Consistent with in vitro and human research, over 60 studies on animals (including rats, mice, roosters, and rabbits) have found that fluoride adversely impacts the male reproductive system. As demonstrated in the excerpts below, these studies have repeatedly found the following effects: (1) decreases in testosterone levels; (2) reduced sperm motility; (3) altered sperm morphology; (4) reduced sperm quantity; (5) increased oxidative stress; (6) and reduced capacity to breed.

While most of the 60 animal studies have used high doses of fluoride, some of the studies have found effects at dosages that would produce blood fluoride levels far lower than the fluoride levels used in vitro. (See, e.g., Sun 2010; Dvoráková-Hortová 2008; Sharma 2008; Reddy 2007; Gupta 2007; Pushpalatha 2005). Moreover, in one of the few studies to monitor blood fluoride concentrations throughout the study, a team of Mexican researchers found that blood fluoride levels of 0.2 to 0.26 ppm for eight weeks caused increased oxidative stress, reductions in sperm motility, and reduced fertility in male rats.  (Izquierdo-Vega 2008). The lower-dose animal studies thus suggest that short-term in vitro studies are less sensitive for detecting fluoride effects than long-term animal studies.

Although some animal studies have not found any effects of high fluoride dosages on the male reproductive system, these studies represent the distinct minority in the field. (Sprando & Collins 1996, 1997, and 1998). One possible explanation for this discrepancy are potential differences in the nutritional health of the animals. As has been demonstrated in many other areas of fluoride research, nutritional deficiencies (e.g., protein) have been found to unequivocally exacerbate fluoride’s reproductive effects, and nutritional supplementation (e.g., protein or anti-oxidants such as vitamin C) has been found to significantly prevent or ameliorate these effects. These findings thus raise the concern that the most vulnerable populations in society (i.e., the poor and malnourished) will be most susceptible to suffering reproductive toxicity from fluoride exposure.

Animal Studies on Fluoride & Male Reproductive System:

“In Group III (fed on sodium fluoride) significant decrease in sperm count (P < 0.001), motility (P < 0.001), progressive motility (P < 0.01), and epididymal weight (P < 0.05) compared to control was seen that was also evident on testicular histology. With vitamin D supplementation, there was a significant improvement in the sperm count (P<0.001), motility (P<0.01), and progressive motility (P<0.05) but remained significantly lower than the control values. With vitamin E supplementation there was significant improvement in the sperm count near normal.”
SOURCE: Kumar N, et al. (2012). To Study the Effect of Vitamin D and E on Sodium-Fluoride-induced Toxicity in Reproductive Functions of Male Rabbits. Toxicology International 19(2):182-87.

“Exposure to fluoride can induce low sperm quality; however, little is known about the molecular mechanisms by which fluoride exerts its toxic effects. This study was conducted to evaluate ultrastructure, oxidative stress, and apoptosis in sperm of mice treated with 150 mg/l NaF for 49 days. Furthermore, microarray analysis was also utilized to characterize the effects of fluoride in gene expression profiling on mice sperm. An increased ROS and a decreased TAC accompanied with distinct morphological changes and significant apoptosis were observed in mice sperm from the fluoride group. Fluoride exposure also significantly elevated the protein expressions of cytochrome c and active caspase-3. In global gene expression profiling, 34 up-regulated and 63 down-regulated genes, which are involved in several sperm biological processes including signal transduction, oxidative stress, apoptosis, electron transport, glycolysis, chemotaxis, spermatogenesis, and sperm capacitation, were significantly differentially expressed. Based on these findings, it was proposed that oxidative stress induced by excessive ROS may trigger sperm apoptosis through mitochondrial impairment, resulting in decreased fertility in mice exposed to fluoride. Microarray analysis also provided several important biological clues for further investigating fluoride-induced damage in sperm morphology and functions.”
SOURCE: Sun Z, et al. (2011). Fluoride-induced apoptosis and gene expression profiling in mice sperm in vivo. Arch Toxicol. 85(11):1441-52.

“The present study demonstrates that fluoride hampers the reproductive functions of male rabbits and is proportional to the duration of fluoride exposure.”
SOURCE: Kumar N, et al. (2010). Effect of duration of fluoride exposure on the reproductive system in male rabbits. J Hum Reprod Sci. 3:148-52.

“A total of 20 Kunming mice at the age of 20 days were divided into four groups randomly. The mice in each group were respectively fed with water containing 0, 50, 100 and 150 mg/L sodium fluoride for 120 d. The lesions of testicular tissue induced by fluoride were verified using paraffin-tissue sections. The results showed that fluoride had great effects on testicular tissue,which were as follows: the wall of convoluted tubule was disrupt, the structure of that was disordered; sperm cells and secondary spermatocytes were shed from seminaferous epithelium; vacuolated changes were found from cytoplasm and nucli of spermatocytes;cellular micronuclei frequency was higher; and deformed sperms were also found.”
SOURCE: Wu PF, et al. (2010). Morphologic observation of mouse testicular tissue lesions induced by fluorine. Animal Husbandry and Feed Science. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-NMXK201004011.htm

“The aim of this study was to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. . . . Spermatozoa from fluoride-treated rats exhibited a significant increase in the generation of ROS, accompanied by a significant increase in NADPH oxidase activity. The increase in ROS generation was significantly diminished by diphenylene iodonium, an inhibitor of NADPH oxidase activity. In contrast, a decrease in the generation of ROS, an increase in SOD activity and the prevention of TBARS formation process were observed in spermatozoa of rats exposed to fluoride plus a-tocopherol. Finally, a-tocopherol treatment prevented the IVF incapacity observed in the spermatozoa from fluoride-treated rats. These results suggest that NADPH oxidase participates in the oxidative stress damage caused by subchronic exposure to fluoride.”
SOURCE: Izquierdo-Vega JA, et al. (2010). NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of a-tocopherol. J Appl Toxicol. 2010 Nov 19. doi: 10.1002/jat.1600. [Epub ahead of print]

“Sperm hyperactivation is crucial for a successful fertilization . . . . The purpose of this study was to investigate the effect of sodium fluoride (NaF) on sperm hyperactivation, Ca2+/CALM-CAMK2 signaling, and CatSper1 and CatSper2 mRNA expression in mice sperm. . . . The results showed that NaF reduced the sperm hyperactivated motility in a dose-dependent manner. Compared with the controls, intracellular Ca2+ concentration and CAMK2 protein were significantly decreased in mice treated with 70 and 150 mg NaF/l, while no effect on CALM was determined in all treatment groups. Furthermore, decreased sperm CatSper1 mRNA expression was also observed in response to middle and higher doses of NaF (70, 150 mg/l) with comparison to the control group, whereas no change in the mRNA expression of CatSper2 was detected in NaF administrated groups. Treatment with 30 mg NaF/l exhibited slight effects on the above indexes with no statistical difference. These findings indicated that exposure to 70 and 150 mg/l NaF for 49 days could result in low hyperactivation via alteration of Ca2+ signaling pathway involving CatSper1 in sperm from mice.”
SOURCE: Sun Z, et al. (2010). Effects of sodium fluoride on hyperactivation and Ca2+ signaling pathway in sperm from mice: an in vivo study. Arch Toxicol. 84(5):353-61.

“Increasing infertility, due to pathological changes on sperm, has become a serious issue. Eco-toxicological effect of rising concentration of fluorides can be enhanced in the presence of aluminium ions by forming fluorometallic complexes, analogues of phosphate groups that interfere with the activity of G-proteins and P-type ATPases, which are part of several signalling pathways during sperm maturation. In order for sperm to gain fertilizing ability, they must undergo in the female reproductive tract, capacitation that includes tyrosine phosphorylation and consequent actin polymerization. The present paper reports the findings of 3-month oral toxicity in mice of fluorides at the concentrations 0, 1, 10, and 100ppm and their synergic action with aluminium at dose of 10ppm. There were no mortalities, clinical signs of discomfort or body weight loss during the experiment. The analysis revealed, for the concentrations of 10 and 100ppm, abnormalities of spermatogenesis and ability of epididymal spermatozoa to capacitate in vitro, as the result of decreased sperm head tyrosine phosphorylation and actin polymerization. The enhancing overload caused by fluorides represents a potential factor, having an impact on function of sperm, hence contributing to a growing infertility in the human population.”
SOURCE: Dvoráková-Hortová K, et al. (2008). The influence of fluorides on mouse sperm capacitation. Anim Reprod Sci. 108(1-2):157-70.

“The aim of the study was to evaluate the effect of environmentally relevant doses of fluoride on in vitro fertilization (IVF) capacity of spermatozoa, and its relationship to spermatozoa mitochondrial transmembrane potential (DeltaPsi(m)). . . . Spermatozoa from fluoride-treated rats exhibited a significant decrease in SOD activity (~33%), accompanied with a significant increase in the generation of O(2)() (~40%), a significant decrease in DeltaPsi(m) (~33%), and a significant increase in lipid peroxidation concentration (~50%), relative to spermatozoa from the control group. Consistent with this finding, spermatozoa from fluoride-treated rats exhibited altered plasmatic membrane. In addition, the percentage of fluoride-treated spermatozoa capable of undergoing the acrosome reaction was decreased relative to control spermatozoa (34 vs. 55%), while the percentage fluoride-treated spermatozoa capable of oocyte fertilization was also significantly lower than the control group (13 vs. 71%). These observations suggest that subchronic exposure to fluoride causes oxidative stress damage and loss of mitochondrial transmembrane potential, resulting in reduced fertility.”
SOURCE: Izquierdo-Vega JA, et al. (2008). Decreased in vitro fertility in male rats exposed to fluoride-induced oxidative stress damage and mitochondrial transmembrane potential loss. Toxicol Appl Pharmacol. 230(3):352-7.

“The healthy, adult male rats (Rattus norvegicus) were treated with fluoride water (F.W.+5.8 ppm), F.W.+ ascorbic acid and F.W. + vitamins (C, D) and Ca+2 for 60 days. Fluoride water ingestion to rats for 60 days resulted in significant reduction of seminal vesicle weight, sperm motility and sperm density of cauda epididymis and testis as compared to control values. The level of testosterone diminished significantly leading to reduced fertility and numbers of litters. The total erythrocytes number, hemoglobin and haematocrit value declined. The concentration of protein, fructose and ascorbic acid decreased, whereas, the cholesterol concentration of testis and enzyme activity of acid phosphatase increased significantly (P<0.001) as compared to control value. The exogenous feeding of ascorbic acid and vitamin C, vitamin D and calcium along with fluoride water for 60 days caused recovery in all altered parameters studied including circulating level of testosterone, blood physiology, sperm function and fertility. The data suggest that ascorbic acid and vitamin C, vitamin D and Ca +2 treatment can play a prophylactic role to maintain normal physiology in fluoride toxicity.”
SOURCE: Sharma JD, et al. (2008). Amelioration of fluoride toxicity in rats through vitamins (C, D) and calcium. Toxicology International 15:111-6. Available from: http://www.toxicologyinternational.com/text.asp?2008/15/2/111/63167

“Objective: To investigate the adverse effect of chronic fluorosis on the testicular structure of rats testis and the antagonism of taurine-zinc. Methods 30 male Wistar rats were randomly divided into 5 groups (6 in each) and treated with fluoride and taurine-zinc through drinking water: control, low fluorine (LF, 100 mg NaF/L), high fluorine (HF, 200 mg NaF/L), low fluorine plus Zn(LF+Zn), high fluorine plus Zn (HF+Zn). After 5 months of fluoride treated, the rats in LF+Zn and HF+Zn groups were given taurine-zinc (0.34 g/L) by added in the drinking water for another month. Six months later, the testicle structure in all groups was examined under the microscope. Results: In LF group, the loosened testicular gland and interstitial edema were seen. In HF group, primary spermatocyte became smaller and sperm head disappeared. However, in LF+Zn and HF+Zn groups there were no so significant damages, the changes were similar to normal testis. Conclusion: Chronic fluorosis can cause testis damage and taurine-zinc presents an obvious ameliorative effect in rats.”
SOURCE: Chen SJ, et al. (2008). Testis damage induced by chronic fluorosis and antagonism of taurine-zinc. Journal of Environment and Health. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-HJYJ200801019.htm

“Sodium fluoride (NaF), a widespread natural pollutant was given to sperm-positive female rats throughout gestation and lactation at a dose of 4.5 and 9.0 ppm via drinking water. The neonates were allowed to grow up to 90 days on tap water, and then sperm parameters, testicular steroidogenic marker enzyme activity levels, and circulatory hormone levels were studied. The sperm count, sperm motility, sperm coiling (hypoosmotic swelling test), and sperm viability were decreased in experimental rats when compared with controls. The activity levels of testicular steroidogenic marker enzymes (3beta hydroxysteroid dehydrogenase and 17beta hydroxysteroid dehydrogenase) were significantly decreased in experimental animals indicating decreased steroidogenesis. The serum testosterone, follicle stimulating hormone and luteinizing hormone levels were also significantly altered in experimental animals. Our data indicate that exposure to NaF during gestation and lactation affects male reproduction in adult rats by decreasing spermatogenesis and steroidogenesis.”
SOURCE: Reddy PS, et al. (2007). Suppression of male reproduction in rats after exposure to sodium fluoride during early stages of development. Naturwissenschaften. 2007 Jul;94(7):607-11.

“The present study was undertaken to evaluate the effect of fluoride toxicity on the reproductive system of male rats. Sexually mature male Wistar rats were exposed to 2, 4, and 6 ppm sodium fluoride in their drinking water for 6 months ad libitum. Sperm motility and density in cauda epididymis were assessed. Biochemical and histological analysis were performed in reproductive organs. Fluoride treatment brought about a significant decrease in the weight of testis, epididymis, and ventral prostate. The sperm motility and density were significantly reduced. There was a marked reduction in the number of primary spermatocyte, secondary spermatocyte, and spermatids. The Sertoli cell counts and their cross sectional surface areas were significantly decreased. The Leydig cell nuclear area and the number of mature Leydig cells were also significantly decreased. The protein content of the testis and epididymis were significantly reduced. Fructose in the seminal vesicles and cholesterol in testes were increased significantly. In conclusion, sodium fluoride administrated in drinking water of 2, 4, and 6 ppm concentration for 6 months to male rats adversely affected their fertility and reproductive system.”
SOURCE: Gupta RS, et al. (2007). The toxic effects of sodium fluoride on the reproductive system of male rats. Toxicol Ind Health. 23(9):507-13.

“Fluoride contamination of drinking water can disrupt male gametogenesis and steroidogenesis and induce testicular oxidative stress. Treatment of rats with sodium fluoride at the dose of 20 mg/kg/day for 28 days resulted in significant diminution of testicular Delta5,3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-hydroxysteroid dehydrogenase (HSD) activities and low plasma levels of testosterone, follicular stimulating hormone (FSH) and leutinizing hormone (LH). Spermatogenesis inhibited after sodium fluoride treatment has been assessed here by the quantification of different generation of germ cells like spermatogonia A (ASg), preleptotene spermatocyte (PLSc), midpachytene spermatocyte (MPSc) and step 7 spermatid (7Sd) at stage VII of seminiferous epithelial cycle. Furthermore, fluoride treatment was associated with low activities of testicular, prostatic and epididymal catalase (CAT), superoxide dismutase (SOD) and peroxidase along with elevation of malondialdehyde (MDA) and conjugated dienes (CD) in those tissues. Co-administration of calcium and Vitamin-E with fluoride resulted in a significant recovery from testicular disorders and oxidative stress in the testis and male accessory sex organs. The results of this study demonstrate that fluoride exposure, at the dose available in drinking water in contaminated areas, led to inhibition of testicular gametogenesis and steroidogenesis in association with oxidative stress in the testis and male accessory sex organs, which are protected significantly by dietary agents like Vitamin-E and calcium.”
SOURCE: Sarkar SD, et al. (2006). Management of fluoride induced testicular disorders by calcium and vitamin-E co-administration in the albino rat. Reprod Toxicol. 22(4):606-12.

“The [fluoride-induced] decrease in sperm motility appears to be related to decline in SMAI and abnormal sperm counts. The significant decrease in sperm viability along with the above parameters would be expected to affect fertility, whereas inhibition of hyaluronidase and to some extent of acrosin could affect fertilizing capacity of the sperm. The results reveal that dietary factors such as increased protein intake can be especially valuable in curbing fluoride fertility toxicity.”
SOURCE: Chinoy NJ, et al. (2006). Effects of fluoride ingestion with protein deficient or protein enriched diets on sperm function of mice. Fluoride 39:11-16.

“To ascertain the effect of chronic fluorosis on rooster sperm quality, chronic fluorosis model of roosters was rebuilt artificially by adding F- to the drinking water. In the 30th, 50th and 70th day, sperms of each animal were collected and the sperm density, sperm vigour and sperm abnormality rate were determined. [Results]: Chronic fluorosis may cause the reduction of sperm density and sperm vigour and raise of sperm abnormality rate. The control group has no discrepancy in different testing time. In the experimental group, sperm density of the 50th and 70th day is lower than 30th day, but there is no statistics discrepancy between the 50th and 70th day; and sperm vigour of the 70th day is lower than the 30th day . . . .”
SOURCE: Cai Z. (2006). Determination the changes of rooster sperm quality induced by chronic fluorosis. Livestock and Poultry Industry. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-XQYI200612009.htm

“In the fluorine group and cadmium group, the contents of lipid peroxide noticeably increased and the conternts of glutathione peroxidase (GSH-Px) were remarkably reduced in the testicle of rats . . . .”
SOURCE: Mou S, et al. (2006). Effect of fluorine, selenium and cadmium
on lipid peroxide and microelements in rat’s testicle. Chinese Journal of Public Health. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZGGW200603045.htm

“Semen analysis including sperm morphology assessment has been suggested to be a useful indication of the factors in man’s macro-environment, which can modulate or damage spermatogenesis (Mac Leod & Gold 1953). The present study was aimed to determine the reproductive toxic effects of male rat after ingestion of NaF [4.5-9 ppm] through drinking water. The route chosen in this study for exposure was via drinking water to mimic human exposure and to reflect the impact on fertility, after chronic ingestion. The decreased sperm number and motility observed in experimental rats might be responsible for decreasing male fertility. Decrease in male reproductive potential was observed in rats and rabbits after exposure to fluoride (Kumar & Susheela 1994, 1995; Narayana & Chinoy 1994; Zhang et al. 2000; Collins et al. 2001). Besides decreased sperm count, sperm motility, the sperm viability and HOS sperm coiling percentages were also adversely affected in NaF-exposed rats. These changes were greater in rats exposed to higher dose of NaF. The decreased testicular steroidogenic enzyme activity levels may lead to decreased steroidogenesis in experimental rats, which in turn may suppress the reproductive activities in the male rats.”
SOURCE: Pushpalatha T, et al. (2005). Exposure to high fluoride concentration in drinking water will affect spermatogenesis and steroidogenesis in male albino rats. Biometals 18:207-12.

“The results of our experiment suggests that fluoride at the dose noted in drinking water in contaminated areas may induce oxidative stress in reproductive and metabolic organs that can be ameliorated significantly by testosterone or vitamin E coadministration. Moreover, as there was no significant variation in body weights among these groups, it may be predicted that this effect of fluoride on reproductive and metabolic organs is specific and is not due to general effect of fluoride.”
SOURCE: Das S, et al. (2005). Induction of oxidative stress on reproductive and metabolic organs in sodium fluoride-treated male albino rats: protective effect of testosterone and vitamin e coadministration. Toxicol Mech Methods. 15(4):271-7.

“The content of NaF in testis and the ratio of apoptotic spermatogenic cell in fluoride treatment groups significantly increased with increased experimental dosage and prolonged experimental period (P < 0.05). Meanwhile, the serum estradiol level significantly decreased (P < 0.05), which was negatively correlated with the content of NaF in testis as well as the ratio of apoptotic spermatogenic cell (P < 0.05). CONCLUSION: Excessive fluoride could lead disturbance to serum estradiol level during some range of dose and time, which is an important factor to spermatogenic cell apoptosis.”
SOURCE: Jiang CX, et al. (2005). [Relationship between spermatogenic cell apoptosis and serum estradiol level in rats exposed to fluoride]. Wei Sheng Yan Jiu. 34:32-4.

“In [fluoride] treated groups there were significant decreases in the sperm count and the rate of sperm motility (P 0.05), while the rate of sperm deformity increased (P 0.05) compared with the control group. Conclusions By inhibiting the expression of PCNA, NaF may decrease the count of germ cells and then damage the male reproductive system.”
SOURCE: Jiang Q, et al. (2005). Effect of fluoride on expression of proliferating cell nuclear antigen in germ cells of rats’ testes. Chinese Journal of Endemiology. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZDFB200505017.htm

“These data suggest that a zinc-enriched diet protects seminiferous tubules against fluoride toxicity by preventing the fluoride-induced testicular zinc deprivation.”
SOURCE: Krasowska A, et al. (2004). Zinc protection from fluoride-induced testicular injury in the bank vole (Clethrionomys glareolus). Toxicology Letters 147: 229-235.

“Conclusions: 200 or 300 mg/L sodium fluoride in drinking water can significantly decrease sperm count and mobility of male mice. Vitamin E was given while administrated with NaF, but effects on mice were not improved.”
SOURCE: An L, et al. (2004). Combined effects of vitamin E and fluoride on reproductive function in male mice. Chinese Journal of Control of Endemic Disease. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-DYBF200403001.htm

“Objective: To study the effects of excessive fluorine on reproductive system of male rats.Methods Sodium fluoride was administered to male rats with drinking water (150 mg/L) for 10 weeks. The sperm count, the rates of sperm mobility and aberration, the levels of biochemical marker enzyme of testis and epididymidis, as well as the levels of gonadal hormone in serum, were examined. And pathological alterations of testes were observed. Results: Contrasted with control rats, the sperm count, the rate of sperm mobility, as well as the levels of serum testosterone (T) and luteinizing hormone (LH), were suppressed by fluoride. While the rate of sperm aberration was elevated. The differences between two groups were significant ( P 0.05). Pathological alterations of testes were also found. Conclusions: The long-term exposure to fluorine of high dose could produce toxic effect on male reproductive system.”
SOURCE: Cui LX, et al. (2003). Experimental study on effect of fluoride on reproductive system of male rats. Chinese Journal of Endemiology. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZDFB406.007.htm

“This study examined the effect of sodium fluoride, a water pollutant important through the world, including India, on testicular steroidogenic and gametogenic activities in relation to testicular oxidative stress in rats. Sodium fluoride treatment at 20mg/kg/day for 29 days by oral gavage resulted in significant diminution in the relative wet weight of the testis, prostate, and seminal vesicle without alteration in the body weight gain. Testicular delta(5),3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities were decreased significantly along with significant diminution in plasma levels of testosterone in the fluoride-exposed group compared to the control. Epididymal sperm count was decreased significantly in the fluoride-treated group and qualitative examination of testicular sections revealed fewer mature luminal spermatozoa in comparison to the control. The seminiferous tubules were dilated in treated animals. Fluoride treatment was associated with oxidative stress as indicated by an increased level of conjugated dienes in the testis, epididymis, and epididymal sperm pellet with respect to control. Peroxidase and catalase activities in the sperm pellet were decreased significantly in comparison to the control. The results of this experiment indicate that fluoride at a dose encountered in drinking water in contaminated areas exerts an adverse effect on the male reproductive system and this effect is associated with indicators of oxidative stress.”
SOURCE: Ghosh D, et al. (2002). Testicular toxicity in sodium fluoride treated rats: association with oxidative stress. Reproductive Toxicolology 16(4):385.

“To study the mechanisms of the antagonistic action of selenite on fluoride-induced male reproductive damages, and find out the optimal level of selenite in drinking water against fluoride toxicity… Results: Fluoride could cause the elevation of fluorine concentrations in blood and urine, the abnormalities of trace elements in serum and testis, as well as the significant increase of lipid peroxide (LPO) levels, and the obvious decreases of activities of glutathione peroxidase (GSH-Px) and ATPase in testis and epididymis of rats exposed to fluoride in drinking water (68 mg/L).”
SOURCE: Yang KD, et al. (2002). [Study on antagonistic effects of selenite on fluoride-induced impairments of testis and epididymis in rats]. Chung-Kuo Kung Kung Wei Sheng 18: 427-9.

“The effects of sodium fluoride (NaF) ingestion (10 mg NaF/kg body weight) and the possible therapeutic effects of ascorbic acid (AA, 15 mg/animal/day) and/or calcium phosphate (Ca, 25 mg/animal/day) on the reproductive functions and fertility of male mice were investigated. NaF-ingestion brought about a significant decline in sperm acrosomal acrosin and hyaluronidase. Cauda epididymal sperm stained with alcoholic acidic silver nitrate reagent revealed acrosomal damage and deflagellation. However, sperm nuclear integrity was not affected by the treatment. The reduced activity of the enzymes as well as the structural and metabolic alterations in the sperm led to a significant decrease in sperm count, and motility and live:dead ratios but an increase in abnormal sperm which ultimately lead to a poor fertility rate. The cessation of NaF-treatment was not conducive to bringing about a complete recovery. However, the administration of AA or Ca to NaF-treated mice revealed significant recovery from fluoride toxicity in all the above parameters.”
SOURCE: Chinoy NJ, Sharma A. (2000). Reversal of fluoride-induced alteration in cauda epididymal spermatozoa and fertility impairment in male mice. Environmental Sciences 7: 29-38.

“Sexually mature male Swiss mice were exposed at 60 days of age to 100, 200 and 300 ppm sodium fluoride (NaF) in their drinking water for 4 weeks or 10 weeks. The effect of NaF exposure on fertility was assessed by breeding these males with untreated female mice after the exposure periods. Fertility was significantly reduced at all three concentrations by exposure for 10 weeks but not for 4 weeks. The number of implantation sites and viable fetuses was significantly reduced in females mated with males that had ingested NaF at a concentration of 200 ppm for 10 weeks. Relative weights of seminal vesicles and preputial glands were significantly increased in mice exposed to 200 and 300 ppm NaF for 4 weeks but not in mice exposed for 10 weeks. These results indicate that long-term ingestion of NaF adversely affects fertility in male mice.”
SOURCE: Elbetieha A, et al. (2000). Fertility effects of sodium fluoride in male mice. Fluoride 33: 128-134.

“Conclusion: The sperm aberration rate of mice were significantly increase after drinking high fluoride water [50 + 100 mg/l F].”
SOURCE: Lu Y, et al. (2000). Effect of water defluoridation by activated magnesia on sperm morphology in mice. Chinese Journal of Control of Endemic Diseases. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-DYBF200003002.htm

“The protective effect of ascorbic acid [vitamin C] at a dose level of 1.0mg/L in drinking water against the fluoride induced damage on reproductive system of rat was studied.150 mg/L sodium fluoride (NaF) in drinking water of male rat can cause significant decreases in sperm count and mobility, increases in serum and testicular lipid peroxides (LPO) contents, and depress the adenosine triphosphatase (ATPase) activity in epididymis. All of these effects are reversible by adding adequate ascorbic acid in drinking water simultaneously. The effects of ascorbic acid against fluoride induced damages are similar to those produced by 2.0 mg/L selenium in the drinking water of rats. However, no significant recovery of fluoride-induced effects on GSH Px activities in the tissues of testis and epididymis were observed in the ascorbic acid and fluoride group. The mechanism of ascorbic acid on fluoride induced damage of male reproductive system needs to be further studied.”
SOURCE: Zhu X. (2000). The primary study of antagonism of selenium on fluoride induced reproductive toxicity of male rat. China Public Health. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZGGW200008013.htm

“These results clearly indicate that protein supplementation is beneficial to overcome the toxic effects of fluoride on testicular steroidogenesis, protein, carbohydrate, and energy and oxidation metabolisms in the reporductive organs of male mice. Protein deficiency, on the other hand, aggravates fluoride toxicity. A protein-supplemented diet might therefore substantially mitigate certain fluoride-induced health hazards in humans living in endemic areas.”
SOURCE: Chinoy NJ, Mehta D. (1999). Effects of protein supplementation and deficiency on fluoride-induced toxicity in reproductive organs of male mice. Fluoride 32: 204-214.

“Studies on the beneficial effects of vitamins E and D supplementation on functions of caput and cauda epididymides, their spermatozoa, vas deferens and seminal vesicle of sodium fluoride (NaF) treated male mice were carried out. The NaF treatment resulted in significant decrease in the body and epididymis weight but those of vas deferens and seminal vesicle were not affected. NaF treatment brought about alterations in epididymal milieu as elucidated by the significant decrease in levels of sialic acid and protein as well as activity of ATPase in epididymides. As a result, the sperm maturation process was affected leading to a significant decline in cauda epididymal sperm motility and viability. This caused a significant reduction in fertility rate. The cauda epididymal sperm count was also significantly reduced. The data obtained suggest that fluoride treatment induced significant metabolic alterations in the epididymides, vas deferens and seminal vesicles of mice.”
SOURCE: Chinoy NJ, Sharma A. (1998). Amelioration of fluoride toxicity by vitamin E and D in reproductive functions of male mice. Fluoride 31: 203-216.

“Conclusions: The modification of some parameters related to fertility by the repeated oral NaF intake, in rodents, suggest that NaF has potential to disturb male fertility.”
SOURCE: Pinto R, et al. (1998). NaF may disturb male fertility in rodents. Toxicology Letters 95(Suppl 1): 214.

“The cauda epididymal spermatozoa were highly sensitive to the effects of sodium fluoride as their structural and metabolic alterations led to marked decreases in their motility, live:dead ratio and sperm mitochondrial activity index but increases in sperm abnormalities and alterations in sperm membrane phospholipids, particularly phosphatidylinositol and phosphatidyl serine. The activities of ATPase and succinate dehydrogenase as well as glutathione levels were decreased in testis by sodium fluoride treatment, revealing disturbances in its metabolism.”
SOURCE: Chinoy NJ, et al. (1997). Fluoride toxicity in the testis and cauda epididymis of guinea pig and reversal by ascorbate. Medical Science Research 25: 97-100.

“The toxic effects were evaluated of sodium fluoride (NaF) ingestion on the physiology of tissue components of testis and epididymis of adult, male albino rats, and the possible reversal of the effects by use of some antidotes. The results revealed that the testis and cauda epididymal proteins were altered, with disappearance of some proteins and induction of some new ones. This is the first report of such changes… On comparing the alterations in protein profile, phospholipds and glutathione in both tissues, it was evident that the protein profile was disturbed more in testis than in cauda epididymis, whereas phospholipids and gluthathione levels were affected more in cauda than in testis… As the proteins of testis and cauda epididymis are known to be involved as androgen carrier proteins, in testicular functions and in sperm motility, it follows that NaF treatment might affect the levels of these proteins as well as alter sperm motility and viability.”
SOURCE: Chinoy NJ, et al. (1997). Fluoride toxicity on rat testis and cauda epididymal tissue components and its reversal. Fluoride 30: 41-50.

“At 16 weeks, the [High-Fluoride] males had a significantly lower mean testes weight than the [Low-Fluoride] males: 1.10 ± 0.11 vs. 1.32 ± 0.18 g, respectively (p < 0.002). The reason for this is not clear.”
SOURCE: Luke J. (1997). The Effect of Fluoride on the Physiology of the Pineal Gland. Ph.D. Thesis. University of Surrey, Guildford. p. 177.

“The present communication addresses the effect of chronic fluoride toxicity on the structure of rabbit Leydig cells using light, scanning and transmission electron microscopy… [T]he extensive degenerative changes (which are progressive) seen in the Leydig cells due to fluoride toxicity may lead to a decrease in testosterone production resulting initially in regression of seminiferous tubules and structural damage of the epididymis and finally cessation of spermatogenesis.”
SOURCE: Susheela AK, Kumar A. (1997). Ultrastructural studies on the leydig cells of rabbits exposed to chronic fluoride toxicity. Environmental Sciences 5:79-94.

“The key point is that high dosage of fluoride may cause testicular lipid peroxidation, wheareas the selenium possesses the antagonistic action against the lipid peroxidation resulting from fluoride.”
SOURCE: Yang K, et al. (1996). Study on effects of selenium on lipid peroxidation and trace elements changes induced by fluorine and selenium in tissue of rat testis. http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZWSX605.008.htm

“The [fluoride] treatment resulted in structural and metabolic alterations in sperm, leading to low sperm motility, a low sperm mitochondrial activity index (SMAI), reduced viability (live:dead ratio), and changes in sperm membrane phospholipids (particularly phosphatidylinositol, phosphatidylserine and phosphatidylethanolamine, which would affect hormone receptor interaction and their functions). A significant reduction in electrolyte levels of sperm also occurred which would also affect their viability. The protein levels in cauda epididymal sperm suspension, vas deferens, seminal vesicle and prostate were significantly decreased after NaF administration, which may be due to altered protein metabolism by interference of fluoride ions. The changes in epididymal protein profile, with absence of some proteins and induction of some new ones, were probably a result of the “stress proteins” in NaF-treated rats affecting the structural and functional integrity of sperm. Glycogen accumulation in vas deferens and a decrease in fructose in seminal vesicles and vas deferens indicated disturbances in carbohydrate metabolism in these organs. However, withdrawal of treatment resulted in partial recovery. A significant recovery from NaF-induced toxic effects occurred following administation of ascorbic acid and/or calcium, while combined treatment (AA + Ca++) for 70 days manifested a synergistic effect. The transient fluoride-induced effects were reversible. The results, corroborated by earlier data from our laboratory, show that fluoride has a definite effect on male reproduction and fertility. Ascorbic acid and calcium are proposed as therapeutic agents in endemic populations for amelioration of effects of fluoride.”
SOURCE: Chinoy NF, et al. (1995). Amelioration of fluoride toxicity in some accessory reproductive glands and spermatozoa of rat. Fluoride 28: 75-86.

“Results showed that the serum testosterone level had decreased with time in rats drinking water containing 100 and 200 mg/L fluoride. [T]estis cholesterol level did not change . . . . Results suggest that fluoride may have some harmful effects on the reproductive system in male rats.”
SOURCE: Zhao ZL, et al. (1995). The influence of fluoride on the content of testosterone and cholesterol in rat. Fluoride 28: 128-130.

“The therapeutic effects of ascorbic acid and calcium (Ca2+) supplementation on reproductive functions of fluoride-treated (10 mg/kg body weight) male rats were investigated. Sodium fluoride treatment resulted in a decrease in almost all parameters studied except concentration of testicular cholesterol, which implies that androgen synthesis might not be affected by NaF treatment. Succinate dehydrogenase activity decreased in testis suggesting that its oxidative metabolism was altered by NaF treatment. Adenosine triposphatase activity, protein, and sialic acid levels in caput and cauda epididymides also showed a decrease. All these changes resulted in a significant decrease in sperm motility and thereby fertility rate.”
SOURCE: Chinoy NF, et al. (1994). Beneficial effects of ascorbic acid and calcium on reproductive functions of sodium fluoride-treated prepubertal male rats. Fluoride 27: 67-75.

“OBJECTIVE–To address the role of fluoride in causing defects to spermatids and epididymal spermatozoa. METHODS–Male rabbits were treated with 10 mg NaF/kg body weight daily for 18 months and maintained under identical laboratory conditions along with the control rabbits not given NaF. Testis and epididymis (caput) were investigated for ultrastructural details of spermatids and spermatozoa. RESULTS–A wide variety of structural defects were observed in the flagellum, the acrosome, and the nucleus of the spermatids and epididymal spermatozoa of fluoride-treated rabbits. Abnormalities included absence of outer microtubules, complete absence of axonemes, structural and numeric aberrations of outer dense fibers, breakdown of the fibrous sheath, and structural defects in the mitochondria of the middle piece of the flagellum. Detachment and peeling off of the acrosome from the flat surfaces of the nucleus were also observed. CONCLUSION–The abnormalities observed render the sperm nonfunctional and ineffective, and thus there is a possible role of fluoride in causing infertility.”
SOURCE: Kumar A, Susheela AK. (1994). Ultrastructural studies of spermiogenesis in rabbit exposed to chronic fluoride toxicity. International Journal of Fertility and Menopausal Studies 39(3):164-71.

“The results revealed that the sperm acrosomal hyaluronidase and acrosin were reduced after 50 days of NaF treatment. Sperm stained with acidic alcoholic silver nitrate revealed acrosomal damage and deflagellation, which might be causative factors for the reduced activity of the enzymes. These alterations also resulted in a decline in sperm motility. The cauda epididymal sperm count was decreased, perhaps because of spermatogenic arrest. Thus, the low sperm motility and count ultimately contributed toward reduction in fertility by NaF treatment. However, withdrawal of NaF treatment for 70 days produced incomplete recovery, while administration of ascorbic acid and calcium, individually and in combination, brought about significant recovery of fluoride-induced effects. Thus, the effects of fluoride on sperm structure and metabolism of rats are transient and reversible.”
SOURCE: Narayana MV, Chinoy NJ. (1994). Reversible effects of sodium fluoride ingestion on spermatozoa of the rat. International Journal of Fertility and Menopausal Studies 39(6):337-46.

“In view of reports of infertility among human populations in fluorosis prevailing regions, we investigated the effect of fluoride ingestion on testicular steroidogenesis in rats. Sodium fluoride (NaF) was administered to the rats orally at a daily dose of 10mg/kg bodyweight for 50 days. The treatment did not cause significant change in testicular cholesterol levels, indicating that metabolism was not altered and that there was no hypo/hypercholesterolemic effect. In addition, activities of the intermediary enzymes in androgenesis, viz., 3ß- and 17ß-hydroxysteroid dehydrogenase were only modestly decreased by NaF ingestion. Subsequently, the determination of circulating androgen levels in NaF-treated rats showed a downward trend compared to those of the control group, suggesting alteration in testosterone concentration. The histomorphometric studies revealed significant change in the Leydig cell diameter m correlation with the androgen levels. These results indicate that fluoride does interfere with steroidogenesis in short-term low-dose exposures in rats.”
SOURCE: Narayana MV, Chinoy NJ. (1994). Effect of fluoride on rat testicular steroidogenesis. Fluoride 27: 7-12.

“The results showed that the level of serum testosterone had the tendency to decrease as the period of time was prolonged in the rats drinking water containing 100 mg/L and 200 mg/L fluoride. The level of cholesterol in testis did not change significantly, but in liver it was significantly declined at the fourth and sixth week as compared with the control group. The results suggest that fluoride may have a harmful effect on the reproductive system.”
SOURCE: Zhao Z, et al. (1994). Influence of fluoride on the contents of testosterone and cholesterol. Chinese Journal of Endemiology. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZDFB406.007.htm

“Sodium fluoride was administered to male rats with drinking water for 6 months. The count, morphological change and motility of sperms were examined. The levels of serum testosterone and activity of testicular lactate dehydrogenase were determined, arid the changes of testes in ultrastucture were observed. The results showed that the long-term exposure to fluoride of high dose may produce toxicity effect on male reproductive system.”
SOURCE: Zhen J, et al. (1993). Experimental study on effect of sodium fluoride on reproductive system of male rats. Industrial Health and Occupational Diseases. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-GYWZ199304005.htm

“In fluorotic rats, testicular cholesterol and serum testosterone levels were not affected. However, succinate dehydrogenase activity in testis was inhibited. Similarly, adenosine triphosphatase activity and sialic acid levels in epididymides were also suppressed with more pronounced effect on cauda epididymis. Consequently, sperm motility and count were decreased leading to a significant decline in fertility by fluoride treatment. Hence, rat is also sensitive to fluoride toxicity.”
SOURCE: Chinoy NJ, et al. (1992). Effects of fluoride ingestion on the physiology of reproductive organs of male rats. Journal of Environmental Biology 13: 55-61.

“Summary: Sodium fluoride (NaF) fed to adult male albino mice at a dose of 10 mg and 20 mg/kg body weight, caused a significant decrease in sperm county and motility. Scanning electron microscopy and silver nitrte staining showed large numbers of deflagellated spermatozoa, with acrosomal, midpiece and tail abnormalities. The treatment caused loss of fertility rate when normal cycling female mice were mated with treated males.”
SOURCE: Chinoy NJ, Sequeira E. (1992). Reversible fluoride induced fertility impairment in male mice. Fluoride 25 71-76.

“Fifty percent of the 100- and 200 ppm F rats after 16 weeks exhibited histopathologic changes in the germinal epithelium of the testes, which resembled those in Zn-deficient rats. The data suggest that a deprivation of testicular Zn due to a high F intake may be directly responsible for the injury of testicular tubules.”
SOURCE: Krasowska A, Wiostowski T. (1992). The effect of high fluoride intake on tissue trace elements and histology of testicular tubules in the rat. Comparative Biochemistry and Physiology: Part C 103(1):31-4.

“A single microdose (50 micrograms/50 microL) injection of sodium fluoride (NaF) into the vasa deferentia of adult male albino rats (Rattus norvegicus) caused arrest of spermatogenesis and absence of spermatozoa in the lumina of the seminiferous tubules of the testes, which consequently led to a decline in the sperm count in the caudae epididymides. Scanning electron microscopy of cauda and vas deferens sperm revealed deflagellation and tail abnormalities. This is probably related to the alterations in the internal milieu of these organs which rendered the spermatozoa immotile and consequently caused fertility impairment in the experimental animals. Thus microdoses of sodium fluoride were found to affect reproductive function and fertility rate.”
SOURCE: Chinoy NJ, et al. (1991). Microdose vasal injection of sodium fluoride in the rat. Reproductive Toxicolology 5(6):505-12.

“Fluoride was orally administered to rabbits at 10 mg NaF/kg body weight for 18 or 29 months. The animals were then killed and the structure of the testis, epididymis and vas deferens studied under light and scanning electron microscopes. In animals treated for 29 months, the spermatogenic cells in the seminiferous tubules were disrupted, degenerated and devoid of spermatozoa. In animals treated for 18 or 29 months, loss of cilia on the epithelial cells lining the lumen of the ductuli efferentes of the caput epididymidis and of stereocilia on the epithelial cells lining the lumen of the vas deferens was observed. In some regions of the epithelial lining of the lumen of the ductuli efferentes and vas deferens, the boundaries of the cells were not clear and appeared to be peeled off. Mucus droplets were abundant in the vas deferens of control animals, but absent in both the treated groups. Spermatogenesis ceased only in animals treated for 29 months. The difference in the structural changes observed in the testes of the 2 treated groups may have been due to the blood-testis barrier. It is concluded that ingestion of high concentrations of fluoride has harmful effects on the male reproductive system.”
SOURCE: Susheela AK, Kumar A. (1991). A study of the effect of high concentrations of fluoride on the reproductive organs of male rabbits, using light and scanning electron microscopy. Journal of Reproductive Fertility 92(2):353-60.

“The aim of the study was to evaluate relationship between infertility and the histological structure of the testes following the subcutaneous administration of different doses of sodium fluoride (5, 10, 20 and 50 mg/kg/day), for 100 days, to groups of six male albino rabbits; the six control animals were given 1 cc distilled water/kg b.w./day for the same length of time. Deficient maturation and differentiation of the spermatocytes and an increase in the amount of interstitial tissue were found in the experimental animals. In the higher dosage groups, spermatogenesis stopped and the seminiferous tubules became necrotic. The study thus established the existence of a definite relationship between fluorosis and testicular damage.”
SOURCE: Shashi A. (1990). Histopathological changes in rabbit testes during experimental fluorosis. Folia Morphol (Praha) 38(1):63-5.

“The results in this experiment suggest that: interstitial cell of testes could be damaged and spermiogenesis could be blocked [by fluoride exposure]. These might supply a morphologic basis for decrease in serum testosterone level and impairment of reproduction during chronic fluorosis.”
SOURCE: Keqin S, et al. (1990). Ultrastructural observations of testes and prostrate gland in rat with chronic fluorosis. Journal of China Medical University. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZGYK199005005.htm

“The effect of high fluoride intake (100 and 200 ppm) in the ration was studied in male rats. After sixty days of treatment, rats showed a decrease in the mean diameter of the seminiferous tubules and the percentage of the tubules containing spermatozia and increase in the in the thickness of the peritubular membranes. The effect was more prominent with the higher dose of fluoride. Serum testosterone level in rats [which] received 200 ppm fluoride showed a sharp decrease, whereas in those treated with 100 ppm did not differ significantly from the control. The fertility performance of treated rats was reduced and the results revealed a reduction in the number of pregnant females and newborns of both treated groups. Lowest dose of fluoride had a similar but less marked effect on the fertility performance than the higher dose. It is concluded that the high fluoride intake causes a decline in the reproductive performance of the adult male rats, although the clinical signs in the teeth are absent.”
SOURCE: Araibi AA, et al. (1989). Effect of high fluoride on the reproductive performance of the male rat. Journal of Biological Sciences Research 20: 19-30.

“The effects of sodium fluoride (NaF) ingestion in two doses (10 and 20 mg/kg body weight) for 30 days on histology and histocytometry of reproductive organs of the adult male mouse were investigated. In order to study reversibility, treatment was withdrawn for one and two months… NaF treatment caused severe disorganization and denudation of germinal epithelial cells of seminiferous tubules with absence of sperm in the lumina. The Leydig cell and nucleus diameters were not affected. The caput epididymis showed fewer changes than the cauda. However, epithelial cell nuclear pyknosis and absence of luminal sperm were observed. A reduction in epithelial cell height, nuclear pyknosis, denudation of cells, and absence of sperm occurred in the cauda epididymis. The vas deferens epithelium showed nuclear pyknosis, clumped stereocilia, and cell debris but no sperm in the lumen and an increase in the lamina propria. The prostate and seminal vesicles were not affected by treatment. Withdrawal of treatment caused marked recovery in the histoarchitecture of these organs. The effects of NaF treatment are therefore transient and reversible.”
SOURCE: Chinoy NJ , Sequeira E. (1989). Effects of fluoride on the histoarchitecture of reproductive organs of the male mouse. Reproductive Toxicolology 3(4):261-7.

“The serum testosterone decreases significantly and there is a dose response relationship between the level of serum testosterone and fluoride concentration of drinking water. The serum [luteinizing hormone] has no significant change.”
SOURCE: Yuan S. (1989). The influence of fluorosis on the function of pituitary-gonadal axis in rat. Chinese Journal of Endemiology. Available online at: http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZDFB198902002.htm

“Reduction of ingested fluoride in a skulk of silver foxes resulted in the reduction of fluoride burden, decreased neonatal mortality and increased kit production during a two breeding and whelping season period.”
SOURCE: Eckerlin RH, et al. (1988). Ameliorative effects of reduced food-borne fluoride on reproduction in silver foxes. Cornell Veterinarian 78(4):385-91.

“Sixty-six eastern screech-owls (Otus asio) were paired and randomly assigned to dietary treatment groups of 0, 40, or 200 ppm (mg/kg) fluoride (as sodium fluoride) in November 1981. Hatching success was adversely affected at the 200 ppm (mg/kg) level, suggesting potential detrimental impacts to wild populations exposed to fluoride pollution.”
SOURCE: Pattee OH, et al. (1988). Effects of dietary fluoride on reproduction in Eastern Screech-Owls. Archives of Environmental Contamination and Toxicology 17: 213-218.

“Genotoxicity of Sodium fluoride was evaluated in mice in vivo with the help of different cytogenetic assays. The frequency of chromosome aberration was dose – and time – dependent but not exactly route-dependent. Fractionated dosing induced less aberration. Incidence of micronucleus and sperm abnormality increased with dose. Relative sensitivity of the three assays has been found to be: Sperm abnormality > Chromosome aberration > Micronucleus. The present results have revealed the mutagenic property of NaF.”
SOURCE: Pati PC, Bhunya SP. (1987). Genotoxic effect of an environmental pollutant, sodium fluoride, in mammalian in vivo test system. Caryologia 40:79-87.

“The study was designed in order to assess the relationship between infertility and histological structure of testes following administration of varying doses of sodium fluoride. One hundred adult male albino mice were fed 10 ppm (Group A), 500 ppm (Group B) and 1000 ppm (Group C) of sodium fluoride in drinking water. The Group A animals were sacrificed at the end of one month, Group B after two and Group C after three months. The testes were removed and, after being processed in the usual manner, they were stained with hematoxylin and eosin. In Groups B and C, the higher dosage groups, there was a lack of maturation and differentiation of spermatocytes. In animals sacrificed at the end of three months, spermatogenesis had stopped and the seminiferous tubules had become necrotic. A definite relationship between fluorosis and damage to the testes has, therefore, been established by this study.”
SOURCE: Kour K, Singh J. (1980). Histological finding of mice testes following fluoride ingestion. Fluoride 13: 160-162.