Abstract
OBJECTIVE: To study effects of fluoride on oxidative stress and apoptosis in rat sertoli cells.
METHODS: Intracellular reactive oxygen species (ROS) , malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, mitochondrial membrane potential and percentage of apoptosis were measured after the rat sertoli cells were incubated with 0, 6, 12 and 24 microg/ml sodium fluorides or 24 hours in vitro.
RESULTS: Fluoride decreased the cell activity significantly (P < 0.01). The results suggested that exposure to fluoride significantly increased the level of ROS and MDA content (P < 0.01), fluoride also decreased SOD activity significantly (P < 0.05 or P < 0.01). In addition, with the NaF dose increased, there is a significantly decreasing in mitochondrial membrane potential and a significantly increasing in early apoptosis rate (P < 0.01).
CONCLUSION: Fluoride can induce excessive oxidative stress and increased apoptosis rate in rat sertoli cells.
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Positive PCNA and Ki-67 Expression in the Testis Correlates with Spermatogenesis Dysfunction in Fluoride-Treated Rats.
The present study aimed to evaluate the effect of fluoride (F) on spermatogenesis in male rats. F- at 50 and 100 mg/L was administered for 70 days, after which the testicular and epididymis tissues were collected to observe the histopathological structure under a light microscope. The ultrastructure of the testis and sperm
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Effects of Fluoride on Surface Structure of Primary Culture Leydig Cells in Mouse.
Fluoride (F) is known to induce reproduction toxicity, and the elucidation of its underlying mechanisms is an ongoing research. These findings aim to provide deeper insights into roles of soduim fluoride (NaF) in testis damage, which could contribute to a better understanding of fluoride-induced male reproductive toxicity. The Leydig cells
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Excessive apoptosis and defective autophagy contribute to developmental testicular toxicity induced by fluoride
Fluoride, a ubiquitous environmental contaminant, is known to impair testicular functions and fertility; however the underlying mechanisms remain obscure. In this study, we used a rat model to mimic human exposure and sought to investigate the roles of apoptosis and autophagy in testicular toxicity of fluoride. Sprague-Dawley rats were developmentally
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N-acetylcysteine alleviates fluoride-induced testicular apoptosis by modulating IRE1?/JNK signaling and nuclear Nrf2 activation.
Highlights NaF exposure triggered testicular apoptosis and sex hormonal disruption. NaF exposure increased the expression of ER stress mediators in testis of rat. NAC pretreatment attenuated IRE1?-JNK-mediated apoptosis induced by NaF. The alteration of Nrf2-dependent redox homeostasis was involved in the protective effect of NAC against NaF-induced testicular apoptosis. We previously
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Vitamin E and Lycopene Reduce Coal Burning Fluorosis-induced Spermatogenic Cell Apoptosis via Oxidative Stress-mediated JNK and ERK Signaling Pathways.
Although fluoride has been widely used in toothpaste, mouthwash, and drinking water to prevent dental caries, the excessive intake of fluoride can cause fluorosis which is associated with dental, skeletal, and soft tissue fluorosis. Recent evidences have drawn the attention to its adverse effects on male reproductive system that include
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Fluoride's Effect on Male Reproductive System -- The "Sprando/Collins" Anomaly
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Fluoride's Effect on Male Reproductive System: Animal Studies
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Fluoride's Effect on Male Reproductive System - Human Studies
Consistent with in vitro and animal research, studies of human populations have reported associations between fluoride exposure and damage to the male reproductive system. Most notably, a scientist at the Food & Drug Administration reported in 1994 that populations in the United States with more than 3 ppm fluoride in their water had lower "total fertility rates" than populations with lower fluoride levels.
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Fluoride's Effect on the Male Reproductive System -- In Vitro Studies
Carefully controlled in vitro studies have found that direct exposure of fluoride to the testes or semen inhibits testosterone production and damages sperm. While researchers have known since the 1930s that mega concentrations of fluoride can completely (but reversibly) immobilize sperm, it was not until the 1970s and 1980s that researchers found that relatively modest concentrations of fluoride could cause damage prior to complete immobilization.
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