Abstract
OBJECTIVE: Investigated the effects of N-acetylcysteine (NAC) on endoplasmic reticulum stress of sertoli cells induced by sodium fluoride (NaF).
METHODS: Rat sertoli cells were exposed to various concentration of (0, 6, 12, 24 µg/ml) sodium fluoride with or without 2 mmol/L NAC for 24 hours. The cell viability was evaluated using trypan blue exclusion test. Intracellular reactive oxygen species (ROS) was measured using the fluorescent probe DCFH-DA. Western blot was used to test the expression of GRP78, PERK and CHOP.
RESULTS: It was found that treatment with NAC (2 mmol/L) restored the reduced cell viability and excessive oxidative stress (P < 0.01). Moreover, fluoride exposure upregulated the expression of GRP7 8, PERK and CHOP protein (P <0. 01 ). NAC was also found to suppress the levels of GRP78, PERK and CHOP expression in NaF-treated cells (p<0.01).
CONCLUSION: Endoplasmic reticulum stress signaling pathways were activated by ROS, and NAC attenuate endoplasmic reticulum stress through inhibiting the levels of ROS in NaF-treated sertoli cells.
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Fluoride-elicited developmental testicular toxicity in rats: roles of endoplasmic reticulum stress and inflammatory response
Long-term excessive fluoride intake is known to be toxic and can damage a variety of organs and tissues in the human body. However, the molecular mechanisms underlying fluoride-induced male reproductive toxicity are not well understood. In this study, we used a rat model to simulate the situations of human exposure
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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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Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPAR?) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity.
Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating
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Effects of sodium fluoride and sulfur dioxide on oxidative stress and antioxidant defenses in rat testes
To assess effects of sodium fluoride and sulfur dioxide on oxidative stress and antioxidant defenses in the testes, 96 sexually mature male Wistar rats were divided randomly into four groups of twenty-four rats each. One group of rats was left untreated as controls, and the other three groups were administered,
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Cell cycle arrest and gene expression profiling of testis in mice exposed to fluoride
Exposure to fluoride results in low reproductive capacity; however, the mechanism underlying the impact of fluoride on male [re]productive system still remains obscure. To assess the potential toxicity in testis of mice administrated with fluoride, global genome microarray and real-time PCR were performed to detect and identify the altered transcriptions.
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Fluoride's Effect on Male Reproductive System: Animal Studies
Over 60 studies on animals (including rats, mice, roosters, and rabbits) have found that fluoride adversely impacts the male reproductive system. 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.
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Fluoride's Effect on Male Reproductive System -- The "Sprando/Collins" Anomaly
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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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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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