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The present study evaluated oxidative stress and apoptosis in Sertoli cells that had been exposed to sodium fluoride (NaF). After TM4 Sertoli cells were exposed to two doses of sodium fluoride (4 ppm and 20 ppm, equivalent to 1.81 mg F/L and 9.05 mg F/L, respectively) in the presence and absence of 50 μM vitamin C for two different exposure periods (24 hr and 48 hr), cell viability, cell proliferation, cytotoxicity, lipid peroxidation, and reactive oxygen species were measured and the apoptosis/necrosis rate was calculated. A significant decrease in the Sertoli cell viability was found with the high dose of NaF (20 ppm). The fluoride ion also caused oxidative damage by increasing cytotoxicity, reactive oxygen species, and lipid peroxidation in a dose- and time-dependent manner. The apoptosis/necrosis rate was significantly increased in both NaF groups. Vitamin C, a strong antioxidant, had a protective effect against the fluoride-induced damage in the Sertoli cells including the increased apoptosis/necrosis rate. In conclusion, the present study showed that oxidative stress plays a possible role in the apoptosis of Sertoli cells induced by NaF, and that these effects can be suppressed with vitamin C. [ABSTRACT FROM AUTHOR]

Background Due to the increased application of titanium dioxide nanoparticles (TiO2 NPs) in the food industry and daily life, their potential toxic effects in humans and animals have been investigated. However, very few studies have focused on testicular oxidative stress and/or apoptosis. Methods In order to understand the possible molecular mechanisms of testicular lesions following exposure to TiO2 NPs, male mice were exposed to 2.5, 5, or 10 mg/kg body weight TiO2 NPs for 90 consecutive days. Testicular oxidative stress and apoptosis were then evaluated, and the testicular mRNA expression of several genes and their proteins involved in oxidative stress and/or apoptosis was investigated. Results TiO2 NPs entered Sertoli cells and caused severe testicular oxidative damage and/or apoptosis, accompanied by excessive production of reactive oxygen species and peroxidation of lipids, proteins and DNA as well as a significant reduction in antioxidant capacity. Furthermore, exposure to TiO2 NPs resulted in the up-regulation of caspase-3, Nrbp2, and cytochrome c expression, and caused down-regulation of SOD, CAT, GPx, GST, GR, Cyp1b1, Car3, Bcl-2, Acaa2, and Axud1 expression in mouse testis. Conclusions TiO2 NPs entered Sertoli cells via the blood-testis barrier and were deposited in mouse seminiferous cord and/or Sertoli cells, causing oxidative damage and apoptosis. [ABSTRACT FROM AUTHOR]