Abstract

This study examined the effect of oxidative stress on the apoptosis of Sertoli cells induced by sodium fluoride (NaF). Cell viability, reactive oxygen species, malondialdehyde content, superoxide dismutase activity, mitochondrial membrane potential, and apoptosis were measured after the rat Sertoli cells were exposed to various concentrations of (0, 6, 12, and 24??g/ml) sodium fluoride in the presence and absence of 2?mM N-acetylcysteine (NAC) for 24?h. The present study showed that decrease in cell viability and excessive oxidative stress were observed in NaF-treated cells. The treatment with NAC restored the decreased cell viability and excessive oxidative stress. Moreover, fluoride exposure decreased mitochondrial membrane potential and increased apoptosis in Sertoli cells. NAC was also found to suppress a loss of mitochondrial membrane potential and the percentage of apoptosis in NaF-treated Sertoli cells. This study proved that oxidative stress probably play a major role in NaF-induced apoptosis of Sertoli cells.

• Related Studies :

  • Selenium may suppress peripheral blood mononuclear cell apoptosis by modulating HSP70 and regulate levels of SIRT1 through reproductive hormone secretion and oxidant stress in women suffering fluorosis.

    Excessive taking fluoride (F) causes severe damage to reproductive system through stimulation of apoptosis and oxidant stress. Selenium (Se) may promote anti-oxidant enzymes and invert cell apoptosis. The aim of this study was to investigate the effect of Se on peripheral blood mononuclear cell (PBMC) apoptosis and oxidant stress in

  • Protective effect of caffeic acid phenethyl ester (CAPE) on fluoride-induced oxidative stress and apoptosis in rat endometrium

    High fluoride intake may affect biological systems by increasing free radicals, which may enhance lipid peroxidation levels of the tissues, thus leading to oxidative damage. Caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, protects tissues from reactive oxygen species mediated oxidative stress in ischemia-reperfusion and toxic injuries. Several

  • Toxic effects of sodium fluoride on reproductive function in male mice

    To investigate the effects and possible mechanisms of the action of fluoride on testis cell cycle and cell apoptosis in male mice, sexually mature male Kunming mice were exposed to 50, 100, 200, and 300 mg NaF/L in their drinking water for 8 weeks. At the end of the exposure

  • Sodium fluoride activates ERK and JNK via induction of oxidative stress to promote apoptosis and impairs ovarian function in rats

    The toxicity of sodium fluoride (NaF) to female fertility is currently recognized; however, the mechanisms are unclear. Previously, we reported a reduction in successful pregnancy rates, ovarian atrophy and dysfunction following exposure to NaF. The purpose of this study was to elucidate the underlying molecular mechanisms. Female Sprague-Dawley rats (10

  • Fluoride Impairs Ovary Development by Affecting Oogenesis and Inducing Oxidative Stress and Apoptosis in Female Zebrafish (Danio Rerio).

    Highlights Fluoride exposure decreased FSH, LH and VTG levels in ovary of zebrafish. Fluoride exposure altered the transcriptional profiles of oogenesis-related genes. Fluoride exposure increased ROS production in ovary of zebrafish. Fluoride exposure induces oxidative stress in ovary of zebrafish. Fluoride exposure induces apoptosis through both extrinsic and intrinsic

• Related FAN Content :

  • Fluoride content in tea and its relationship with tea quality.

    J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected

  • Fluoride & Oxidative Stress

    A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure

  • 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.

  • 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.

  • Nutrient Deficiencies Enhance Fluoride Toxicity

    It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,