Acrylamide (AA) is a common chemical, produced during food processing and widely used in various industries and laboratory processes. Thus, AA causes a significant risk for human and animal health. Recently published studies have suggested that reproductive toxicity of AA and glycidamide (GA) was mainly due to the oxidative stress which can lead to cell apoptosis. The present experiment was conducted to investigate the effect of oxidative stress on the apoptosis of mouse Leydig (TM3) and Sertoli (TM4) cells induced by AA and its metabolite GA. TM3 and TM4 cells were exposed to AA (10 µM and 1 mM) and GA (1 µM and 0.5 mM) for 24 h. Following the exposure time, the Leydig and Sertoli cells were evaluated for measurement of cell viability, lactate dehydrogenase activity, lipid peroxidation and hydrogen peroxide levels, apoptosis/necrosis rate, and mRNA expression levels of apoptotic genes (caspase3, Bcl-2, Bax, and p53). The present study showed that AA and GA exposure caused decrease in cell viability and increase in excessive oxidative stress and apoptosis in both cell types. In conclusion, our in vitro results demonstrate that oxidative stress probably plays a major role in AA- and GA-induced apoptosis of Leydig and Sertoli cells.

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Arsenic is commonly found in the natural environment and is toxic agent for living organism in many countries in the world. Studies on animal models suggest that exposure to arsenic may cause reproductive toxicity; however, effect of arsenic on reproductive toxicity has still not been clearly described. This study was focused on cytotoxicity, oxidative stress, and the antioxidant defense system induced with exposure to sodium arsenite in Mus musculus Leydig and Sertoli cells. The cells were exposed to two different concentrations of sodium arsenite of 50 ppb (0.4 μM) and 1000 ppb (7.7 μM) for 24, 48, and 72 h. Following the exposure time, cell viability, cell proliferation, and lactate dehydrogenase (LDH) activity were determining using colorimetric method. Also, we evaluated oxidative stress markers such as glutathione (GSH), lipid peroxidation, hydroxyl radical, hydrogen peroxide levels, and cellular enzymatic antioxidants such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-s-transferase, and γ-glutamyl transpeptidase (γ-GT). As a result, sodium arsenite exposure in Leydig and Sertoli cells caused cellular cytotoxicity and downregulated the antioxidant defense system by inducing oxidative stress depending on concentration and time. Furthermore, this study demonstrated that when compared with Sertoli cells, Leydig cells were more affected by arsenite toxicity.

The present study was aimed at determining the oxidative damage caused by sodium arsenite in 3T3 fibroblast cells and the possible protective role of curcumin (Cur) against sodium arsenite toxicity. Embryonic fibroblast cells were exposed to sodium arsenite (0.01, 0.1, 1, and 10 μM) in the presence and absence of Cur (2.5 μM) for 24 hours. Cell viability, cytotoxicity, lipid peroxidation, hydroxyl radical, hydrogen peroxide, antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) and expression levels of antioxidant genes (superoxide dismutase, catalase, and glutathione peroxidase) were measured in embryonic fibroblast cells. Results demonstrated that sodium arsenite directly affects antioxidant enzymes and genes in 3T3 embryonic fibroblast cells and induces oxidative damage by increasing the amount of hydrogen peroxide, hydroxyl radical, and lipid peroxidation in the cell. Furthermore, the study indicated that Cur might be a potential ameliorative antioxidant to protect the fibroblast cell toxicity induced by sodium arsenite. K E Y W O R D S curcumin, embryonic fibroblast, oxidative damage, sodium arsenite

The aim of this study was to investigate the possible therapeutic effects of curcumin