Abstract
The present study evaluated the mechanism underlying the protective effect of sulforaphane (SFN) on cadmium (Cd)-induced Sertoli cell (TM4 cells) injury in mice. The apoptosis rate of cells in each group was detected by flow cytometry. It was determined the effect of SFN on the expression of downstream molecular targets of Nrf2/ARE axis and on the lipid peroxide content. The related genes involved in the nuclear factor E2-related factor 2(Nrf2)/antioxidant response element (ARE) signaling pathway were evaluated by RT-PCR; for example, the mRNA expression levels of Nrf2, heme oxygenase-1 (HO-1), glutathione peroxidase (GSH-Px), quinone oxidoreductase 1 (NQO1), and γ-glutamylcysteine synthetase (γ-GCS), while the protein expression levels were assessed by Western blot. Our results showed that the mRNA and protein expression levels of Nrf2, HO-1, NQO1, GSH-Px, and γ-GCS were increased in various degree when the Sertoli cells were to added different concentrations of SFN. Our results also showed that SFN reduced the apoptosis rate, increased the activity of T-SOD, inhibited the increase of the MDA content caused by Cd. Meanwhile, SFN could increase the mRNA and protein expression levels of Nrf2, HO-1 and NQO1 and reduced the mRNA and protein expression levels of GSH-Px and γ-GCS caused by Cd in Sertoli cells (p < 0.01). Taken together, SFN could improve the antioxidant capacity of Sertoli cells, and exert a protective effect on the oxidative damage and apoptosis of Cd-induced Sertoli cells through the activation of Nrf2/ARE signal transduction pathway.
Highlights
Cadmium (Cd) is a well-known environmental pollutant and a major industrial raw material, wherein it is primarily used for manufacturing batteries, metal electroplating, pigments, plastic cement, and alloy
The organisms are poisoned by ingesting Cd-contaminated food and drinking water, while humans could be poisoned when they are engaged in the processing and use of batteries and pigments; some poisoning could be attributed to smoking [1,2]
Cd increased the level of lipid peroxidation and the number of abnormal sperm in rat testis, reduced the level of plasma testosterone, testicular steroid synthesis as well as the number and motility of sperms in the epididymis [7], which caused a severe weight loss of rats, testicular atrophy, necrosis, fibrosis, calcification, and significant peripheral lymphocyte infiltration [8]
Summary
Cadmium (Cd) is a well-known environmental pollutant and a major industrial raw material, wherein it is primarily used for manufacturing batteries, metal electroplating, pigments, plastic cement, and alloy. Another study showed that the final body weight, relative testicular weight, the weight of epididymis, the weight of the epididymis, the weight of semen, the weight of prostate of Cd-poisoned rats, the activity of antioxidant enzymes in the testicular tissues, and the androgen receptors in rat testis decreased, while the protein expression of caspase-3 increased [9]. It was used to infuse the rats that were polluted with Cd, SFN exhibited a robust antioxidant effect, the concentration of serum testosterone and daily sperm production in rats increased significantly, and the Cd-induced reproductive toxicity was antagonized [23]. Our previous study found that SFN could significantly reduce the Cd-induced oxidative damage of testicular tissues and the reproductive toxicity [24]. The present study investigated the protective effect of SFN on Cd-induced oxidative cellular damage in rat testis and explore its mechanism. The results provided a theoretical basis for the prevention and control of the cytotoxicity of Cd, as well as, the application of SFN in production practice
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