Abstract
Sulforaphane (SFN) is a natural and highly effective antioxidant. Studies suggest that SFN protects cells and tissues against cadmium (Cd) toxicity. This study investigated the protective effect of SFN against oxidative damage in the testes of Kunming mice exposed to cadmium, and explored the possible molecular mechanisms involved. Cadmium greatly reduced the serum testosterone levels in mice, reduced sperm motility, total sperm count, and increased the sperm deformity rate. Cadmium also reduces superoxide dismutase (T-SOD) and glutathione (GSH) levels and increases malondialdehyde (MDA) concentrations. SFN intervention improved sperm quality, serum testosterone, and antioxidant levels. Both mRNA and protein expression of mouse testicular nuclear factor-erythroid 2-related factor 2 (Nrf2) was reduced in cadmium-treated group. Furthermore, the downstream genes of Nrf2, glutathione peroxidase (GSH-Px), γ-glutamyl cysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) were also decreased in cadmium-treated group. SFN intervention increases the expression of these genes. Sulforaphane prevents cadmium-induced testicular damage, probably via activation of Nrf2/ARE signaling.
Highlights
Cadmium chloride (CdCl2) is an important industrial raw material
The rates of sperm motility, count and deformity in mice treated with SFN were not significantly different than in the control group (p > 0.05; Figure 1A–C)
This study investigated the role of sulforaphane in the altered nuclear factor-erythroid 2-related factor 2 (Nrf2) expression and Nrf2-mediated phase 2 enzymatic activity following testicular exposure to cadmium toxicity in mice
Summary
Cadmium chloride (CdCl2) is an important industrial raw material. It is widely used in the manufacture of batteries, metal plates, paints, plastics, and alloys. The Cap-N-Collar basic leucine zipper (bZip) transcription factor Nrf is a master regulator of cellular detoxification responses and redox status [23] It regulates the expression of more than 200 genes [24], acting as an endogenous antioxidant. Studies suggest that SFN decreases the incidence of apoptosis in mouse testicular cells induced by diabetes types 1 and 2, via activation and upregulation of Nrf2 [30]. Recent studies report epigenetic control by SFN of Nrf expression in prostate cancer cells [31]. It is unclear whether SFN prevents cadmium-induced testicular injury, via similar mechanisms. We have created a mouse model of cadmium poisoning, and investigated the protective role of SFN intervention and Nrf2-signaling mechanisms against cadmium toxicity in testicular cells
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