Selenium Could Alleviate Potassium Dichromate-Induced Epididymal, Prostatic and Seminal Vesicle Changes in Adult Rats: Potential Role of Inhibiting NF-κB Pathway

Abstract

Background: Chromium is generated as a waste product from different industries. Its reproductive toxicity has been addressed in many studies that considered oxidative stress the main contributing factor for such toxicity. Selenium is essential for male reproductive health and crucially involved in regulation of cellular redox status. Aim: To elucidate the potential impacts of potassium dichromate (PDC) on the structure of the epididymis, prostate and seminal vesicles and to investigate the efficacy of selenium on counteracting these impacts. Methods: Thirty-six adult male rats were assigned into four groups: control, selenium, PDC, and PDC+selenium. The animals were subjected for a treatment period of four weeks. At the end of experimental period, blood and semen samples, epididymides, prostates and seminal vesicles were collected and processed for biochemical, morphological and immunohistochemical analyses. Results: PDC administration significantly deteriorated sperm parameters and triggered alteration of cellular redox homeostasis, evidenced by increased serum malonaldehyde levels with decreased enzymatic activity of the antioxidants: superoxide dismutase and catalase. Furthermore, PDC significantly unregulated the expression of the serum inflammatory markers; nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha and interleuken-1beta. Microscopically, all the examined tissues of PDC-treated rats displayed deteriorated microarchitecture as well as elevated 8-hydroxy-2-deoxyguanosine and microtubuleassociated protein light chain3 immunoexpression, indicating increased oxidative DNA damage and autophagy activity. Selenium supplements to PDC-treated rats effectively alleviated all the tested parameters. Conclusion: Selenium supplements could effectively mitigate PDC-induced damage of the epididymis, prostate and seminal vesicles through counteracting oxidative stress, and reducing NF-κB activation and excessive autophagy evoked by PDC.