Abstract
Mono-(2-ethylhexyl) phthalate (MEHP) and genistein are two of the most prevalent endocrine-disrupting chemicals (EDCs) that present in the environment and food. However, how these two EDCs would affect prepubertal Sertoli cells development was rarely studied. In this study, primary prepubertal Sertoli cells were isolated from 22-day-old Sprague Dawley rats and exposed to MEHP at 1 μmol/L, 10 μmol/L, and 100 μmol/L (M1, M10, and M100), genistein at 10 μmol/L (G), and their combination (G + M1, G + M10, and G + M100). Cell proliferation inhibition rate, apoptosis and necrosis rate, and cellular redox state were evaluated. Our results revealed that MEHP could significantly increase cell proliferation inhibition rate, apoptosis rate, necrosis rate, and intracellular reactive oxidative species level. However, coadministration of genistein could partially alleviate MEHP-induced prepubertal Sertoli cells oxidative injuries via enhancement of testicular antioxidative enzymes activities and upregulation of Nrf2 and HO-1, indicating that genistein could partially attenuate MEHP-induced prepubertal Sertoli cells damage through antioxidative action and may have promising future on its curative role for attenuating other EDCs-induced reproductive disorders.
Highlights
It is widely acknowledged that endocrine-disrupting chemicals (EDCs) may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife [1]
Multiple studies revealed that exposure to EDCs including bisphenol A and beta-cypermethrin was closely related to male reproductive system impairment [2, 3], if exposure occurred during early development [4]
Sertoli cells are mainly activated and regulated by FSH to ensure the normal spermatogenesis in the adult, and this process is mainly mediated by the bonding of FSH and FSH receptor (FSHR), which is uniquely expressed in the membrane of Sertoli cells
Summary
It is widely acknowledged that endocrine-disrupting chemicals (EDCs) may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife [1]. Multiple studies revealed that exposure to EDCs including bisphenol A and beta-cypermethrin was closely related to male reproductive system impairment [2, 3], if exposure occurred during early development [4]. Previous studies revealed isoflavones could mimic the actions of oestrogens and clinical reports did not find any adverse effects on male reproductive physiology [5]. Isoflavones including genistein were reported to modulate activity of antioxidative defence system and alleviate the oxidative stress induced by the other EDCs cadmium, TPA [8, 9]
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