Nna Victor Udo, Usman Umar Zayyanu, Ofutet Emmanuel Oleba, Owu Daniel Udofia
Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, P.M.B. 1115, Calabar, Cross River State, Nigeria; Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kelantan, Malaysia.
Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, Kelantan, Malaysia; Usmanu Danfodiyo University, Sokoto State, Nigeria.
Food Chem Toxicol. 2017 Apr;102:143-155. doi: 10.1016/j.fct.2017.02.010. Epub 2017 Feb 14.
This study examined the possible protective effect of quercetin(QE) on cadmium chloride (CdCl) - induced reproductive toxicity in female rats. Cadmium (Cd) accumulated in the uterus and ovaries of rats, decreased antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione (GSH)], and raised the concentrations of malondialdehyde (MDA) and hydrogen peroxide (HO) in the uterus and ovaries of rats. Serum concentrations of estradiol, progesterone, follicle stimulating hormone and luteinizing hormone decreased significantly after CdCl administration. Caspase-3 activity significantly increased in the ovaries, with an increase in Bax and a decrease in Bcl-2 protein expressions after CdCl treatment. Histopathology of the ovaries revealed significant decrease in follicle number, while the uterus showed cyst-like endometrial glands. All three models of QE treatment [pre-treatment (QE + CdCl), post-treatment (CdCl+QE), simultaneous treatment (CdCl/QE)] decreased Cd accumulation, MDA, HO, and increased SOD, CAT and GPx activities in the uterus and ovaries, decreased apoptosis of follicular cells, and increased serum reproductive hormones. However, the QE pre-treated model offered better protection against CdCl relative to the other two models. These results suggest that, QE exerts multi-mechanistic protective effects against cadmium toxicity attributable to its antioxidant and anti-apoptotic actions.
本研究考察了槲皮素（QE）对氯化镉（CdCl）诱导的雌性大鼠生殖毒性的可能保护作用。镉（Cd）在大鼠子宫和卵巢中蓄积，降低抗氧化剂[超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽（GSH）]水平，并提高大鼠子宫和卵巢中丙二醛（MDA）和过氧化氢（HO）的浓度。给予CdCl后，血清雌二醇、孕酮、卵泡刺激素和黄体生成素浓度显著降低。CdCl处理后，卵巢中半胱天冬酶-3活性显著增加，Bax增加，Bcl-2蛋白表达减少。卵巢组织病理学显示卵泡数量显著减少，而子宫显示出囊状子宫内膜腺体。QE治疗的三种模式[预处理（QE + CdCl）、后处理（CdCl + QE）、同时处理（CdCl/QE）]均降低了子宫和卵巢中的Cd蓄积、MDA、HO水平，并提高了SOD、CAT和GPx活性，减少了卵泡细胞凋亡，增加了血清生殖激素。然而，与其他两种模式相比，QE预处理模式对CdCl的保护作用更好。这些结果表明，QE通过其抗氧化和抗凋亡作用对镉毒性发挥多机制保护作用。
