Polycystic ovary syndrome (PCOS) is a multifaceted disease of women with infertility that has diverse etiologic factors. Some women may have only a few PCOS-linked symptoms or mild symptoms, whereas others will have severe or all PCOS-linked symptoms. Therefore, PCOS symptoms can differ among women. PCOS is a state of hormonal imbalance, excess terminal hair (hirsutism), hair loss (alopecia), menstruation impairments, metabolic disorders, and cystic appearance on the ovaries. The cysts hamper ovulation, thus reducing the ability of women to become pregnant and result in infertility. The available data suggest that PCOS might originate in utero and the phenotypic appearance of PCOS symptoms may be developed in later life, which could be linked with host factors (endogenous) and exogenous factors like lifestyle, and dietary, environmental or occupational factors. Based upon the available information, it can be postulated that prenatal exposure to excessive androgens might be responsible for androgenization of the fetus, which in turn may alter the program of differentiating target tissues and the phenotypic characteristics of PCOS can be persuaded by exposure of female offspring to various endogenous and exogenous factors at later life. Genetic/host and environmental/lifestyle factors might be related to the pathophysiology of PCOS after prenatal exposure to androgen. Additional studies are necessary to understand the exact mechanism responsible for the manifestation of PCOS because it is a very important issue in female reproduction.
Arsenic toxicity becomes one of the major public health issues in several countries. Chronic and acute exposure to arsenic has been reported to be toxic to various systems of the human body and also observed in controlled experimental studies. The study was conducted to evaluate the neurotoxic effect of arsenic in Swiss albino mice and its amelioration by Vitamin E, Coenzyme Q10 and their combination. Swiss albino mice were treated with arsenic of 136 ppm for 15 days. The daily dose is 1/3 of LD 50 (acute) reported dose of arsenic. Thereafter, the animals were maintained either on drinking water or treated with Vitamin E (50 mg/kg bwt), Coenzyme Q10 (10 mg/kg bwt), and their combination by i.p.daily for 15 days. After the treatment, animals were sacrificed. The weight of the brain was marginally lower (ns), in arsenic-treated group as compared to control and antioxidant-protected groups. The LPO (lipid peroxidation) level was higher in arsenic-treated group, and this elevation was checked to some extent by the selected antioxidants which were statistically significant in combination of antioxidant-protected group. A significant reduction was found in GSH (reduced glutathione) level in the brain of arsenic-treated mice whereas GSH level was considerably higher in antioxidant-protected groups. Further, total thiol and total protein level were lower in arsenic-treated group. However, total thiol was significantly higher in antioxidant-protected groups. CAT (catalase) activity was significantly lower while SOD (superoxide dismutase) activity was marginally lowered in arsenic-treated group, and it was slightly higher in antioxidant-protected groups. Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups. Whereas, a higher AChE, BChE, and motor coordination activity was observed in antioxidant-protected group. These data indicate a positive role of selected antioxidant against the toxicity of arsenic in the brain of mice.
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