اثر سولفات منيزيم بر استرس اكسيداتيو القاء‌شده توسط لتروزول در بافت تخمدان موش‌هاي صحرايي ماده بالغ نژاد ويستار

Effect of magnesium sulfate on letrozole-induced oxidative stress in ovarian tissue of adult female Wistar rats

منيزيم دومين عنصر فراوان بعد از پتاسيم در سلول مي ­باشد و نقش مهمي در عملكردهاي گوناگون بيولوژيكي ايفا مي­ كند. سندرم تخمدان پلي­كيستيك (polycystic ovary syndrome, PCOS) يك بيماري شايع غدد درون­ريز در زنان در سنين باروري مي­باشد كه اغلب با سندرم متابوليك همراه است. شواهد نشان مي ­دهند كه استرس اكسيداتيو و درجات پايين التهاب مزمن نقش مهمي را در پاتوژنز PCOS ايفا مي‌كنند. هدف از مطالعه حاضر، بررسي اثر سولفات منيزيم بر استرس اكسيداتيو القاء­شده توسط لتروزول در بافت تخمدان موش­هاي صحرايي ماده بالغ نژاد ويستار بود. بدين منظور تعداد 36 سر موش صحرايي ماده به صورت تصادفي به 6 گروه 6تايي شامل كنترل سالم (بدون تيمار)، تيمار سالم (تيمار با سولفات منيزيم خوراكي با دوز 100 ميلي­گرم بركيلوگرم وزن بدن)، كنترل آسيب تخمداني (تيمار با لتروزول به ­طور خوراكي به ميزان 1 ميلي­گرم بر كيلوگرم وزن بدن) و تيمار تجربي آسيب تخمداني (تيمار با سولفات منيزيم در دوزهاي 10، 50 و 100 ميلي­گرم بر ­كيلوگرم وزن بدن همراه با لتروزول) تقسيم شدند. حيوانات 24 ساعت پس از آخرين دوز درمان در روز 31 آسان­كشي شده و فعاليت آنزيم ­هاي سوپراكسيد ديسموتاز (superoxide dismutase, SOD)، كاتالاز (catalase, CAT) و گلوتاتيون پراكسيداز (glutathione peroxidase, GPX) در بافت تخمدان آن­ها بررسي گرديد. تيمار سولفات منيزيم باعث افزايش معني­دار ميزان فعاليت آنزيم ­هاي SOD، CAT و GPX بافت تخمدان نسبت به گروه كنترل شد (0/05

Background and Purpose: Magnesium is the fourth most abundant cation and the second most abundant intracellular cation in the human body. Magnesium is involved in many essential physiological functions. It is a co-factor for over 300 enzymatic reactions, many of which involve generation of adenosine triphosphate (ATP), it regulates transmembrane transport of other ions, including calcium and potassium, and stabilizes secondary structures of DNA and RNA. Consequently, magnesium is essential for muscle contraction and relaxation, cardiac rhythm, vascular tone, neurological function, and cell proliferation. Magnesium is required for cell proliferation, cellular energy production, mineral metabolism, bone development, and glucose homeostasis. Nutrition surveys in North America indicate that magnesium consumption is below recommended intakes for a large segment of the population. Furthermore, diseases such as type 2 diabetes and use of certain medications can increase magnesium loss and predispose individuals to magnesium deficiency. The low magnesium intakes in comparison to current recommendations combined with the high prevalence of factors that can increase magnesium requirements raise a concern about widespread Mg deficiency. Biochemical data lend further support. Hypomagnesemia exists in the general population and the incidence is high in certain subpopulations. Since magnesium is required for many enzymatic reactions, Magnesium deficiency can presumably affect numerous physiological processes. Some studies have reported changes in body composition with dietary magnesium restriction. In rats, maternal and postnatal feeding of a magnesium-deficient diet decreased body weight, lean body mass, and fat-free mass and increased percentage body fat in the offspring. In contrast, body weight, fat mass, and lean mass were similar in rats fed a high-fat diet containing normal or low magnesium beginning after weaning. Polycystic ovary syndrome (PCOS) is a prevalent endocrinological disorder in reproductive-age women and is often associated with metabolic syndrome. Evidence suggests that oxidative stress and low degrees of chronic inflammation play an important role in the pathogenesis of PCOS. PCOS is the most common endocrine disorder in premenopausal women. PCOS is a common and multifactorial disease that affects approximately 4-18% of all reproductive-aged women in the world. In the clinic, hyperandrogenism and insulin resistance appear to be the major etiological drivers for reproductive and metabolic abnormalities in women with PCOS. While it is believed that anovulation is the main reason for infertility in PCOS patients, accumulating evidence from clinical studies also indicates that the impairment of endometrial function likely causes recurrent pregnancy loss, premature delivery, endometrial hyperplasia, and carcinoma in women with PCOS. Additionally, several lines of evidence suggest that the systemic low-grade inflammation that often coincides with PCOS compromises multiple aspects of fertility. A deficiency in the activity of aromatase was one reasonable intraovarian disturbance in steroidogenesis thought to cause PCOS. Because aromatase catalyzes the rate-limiting step in the biosynthesis of oestrogens from androgens, a decrease in the activity of this enzyme could be expected to result in increased ovarian androgen production and development of PCOS. The purpose of this study, the effect of magnesium sulfate on letrozole-induced oxidative stress was investigated in ovarian tissue of adult female Wistar rats. Materials and Methods: In this study, a total of 36 female rats were randomly divided into 6 groups of 6: The normal control group (intact), the healthy experimental group (magnesium sulfate 100 mg/kg body weight, gavage), ovarian damage control group (letrozole 1 mg/kg body weight, gavage), ovarian damage experimental group (magnesium sulfate 10, 50, and 100 mg/kg body weight together letrozole). The animals were euthanized 24 h after the last dose of the treatment on day 31. Ovaries were immediately obtained after the animals were sacrificed. The ovaries were homogenized and centrifuged. The supernatant was used to assay the activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in ovarian tissue were investigated. Data were analyzed using one-way ANOVA and Tukey test. The criterion was significant (p