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N-乙酰半胱氨酸对亚砷酸钠诱导的子宫氧化应激的影响。

The consequence of NAC on sodium arsenite-induced uterine oxidative stress.

作者信息

Dash Moumita, Maity Moulima, Dey Arindam, Perveen Hasina, Khatun Shamima, Jana Lipirani, Chattopadhyay Sandip

机构信息

Department of Biomedical Laboratory Science and Management, and Clinical Nutrition and Dietetics division (UGC Innovative Department), Vidyasagar University, Midnapore, West Bengal 721102, India.

出版信息

Toxicol Rep. 2018 Feb 13;5:278-287. doi: 10.1016/j.toxrep.2018.02.003. eCollection 2018.

Abstract

Arsenic consumption through drinking water is a worldwide major health problem. Management of arsenic intoxication with invasive, painful therapy using metal chelators is usually used as a conventional treatment strategy in human. In this present study, we examined the efficacy of oral administration of N-acetyl l-cysteine (NAC) in limiting arsenic-mediated female reproductive disorders and oxidative stress in female Wistar rats. The treatment was continued for 8 days (2 estrus cycles) on rats with sodium arsenite (10 mg/Kg body weight) orally. We examined the electrozymographic imprint of three different enzymatic antioxidants in uterine tissue. Rats fed with sodium arsenite exhibited a significant lessening in the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx). Uterine DNA breakage, necrosis, ovarian and uterine tissue damage, disruption in steroidogenesis were also found in arsenic treated rats. Co-administration of NAC at different doses (50 mg/kg body weight, 100 mg/kg body weight, respectively) significantly reversed the action of uterine oxidative stress markers like malondialdehyde (MDA), conjugated dienes (CD) and non protein soluble thiol (NPSH); and noticeably improved antioxidant status of the arsenic fed rats. This ultimately resulted in the uterine tissue repairing followed by improvement of ovarian steroidogenesis. However, this effective function of NAC might be crucial for the restoration of arsenic-induced female reproductive organ damage in rats.

摘要

通过饮用水摄入砷是一个全球性的重大健康问题。使用金属螯合剂进行侵入性、痛苦的治疗来管理砷中毒,通常是人类的传统治疗策略。在本研究中,我们检测了口服N-乙酰半胱氨酸(NAC)对限制雌性Wistar大鼠砷介导的生殖系统紊乱和氧化应激的效果。对口服亚砷酸钠(10毫克/千克体重)的大鼠持续治疗8天(2个发情周期)。我们检测了子宫组织中三种不同酶促抗氧化剂的酶谱印记。喂食亚砷酸钠的大鼠超氧化物歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶(GPx)的活性显著降低。在砷处理的大鼠中还发现了子宫DNA断裂、坏死、卵巢和子宫组织损伤以及类固醇生成紊乱。分别以不同剂量(50毫克/千克体重、100毫克/千克体重)共同给予NAC,显著逆转了子宫氧化应激标志物如丙二醛(MDA)、共轭二烯(CD)和非蛋白可溶性硫醇(NPSH)的作用;并显著改善了喂食砷的大鼠的抗氧化状态。这最终导致子宫组织修复,随后卵巢类固醇生成得到改善。然而,NAC的这种有效作用可能对恢复大鼠砷诱导的雌性生殖器官损伤至关重要。

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