Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Nigeria.
Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Ibadan, Nigeria.
Endocr Regul. 2020 Jan 1;54(1):14-21. doi: 10.2478/enr-2020-0003.
Bisphenol A (BPA) has been reported that among other male reproductive dys-functions, it can cause marked estrogenic effects including alteration in serum hormones as well as testicular lesions in exposed animals. This work sought to study the role of gallic acid (GA), a known antioxidant, on the BPA-induced testicular oxidative stress in adult male Wistar rats using serum hormone analysis, histopathology, and biochemical assays.
Adult male rats were divided into four groups (n=10) including control (0.2 ml of corn oil), GA (20 mg/kg/day), BPA (10 mg/kg/day), BPA+GA (BPA, 10 mg/kg/day + GA, 20 mg/kg/day). All medications were given by oral gavage for 45 consecutive days. The body and testicular weights were measured. Blood and organ samples were collected for the serum hormonal assay: testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL), and tissue biochemistry analysis: superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-S-transferase (GST), malondialdehyde (MDA), hydrogen peroxide (H2O2), respectively.
The BPA-treated rats showed significant reduction in the gonadosomatic index. BPA also caused significant decrease in the levels of the serum testosterone and prolactin. Furthermore, BPA induced testicular oxidative stress by decreasing the activities of antioxidant enzymes and increasing reactive oxygen species. However, co-treatment with GA protected against these alterations.
Findings from the present study confirmed the previously reported data and show that the ability of GA, as a potent antioxidant, may protect against BPA-induced alterations in the male reproductive function. Hence, GA protects against testicular oxidative stress in adult male Wistar rats following chronic exposure to BPA.
已有报道称,双酚 A(BPA)除了其他男性生殖功能障碍外,还会引起明显的雌激素效应,包括改变血清激素以及暴露于该物质的动物的睾丸损伤。本研究旨在通过血清激素分析、组织病理学和生化分析来研究没食子酸(GA)在 BPA 诱导的成年雄性 Wistar 大鼠睾丸氧化应激中的作用,GA 是一种已知的抗氧化剂。
成年雄性大鼠分为四组(每组 10 只),包括对照组(0.2ml 玉米油)、GA 组(20mg/kg/天)、BPA 组(10mg/kg/天)、BPA+GA 组(BPA,10mg/kg/天+GA,20mg/kg/天)。所有药物均经口灌胃连续 45 天。测量体质量和睾丸质量。采集血液和器官样本,用于血清激素测定:睾酮(T)、促黄体生成素(LH)、促卵泡激素(FSH)和催乳素(PRL),以及组织生化分析:超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、谷胱甘肽-S-转移酶(GST)、丙二醛(MDA)、过氧化氢(H2O2)。
BPA 处理的大鼠性腺指数显著降低。BPA 还导致血清睾酮和催乳素水平显著降低。此外,BPA 通过降低抗氧化酶的活性和增加活性氧来诱导睾丸氧化应激。然而,GA 共同治疗可防止这些改变。
本研究的结果证实了之前的报道数据,并表明 GA 作为一种有效的抗氧化剂,可能能够预防 BPA 引起的雄性生殖功能改变。因此,GA 可防止成年雄性 Wistar 大鼠在慢性 BPA 暴露后发生睾丸氧化应激。