Federal College of Animal Health and Production Technology, Moor Plantation, Ibadan, Nigeria.
Department of Veterinary Physiology and Biochemistry, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
Animal Model Exp Med. 2023 Apr;6(2):168-177. doi: 10.1002/ame2.12315.
The important roles of liver and kidney in the elimination of injurious chemicals make them highly susceptible to the noxious activities of various toxicants including cobalt chloride (CoCl ). This study was designed to investigate the role of glycine in the mitigation of hepato-renal toxicities associated with CoCl exposure.
Forty-two (42) male rats were grouped as Control; (CoCl ; 300 ppm); CoCl + Glycine (50 mg/kg); CoCl + Glycine (100 mg/kg); Glycine (50 mg/kg); and Glycine (100 mg/kg). The markers of hepatic and renal damage, oxidative stress, the antioxidant defense system, histopathology, and immunohistochemical localization of neutrophil gelatinase associated lipocalin (NGAL) and renal podocin were evaluated.
Glycine significantly reduced the markers of oxidative stress (malondialdehyde content and H O generation), liver function tests (ALT, AST, and ALP), markers of renal function (creatinine and BUN), and decreased the expression of neutrophil gelatinase-associated lipocalin (NGAL) and podocin compared with rats exposed to CoCl toxicity without glycine treatment. Histopathology lesions including patchy tubular epithelial necrosis, tubular epithelial degeneration and periglomerular inflammation in renal tissues, and severe portal hepatocellular necrosis, inflammation, and duct hyperplasia were observed in hepatic tissues of rats exposed to CoCl toxicity, but were mild to absent in glycine-treated rats.
The results of this study clearly demonstrate protective effects of glycine against CoCl -induced tissue injuries and derangement of physiological activities of the hepatic and renal systems in rats. The protective effects are mediated via augmentation of total antioxidant capacity and upregulation of NGAL and podocin expression.
肝脏和肾脏在清除有害物质方面起着重要作用，因此容易受到各种有毒物质（包括氯化钴[CoCl]）的毒害。本研究旨在探讨甘氨酸在减轻氯化钴暴露引起的肝肾功能毒性中的作用。
将 42 只雄性大鼠分为对照组；（CoCl，300ppm）；CoCl+甘氨酸（50mg/kg）；CoCl+甘氨酸（100mg/kg）；甘氨酸（50mg/kg）；和甘氨酸（100mg/kg）。评估了肝肾功能损伤、氧化应激、抗氧化防御系统、组织病理学和中性粒细胞明胶酶相关脂质运载蛋白（NGAL）和肾足细胞的免疫组织化学定位的标志物。
与未用甘氨酸处理的 CoCl 毒性暴露大鼠相比，甘氨酸显著降低了氧化应激标志物（丙二醛含量和 H2O2生成）、肝功能试验（ALT、AST 和 ALP）、肾功能标志物（肌酐和 BUN）以及中性粒细胞明胶酶相关脂质运载蛋白（NGAL）和足细胞的表达。暴露于 CoCl 毒性的大鼠肾组织中观察到片状肾小管上皮坏死、肾小管上皮变性和肾小球周围炎症以及严重的门脉肝细胞坏死、炎症和胆管增生等组织病理学损伤，但在甘氨酸处理的大鼠中则较轻或不存在。
本研究结果清楚地表明甘氨酸对 CoCl 诱导的组织损伤和大鼠肝肾功能系统生理功能紊乱具有保护作用。保护作用是通过增强总抗氧化能力和上调 NGAL 和 podocin 的表达来介导的。
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