Awoyemi Omolola Victoria, Okotie Ufuoma Jowafe, Oyagbemi Ademola Adetokunbo, Omobowale Temidayo Olutayo, Asenuga Ebunoluwa Racheal, Ola-Davies Olufunke Eunice, Ogunpolu Blessing Seun
Federal College of Animal Health and Production Technology, Moor Plantation, Ibadan, Nigeria.
Department of Veterinary Physiology, Biochemistry and Pharmacology, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
Environ Toxicol. 2017 Jul;32(7):1899-1907. doi: 10.1002/tox.22412. Epub 2017 Mar 17.
Cobalt chloride (CoCl ) is one of the many environmental contaminants, used in numerous industrial sectors. It is a pollutant with deadly toxicological consequences both in developing and developed countries. We investigated toxicological impact of CoCl on hepatic antioxidant status, apoptosis, and genotoxicity. Forty Wistar rats were divided into four groups, 10 rats per group: Group 1 served as control and received clean tap water orally; Group 2 received CoCl solution (150 mg/L); Group 3 received CoCl solution (300 mg/L); and Group 4 received CoCl (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl led to a significant decline in hepatic antioxidant enzymes together with significant increase in markers of oxidative stress. Immunohistochemistry revealed dose-dependent increase in cyclooxygenase-2 and BAX expressions together with increased frequency of Micronucleated Polychromatic Erythrocytes. Combining all, CoCl administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.
氯化钴（CoCl）是众多环境污染物之一，在许多工业领域都有应用。它是一种污染物，在发展中国家和发达国家都会造成致命的毒理学后果。我们研究了CoCl对肝脏抗氧化状态、细胞凋亡和遗传毒性的毒理学影响。将40只Wistar大鼠分为四组，每组10只：第1组作为对照组，口服清洁自来水；第2组接受CoCl溶液（150毫克/升）；第3组接受CoCl溶液（300毫克/升）；第4组在饮用水中分别接受CoCl（600毫克/升），持续7天。大鼠接触CoCl导致肝脏抗氧化酶显著下降，同时氧化应激标志物显著增加。免疫组织化学显示环氧化酶-2和BAX表达呈剂量依赖性增加，同时微核多染红细胞频率增加。综合来看，CoCl给药通过诱导氧化应激、炎症和细胞凋亡导致肝脏损伤。
