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Cobalt chloride exposure dose‐dependently induced hepatotoxicity through enhancement of cyclooxygenase‐2 (COX‐2)/B‐cell associated protein X (BAX) signaling and genotoxicity in Wistar rats
Author(s) -
Awoyemi Omolola Victoria,
Okotie Ufuoma Jowafe,
Oyagbemi Ademola Adetokunbo,
Omobowale Temidayo Olutayo,
Asenuga Ebunoluwa Racheal,
OlaDavies Olufunke Eunice,
Ogunpolu Blessing Seun
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22412
Subject(s) - genotoxicity , oxidative stress , antioxidant , apoptosis , pharmacology , chemistry , toxicity , toxicology , biology , biochemistry , organic chemistry
Cobalt chloride (CoCl 2 ) 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 2 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 2 solution (150 mg/L); Group 3 received CoCl 2 solution (300 mg/L); and Group 4 received CoCl 2 (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl 2 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 2 administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.