Ademola Adetokunbo Oyagbemi1, Temidayo Olutayo Omobowale2, Ebunoluwa Racheal Asenuga3, Grace Onyeche Ochigbo1, Abiola Olumuyiwa Adejumobi2, Adeolu Alex Adedapo1, Momoh Audu Yakubu4. 1. a Department of Veterinary Physiology, Biochemistry and Pharmacology, Faculty of Veterinary Medicine , University of Ibadan , Nigeria. 2. b Department of Veterinary Medicine, Faculty of Veterinary Medicine , University of Ibadan , Nigeria. 3. c Department of Veterinary Medicine, Faculty of Veterinary Medicine , University of Benin , Nigeria. 4. d Department of Environmental and Interdisciplinary Sciences , COSET, Texas Southern University , Houston , TX , USA.
Abstract
OBJECTIVES: Arsenic is a ubiquitous element that is widely distributed in the environment to which man and animals are exposed. Cardiovascular disease is one of the aftermaths of chronic arsenic exposure-related morbidity and mortality. This study sought to investigate the possibility of reversal from arsenic-induced cardio-renal toxicity following exposure and subsequent withdrawal. The study also seeks to understand the mechanism of action of this reversal. METHODS: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal. RESULTS: Exposure to arsenic caused a significant increase in malondialdehyde, H2O2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.
OBJECTIVES: Arsenic is a ubiquitous element that is widely distributed in the environment to which man and animals are exposed. Cardiovascular disease is one of the aftermaths of chronic arsenic exposure-related morbidity and mortality. This study sought to investigate the possibility of reversal from arsenic-induced cardio-renal toxicity following exposure and subsequent withdrawal. The study also seeks to understand the mechanism of action of this reversal. METHODS: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal. RESULTS: Exposure to arsenic caused a significant increase in malondialdehyde, H2O2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.
Entities:
Keywords:
Arsenic acid; cardiotoxicity; nephrotoxicity; oxidative stress; protein kinase B
Authors: Bozho Todorich; James O Olopade; Nodar Surguladze; Xuesheng Zhang; Elizabeth Neely; James R Connor Journal: Neurotox Res Date: 2010-03-17 Impact factor: 3.911