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Saba, Adebowale Bernard
- Effect of Exposure and Withdrawal on Lead-Induced Toxicity and Oxidative Stress in Cardiac Tissues of Rats
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Authors
Temidayo Olutayo Omobowale
1,
Ademola Adetokunbo Oyagbemi
2,
Akinleye Stephen Akinrinde
2,
Ola-Davies Olufunke Eunice
2,
Adebowale Bernard Saba
2,
Olopade James Olukayode
3,
Adedapo Alex Adeolu
4
Affiliations
1 Departments of Veterinary Medicine, University of Ibadan, Ibadan, NG
2 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, NG
3 Department of Veterinary Anatomy, University of Ibadan, Ibadan, NG
4 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, IN
1 Departments of Veterinary Medicine, University of Ibadan, Ibadan, NG
2 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, NG
3 Department of Veterinary Anatomy, University of Ibadan, Ibadan, NG
4 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, IN
Source
Toxicology International (Formerly Indian Journal of Toxicology), Vol 23, No 1 (2016), Pagination: 12-17Abstract
Lead poisoning continues to pose a serious health challenge and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being resettled from leadcontaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead in cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate (PbA) at doses of 0.25, 0.5, and 1.0 mg/ml for 6-week duration, after which one-half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to PbA produced significant decline (P < 0.05) in the activities of antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT), and reduced glutathione (GSH), whereas malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited a similar pattern of alterations, with a significant (P < 0.05) reduction in GSH, GPx, and SOD and a significant elevation in MDA and H2O2 concentrations. However, GST activity was elevated, whereas CAT activity remained unaltered in the withdrawal period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters failed to resolve upon withdrawal of lead exposure in male rats during the period of study.Keywords
Antioxidants, Cardiotoxicity, Lead Acetate, Oxidative Stress, Rats.
References
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- Modulatory Role of Kolaviron (KV), a Biflavonoid from Garcinia kola, in Sodium Arsenite-Induced Hepatotoxicity and Haematotoxicity in Rats
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Authors
Olalekan Samson Agboola
1,
Ademola Adetokunbo Oyagbemi
1,
Temidayo Olutayo Omobowale
2,
Ebunoluwa Rachel Asenuga
1,
Adebowale Bernard Saba
1
Affiliations
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
Source
Toxicology International (Formerly Indian Journal of Toxicology), Vol 23, No 1 (2016), Pagination: 54-62Abstract
Arsenic acid (NaAsO2) is an environmental pollutant that is widely distributed in air, water and soil. Exposure to this silent killer in drinking water has posed a major health threat to both developing and developed countries of the world. The use of phytochemicals has gained acceptance in the recent years. Hence, the purpose of this study was to explore the chemopreventive effect of Kolaviron, a biflavonoid from Garcinia kola seed on NaAsO2 induced hepatoxicity and haematotoxicity. Rats were pre-treated with KV (100&200mg/kg) for 7 days prior to NaAsO2 (10mg/kg; i.p.) intoxication on day 8. Complete blood counts (CBC), liver function tests, hepatic antioxidant, markers of oxidative stress and histological sections of the liver were assessed. NaAsO2 intoxication caused a significant (p<0.05) increase in the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP). Also, the hepatic catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD) and reduced glutathione (GSH) content were significantly (p<0.05) reduced whereas markers of oxidative stress such as malondialdehyde (MDA), hydrogen peroxide (H2O2) and nitric oxide (NO) contents were also severely (p<0.05) elevated. NaAsO2 intoxication caused a significant (p<0.05) reduction in packed cell volume (PCV), red blood cell (RBC) counts and haemoglobin (Hb) concentration. KV pre-treatment significantly suppressed markers of oxidative stress and prevented the depletion of antioxidant defence system. Normochromic normocytic anaemia precipitated by NaAsO2 intoxication was attenuated by KV administration. Histopathological examination showed that liver tissue injury mediated by arsenic was ameliorated by KV pre-treatment. It was concluded that KV may represent a potential drug candidate to protect against liver damage and other detrimental effects of arsenic toxicity.Keywords
Hepatotoxicity, Arsenite, Kolaviron (KV), Oxidative Stress, Chemoprevention.References
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