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Failure of recovery from lead‐acetate‐induced oxidative stress and cardiotoxicity in Wistar rats (648.14)
Author(s) -
Omobowale Temidayo,
Ademola Oyagbemi,
Saba Adebowale,
Akinrinde Stephen,
Daramola Temilade,
Ogunpolu Blessing
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.648.14
Subject(s) - lead acetate , malondialdehyde , oxidative stress , cardiotoxicity , glutathione , glutathione peroxidase , superoxide dismutase , antioxidant , chemistry , lead poisoning , catalase , toxicity , pharmacology , medicine , endocrinology , biochemistry , enzyme , psychiatry , organic chemistry
Lead poisoning continues to be a serious health problem and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being re‐settled from lead‐contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead to cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate at doses of 0.25, 0.5 and 1.0mg/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 lead acetate produced significant decline (p<0.05) in the activities of antioxidant parameters, including Glutathione peroxidase (GPx), Glutathione S‐transferase (GST), Catalase (CAT), Superoxide dismutase (SOD) and Reduced glutathione (GSH), while Malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited similar pattern of alterations, with significant (p<0.05) reduction in GSH, GPx and SOD and significant elevation in MDA and H 2 O 2 concentrations. However, GST activity was elevated, while CAT activity remained unaltered in the recovery period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters in this study failed to resolve upon withdrawal of lead exposure in male rats during the period of study.