Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats
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Date
2014
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Publisher
Comparative Clinical Pathology (Springer-Verlag London, UK)
Abstract
There is no clear-cut understanding yet of the effect of a sustained production of nitric oxide (NO) either through endogenous or exogenous source on the iron (Fe) metabolism in living cells. Albeit, there are evidences linking decreased NO production to increased iron levels. A high level of free iron in living cells, predispose such systems to oxidative damage through the promotion of free hydroxyl radical generation. On the other hand, a continuous and sustained high level of NO could contribute to cellular damage arising from the debilitating effect of peroxynitrite, a very reactive free radical formed between free NO and superoxide anion. This study investigated the biochemical influence of individual or co-administration of two drugs; nitroglycerin (NGC) and ferrous sulphate (FeSO4) in rats. Data revealed elevated levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase as well as high malondialdehyde concentrations. Consequently, the levels of superoxide dismutase and catalase were raised. The histopathological presentations show the presence of gradual and subtle cellular damage. We present evidence that individual or co-administration of FeSO4 or NGC promoted the generation of free radical species which might have caused the tissue damage observed.
Description
In this research, we present evidence that individual or co-administration of FeSO4 or NGC promoted the generation of free radical species which might have caused the tissue damage observed.
Keywords
Lipid peroxidation, Pathology, Marker enzymes, Free radical, Drug interaction
Citation
Adeyemi, O. S. & Sulaiman, F. A. (2014): Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats. Comparative Clinical Pathology (Springer-Verlag London, UK) (2014). 23(5): 1525-1533. Doi 10.1007/s00580-013-1817-2. Published by Springer, Journal is based in U.K. www.sciencedirect.com (Springer; ISI/SCOPUS)