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Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats

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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.

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Abbreviations

SOD:

Superoxide dismutase

MDA:

Malondialdehyde

CAT:

Catalase

ALT:

Alanine transaminase

AST:

Aspartate transaminase

ALP:

Alkaline phosphatase

NO:

Nitric oxide

Fe:

Iron

MPO:

Myeloperoxidase

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Acknowledgments

The authors would like to acknowledge Awah, Lawrence and their entire team (2011).

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The authors declare no conflict of interest.

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Correspondence to O. S. Adeyemi.

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Adeyemi, O.S., Sulaiman, F.A. Co-administration of iron sulphate and nitroglycerin promoted oxidative stress and mild tissue damage in Wistar rats. Comp Clin Pathol 23, 1525–1533 (2014). https://doi.org/10.1007/s00580-013-1817-2

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