Protective effect of aminoguanidine against paraquat-induced oxidative stress in the lung of mice

The effect of aminoguanidine (AG) against toxicity of paraquat (PQ), an oxidative-stress inducing substance, in mice was investigated. A single dose of PQ (50 mg/kg, i.p.) induced lung-toxicity, manifested by significant decrease of the activity of angiotensin converting enzyme (ACE) in lung tissue...

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Published inComparative biochemistry and physiology. Toxicology & pharmacology Vol. 132; no. 3; pp. 391 - 397
Main Authors Mustafa, Adel, Gado, Ali M, Al-Shabanah, Othman A, Al-Bekairi, Abdullah M
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.2002
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Summary:The effect of aminoguanidine (AG) against toxicity of paraquat (PQ), an oxidative-stress inducing substance, in mice was investigated. A single dose of PQ (50 mg/kg, i.p.) induced lung-toxicity, manifested by significant decrease of the activity of angiotensin converting enzyme (ACE) in lung tissue indicating pulmonary capillary endothelial cell damage. Lung toxicity was further evidenced by significant decrease of total sulfhydryl (–SH) content and significant increase in lipid peroxidation measured as malondialdehyde (MDA) in lung tissues. Oral pretreatment of mice with AG (50 mg/kg) in drinking water, starting 5 days before PQ injection and continuing during the experimental period, ameliorated the lung toxicity induced by PQ. This was evidenced by a significant increase in the levels of ACE activity, a significant decrease in lung MDA content and a significant increase in the total sulfhydryl content 24 h after PQ administration. Moreover, pretreatment of mice with AG leads to an increase of the LD 50 value of paraquat. These results indicate that AG is an efficient cytoprotective agent against PQ-induced lung toxicity.
ISSN:1532-0456
1878-1659
DOI:10.1016/S1532-0456(02)00095-9