Avaliação da capacidade do disseleneto de difenila em reduzir a falência hepática aguda induzida por paracetamol em camundongos

Abstract

Paracetamol (APAP) is commonly used analgesic and antipyretic, however high doses can induce damage hepatic. The metabolic N-acetyl-p-benzoquinone imine (NAPQI) is responsible for the toxic effects. The accumulation of this metabolic causes oxidative stress, cellular death and tissue necrosis. Toxicity of APAP is also related to development of inflammation, accumulation of neutrophils and release of proinflammatory mediators. The treatment consists of the N-acetylcysteine administration, which it must be administered quickly. The diphenyl diselenide (PhSe)2 is an organoselenium compound that exhibit antioxidant activity and pharmacological proprieties. The aim of this study is evaluate the ability of (PhSe)2 in reducing acute liver failure induced by APAP in mice. The animals received APAP 600 mg/kg, and after 1h were treated with (PhSe)2 15.6 mg/kg. After 4h APAP administration was collected serum and hepatic tissue for analysis. APAP administration caused severe damage hepatic, oxidative stress induction and glutathione levels reduction. APAP also caused increase of myeloperoxidase activity. The treatment with (PhSe)2 was effective in reduction of alterations caused by APAP, suggesting a promising therapeutic option for the treatment of acute liver failure.