Home Bratislava Medical Journal 2019 Bratislava Medical Journal Vol.120, No.4, p.270–276, 2019

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Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.564

 

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Bratislava Medical Journal Vol.120, No.4, p.270–276, 2019

Title: Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine
Author: N. Tas, A. Altinbas, T. Noyan, S. Kokturk, S. Ayhan, E. Canakci

Abstract: OBJECTIVE AND BACKGROUND: Acute acetaminophen (APAP) overdose has been shown to cause toxicity and the primary treatment medication is N-acetylcysteine (NAC). Dexmedetomidine (DEX) is a sedative drug with known antioxidant properties. We researched whether DEX has an injury-reducing effect on toxicity.
METHODS: Rats were divided into: Group I (control), Group II (APAP) Group III (NAC) Group IV (DEX) and Group V (NAC+DEX). Histopathologic investigations of tissues were performed and glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), myeloperoxidase (MPO) and beta trace protein (PGD2S) levels were studied in blood samples.
RESULTS: DEX administration for hepatotoxicity and nephrotoxicity induced with APAP, caused a significant reduction in oxidative injury markers like MDA and MPO, a significant increase in GSH-Px level and a significant degree of amelioration in liver histopathologic scores.
CONCLUSION: DEX administration for APAP toxicity causes a reduction in oxidative injury biomarkers, increased antioxidant biomarker levels and significant reduction in liver histopathologic scores. The beneficial effect of DEX use for detection of toxicity induced by acute APAP overdose, was shown in this study for the first time (Tab. 5, Fig. 2, Ref. 41).

Keywords: acetaminophen, dexmedetomidine, hepatotoxicity, nephrotoxicity
Published online: 26-Apr-2019
Year: 2019, Volume: 120, Issue: 4 Page From: 270, Page To: 276
doi:10.4149/BLL_2019_047


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