Amifostine inhibits acrylamide-induced hepatotoxicity by inhibiting oxidative stress and apoptosis

Publish Year: 1402
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:

JR_IJBMS-26-6_007

تاریخ نمایه سازی: 21 اردیبهشت 1402

Abstract:

Objective(s): Acrylamide (ACR) is a toxic chemical agent that can induce hepatotoxicity through different mechanisms including oxidative stress and apoptosis. Amifostine is an important hepatoprotective and anti-oxidant compound. In this research, the hepatoprotective effect of amifostine on ACR-induced hepatotoxicity in rats has been investigated.Materials and Methods: Male Wistar rats were randomly divided into ۷ groups, including: ۱. Control group, ۲. ACR (۵۰ mg/kg, ۱۱ days, IP), ۳-۵. ACR+ amifostine (۲۵, ۵۰, ۱۰۰ mg/kg, ۱۱ days, IP), ۶. ACR+ N-acetyl cysteine (NAC) (۲۰۰ mg/kg, ۱۱ days, IP), and ۷. Amifostine (۱۰۰ mg/kg, ۱۱ days, IP). At the end of the injection period, animals’ liver samples were collected to determine the content of glutathione (GSH), malondialdehyde (MDA), and apoptotic proteins (B-cell lymphoma ۲ (Bcl۲), Bcl-۲-associated X protein (Bax), and cleaved caspase-۳. Serum samples were also collected to measure alanine transaminase (ALT) and aspartate transaminase (AST) levels. Results: Administration of ACR increased MDA, Bax/Bcl۲ ratio, cleaved caspase-۳, ALT, and AST levels, and decreased GSH content compared with the control group. The administration of amifostine with ACR decreased MDA, Bax/Bcl۲ ratio, cleaved caspase-۳, ALT, and AST levels, and increased GSH content compared with the ACR group. Receiving NAC along with ACR reversed the alterations induced by ACR. Conclusion: This study shows that pretreatment with amifostine can reduce ACR-induced toxicity in the liver tissue of rats. Since oxidative stress is one of the most important mechanisms in ACR toxicity, amifostine probably reduces the toxicity of ACR by increasing the anti-oxidant and anti-apoptotic capacity of the hepatic cells.

Authors

Mostafa Karimi

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Mahboobeh Ghasemzadeh Rahbardar

Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Bibi Marjan Razavi

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Hossein Hosseinzadeh

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

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