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Karimi, Mostafa, Ghasemzadeh Rahbardar, Mahboobeh, Razavi, Bibi Marjan, Hosseinzadeh, Hossein. (1402). Amifostine inhibits acrylamide-induced hepatotoxicity by inhibiting oxidative stress and apoptosis. , 26(6), 662-668. doi: 10.22038/ijbms.2023.67815.14837
Mostafa Karimi; Mahboobeh Ghasemzadeh Rahbardar; Bibi Marjan Razavi; Hossein Hosseinzadeh. "Amifostine inhibits acrylamide-induced hepatotoxicity by inhibiting oxidative stress and apoptosis". , 26, 6, 1402, 662-668. doi: 10.22038/ijbms.2023.67815.14837
Karimi, Mostafa, Ghasemzadeh Rahbardar, Mahboobeh, Razavi, Bibi Marjan, Hosseinzadeh, Hossein. (1402). 'Amifostine inhibits acrylamide-induced hepatotoxicity by inhibiting oxidative stress and apoptosis', , 26(6), pp. 662-668. doi: 10.22038/ijbms.2023.67815.14837
Karimi, Mostafa, Ghasemzadeh Rahbardar, Mahboobeh, Razavi, Bibi Marjan, Hosseinzadeh, Hossein. Amifostine inhibits acrylamide-induced hepatotoxicity by inhibiting oxidative stress and apoptosis. , 1402; 26(6): 662-668. doi: 10.22038/ijbms.2023.67815.14837

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

Iranian Journal of Basic Medical Sciences
مقاله 7، دوره 26، شماره 6، شهریور 2023، صفحه 662-668    اصل مقاله (705.16 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.67815.14837
نویسندگان
Mostafa Karimi1؛ Mahboobeh Ghasemzadeh Rahbardar2؛ Bibi Marjan Razavi* 1، 3؛ Hossein Hosseinzadeh* 1، 2
1Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
2Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
3Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
چکیده
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 7 groups, including: 1. Control group, 2. ACR (50 mg/kg, 11 days, IP), 3-5. ACR+ amifostine (25, 50, 100 mg/kg, 11 days, IP), 6. ACR+ N-acetyl cysteine (NAC) (200 mg/kg, 11 days, IP), and 7. Amifostine (100 mg/kg, 11 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 2 (Bcl2), Bcl-2-associated X protein (Bax), and cleaved caspase-3. Serum samples were also collected to measure alanine transaminase (ALT) and aspartate transaminase (AST) levels. 
Results: Administration of ACR increased MDA, Bax/Bcl2 ratio, cleaved caspase-3, ALT, and AST levels, and decreased GSH content compared with the control group. The administration of amifostine with ACR decreased MDA, Bax/Bcl2 ratio, cleaved caspase-3, 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.
کلیدواژه‌ها
Antioxidants؛ Malondialdehyde؛ Glutathione؛ Apoptosis؛ bcl-2-Associated X Protein؛ Caspase 3؛ Hepatocytes؛ Aspartate Aminotransferases
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