title: Resveratrol protects against experimental induced Reye's syndrome by prohibition of oxidative stress and restoration of complex I activity.
abstract: This study was designed to investigate whether resveratrol could provide protection against Reye's syndrome induced by 4-pentenoic acid in Wistar albino rats. Compared with rats with untreated Reye's syndrome, 1 h pretreatment by low dose resveratrol (10 mg/kg by oral gavage) resulted in marked amelioration in liver functions in the form of significant decrease in serum transaminases (AST, ALT) and plasma ammonia levels, shortening of prothrombin time, and increase in serum albumin levels. In addition, resveratrol prohibited oxidative stress markers, as indicated by a significant increase in GSH and decrease in MDA, with restoration of complex I activity in liver tissues. The classical histopathological presentation in Reye's syndrome of microvesicular steatosis by light microscope and mitochondria distortion by electron microscope has been improved by resveratrol pretreatment. The efficient protection by resveratrol was determined by normalization in serum levels of AST and albumin, as well as complex I activity, GSH, and MDA. In conclusion, pretreatment by resveratrol in low doses could protect against Reye's syndrome partially via prohibition of oxidative stress and restoration of complex I activity. This may provide the opportunity to reconsider aspirin therapy for infants and young children. However, the verification of such results in clinical practice remains a challenge.
authors.affiliation: a Department of Pharmacology, Faculty of Medicine, Tanta University, Al-Geish Street, Postal No. 31527, Egypt.
authors.forename: Amany
authors.initials: A
authors.lastname: Abdin
authors.forename: Naglaa
authors.initials: N
authors.lastname: Sarhan
mesh_terms: D000641:Ammonia / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D042967:Electron Transport Complex I / Q000378:metabolism*; D005229:Fatty Acids, Monounsaturated; D008315:Malondialdehyde / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011516:Prothrombin / Q000378:metabolism; D017208:Rats, Wistar; D000077185:Resveratrol; D012202:Reye Syndrome / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D012709:Serum Albumin / Q000378:metabolism; D000075462:Serum Albumin, Human; D013267:Stilbenes / Q000494:pharmacology / Q000627:therapeutic use*; D000637:Transaminases / Q000097:blood
chemical_list: C422455:ALB protein, human; D000975:Antioxidants; D005229:Fatty Acids, Monounsaturated; D026901:Membrane Transport Proteins; D012709:Serum Albumin; D013267:Stilbenes; C086860:glutathione transporter; D008315:Malondialdehyde; D000641:Ammonia; D011516:Prothrombin; C009785:4-pentenoic acid; D000637:Transaminases; D042967:Electron Transport Complex I; D000077185:Resveratrol; D000075462:Serum Albumin, Human
keywords: Reye’s syndrome; antioxidant; antioxydant; aspirin; aspirine; dysfonction mitochondriale; dérivé du stilbène; mitochondrial dysfunction; stilbene derivative; syndrome de Reye