Type of presentation: Poster

LS-11-P-5932 Resveratrol Protects Against Experimental Induced-Reye's Syndrome by Prohibition of Oxidative Stress and Restoration of Complex I Activity

Abdeen A. A.1, Sarhan N. I.2
1Departemnt of Pharmacology ,Faculty of medicine ,Tanta University , 2Departement of histology and cell biology FAculty of medicine Tanta university
nsarhan2006@hotmail.com

Reye's syndrome is the main contraindication of using aspirin in
young children during fever-causing illnesses. The safety of paracetamol as a classical
alternate therapy is now questionable due to increasing evidence of its correlation to
increased incidence of autism. Therefore, this study was designed to investigate if
resveratrol could provide protection against Reye's syndrome induced by 4-pentenoic
acid in Wister albino rats. Methods and results: Compared to rats with untreated
Reye's syndrome; 1 hour pre-treatment 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 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 pre-treatment. 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. Conclusion: It could be concluded that pre-treatment with resveratrol in low
dose 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 result
in clinical practice remains a real challenge.

Fig. 1: Induced Reye's syndrome(group II) showing multiple microvesicular steatosis (►) and mononuclear cellular infiltrate (→). (×200). [

Fig. 2: Induced Reye'ssyndrome (group II) showing multiple microvesicular steatosis (→) and extracellular vacuoles with wide separation of thecells (*). Notice nuclear fragmentation (►). (×1000).

Fig. 3: Hepatocytes of induced Reye's syndrome (group II) showing crescents of chromatin margination inside the nucleus (N) with focal swelling (*) and disrupted nuclear envelope (wavy arrow), few mitochondriawith destroyed cristae (►) and multiple vacuoles (→). Notice also focal disruption of the plasma membrane (curved arrow).(×11700|). 

Fig. 4:  Hepatocytes of induced Reye's syndrome (group II) showing irregular contoured nucleus (N), Few mitochondria (M), large sized cytoplasmic lipid droplets (L), multiple vacuoles (►) and electron dense bodies (→).(×11700).