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Effects of Sesame Oil Against After the Onset of Acetaminophen‐Induced Acute Hepatic Injury in Rats
Author(s) -
Chandrasekaran Victor Raj Mohan,
Chien SePing,
Hsu DurZong,
Chang YuChung,
Liu MingYie
Publication year - 2010
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607110362584
Subject(s) - acetaminophen , pharmacology , liver injury , glutathione , lipid peroxidation , antipyretic , centrilobular necrosis , medicine , antioxidant , analgesic , chemistry , oxidative stress , biochemistry , enzyme
Background: Acetaminophen (APAP) is a safe and effective analgesic and antipyretic when used at therapeutic levels. However, an acute or cumulative overdose can cause severe liver injury with the potential to progress to liver failure in humans and experimental animals. Much attention has been paid to the development of an antioxidant that protects against APAP‐induced acute hepatic injury. Hence, we aimed to investigate the effect of sesame oil against after the onset of acute hepatic injury in APAP‐overdosed rats. Methods: Male Wistar rats were first given 2 oral doses (1,000 mg/kg each) of APAP (at 0 and 24 hours) and then 1 oral dose of sesame oil (8 mL/kg at 24 hours). Results: After 48 hours, APAP increased aspartate and alanine aminotransferase levels in the rats' serum and centrilobular necrosis in liver tissue. In addition, APAP significantly decreased the rats' glutathione levels and mitochondrial aconitase activity, but increased superoxide anion, hydroxyl radical, and lipid peroxidation levels. Oral sesame oil (8 mL/kg, given at 24 hours) reversed all APAP‐altered parameters and protected the rats against APAP‐induced acute liver injury. Conclusion: We hypothesize that sesame oil acts as a useful agent that maintains intracellular glutathione levels and inhibits reactive oxygen species, thereby protecting rats against after the onset of APAP‐induced acute oxidative liver injury.