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Background: Acetaminophen, a widely used analgesic and antipyretic is known to cause hepatic injury in humans and experimental animals when administered in high doses. It was reported that toxic effects of acetaminophen are due to oxidative reactions that take place during its metabolism. L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing to the betaoxidation of fatty acid in the mitochondria. It is a known antioxidant with protective effects against lipid peroxidation. This study aimed to investigate the possible beneficial effect of L-carnitine as an antioxidant agent against acetaminophen induced hepatic toxicity in rats. Material and Methods: Four rat groups (N=7 in each group). Group I is the control, group II received 500 mg/kg/ body weight of L-carnitine for 7 days by oral route, group III received 640/kg/ bw of acetaminophen by oral route, group IV acute acetaminophen group pretreated with L-carnitine for 7 days by gastric tube gavage tube. The liver of all rats were removed for investigation using light and electro microscopic studies. Results: Acetaminophen caused massive centrilobular necrosis and massive degenerative changes. The electron-microscopic study showed few mitochondria, increased fat droplets and scanty smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER).These changes were reduced by L-carnitine pretreatment. Conclusion: those results suggest that acetaminophen results damage in the liver as an acute effect and L-carnitine ameliorated the adverse effects of acetaminophen via its antioxidant role. Keyword: Acetaminophen, L-carnitine, Liver & Rat. INTRODUCTION Liver diseases remain one of the serious health problems. Hepatic dysfunction due to ingestion of hepatotoxin is increasing worldwide Acetaminophen (N-acetyl-P-aminophenol, (APAP), paracetamol) is one of the most commonly consumed drugs available on the market, but unfortunately it is also the most frequent cause of drug – induced liver failure world wide (Larson et al., 2005). About 500 fatal cases of acute liver failure are reported annually in the United States alone (Lee, 2004) and he added that acetaminophen toxicity is the leading cause of drug-induced acute liver failure in the U.S and Europe. Acetaminophen, a commonly used analgesic and antipyretic drug causes fulminate hepatic necrosis in human and experimental animals when used in high doses. The biochemical mechanism by which Role of Protective Effect of L-Carnitine.... 988 acetaminophen induced liver injury is believed to be due to its metabolic conversion to highly reactive intermediate N-acetyl p-benzoquinonimine (NAPQI) by cytochrome p-50 mediated oxidases, this metabolite binds covalently to essential hpatao-cellular protein and is known to be detoxified by glutathione (GSH) (Jaw and Jeffery, 1993). Overdose with APAP depletes cellular GSH, resulting dysfunction, ATP depletion, oxidative stress, DNA damage and oncotic necrosis of parenchymal cells (Kaplowitz, 2004; Jaeschke et al., 2011). The hepatocellular necrosis is accompanied by release of death-associated molecular pattern molecules (DAMPs), such as HMGB1, HSP70, and damaged DNA, which can activate non parenchymal cells, including Kupffer cells and neutrophils (Scaffidi et al., 2002; Bianchi, 2007; Martin-Murphy et al.,

Role of Protective Effect of L-Carnitine against Acute Acetaminophen Induced Hepatic Toxicity in Adult Albino Rats