title: Protective effect of arabic gum against acetaminophen-induced hepatotoxicity in mice.
abstract: Overdose of acetaminophen, a widely used analgesic drug, can result in severe hepatotoxicity and is often fatal. This study was undertaken to examine the effects of arabic gum (AG), which is commonly used in processed foods, on acetaminophen-induced hepatotoxicity in mice. Mice were given arabic gum orally (100 g l(-1)) 5 days before a hepatotoxic dose of acetaminophen (500 mg kg(-1)) intraperitoneally. Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen-induced hepatic lipid peroxidation was reduced significantly by arabic gum pretreatment. The protection offered by arabic gum does not appear to be caused by a decrease in the formation of toxic acetaminophen metabolites, which consumes glutathione, because arabic gum did not alter acetaminophen-induced hepatic glutathione depletion. Acetaminophen increased nitric oxide synthesis as measured by serum nitrate plus nitrite at 4 and 6 h after administration and arabic gum pretreatment significantly reduced their formation. In conclusion, arabic gum is effective in protecting mice against acetaminophen-induced hepatotoxicity. This protection may involve the reduction of oxidative stress.
authors.affiliation: Department of Pharmacology, College of Pharmacy, King Saud University, PO Box 2457, Riyadh 11451, Saudi Arabia.
authors.forename: Ayman M
authors.initials: AM
authors.lastname: Gamal el-din
authors.forename: Adel M
authors.initials: AM
authors.lastname: Mostafa
authors.forename: Othman A
authors.initials: OA
authors.lastname: Al-Shabanah
authors.forename: Abdullah M
authors.initials: AM
authors.lastname: Al-Bekairi
authors.forename: Mahmoud N
authors.initials: MN
authors.lastname: Nagi
mesh_terms: D000082:Acetaminophen / Q000008:administration & dosage* / Q000633:toxicity; D000284:Administration, Oral; D000410:Alanine Transaminase / Q000097:blood; D018712:Analgesics, Non-Narcotic / Q000008:administration & dosage* / Q000633:toxicity; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury; D005978:Glutathione / Q000378:metabolism; D006170:Gum Arabic / Q000494:pharmacology* / Q000627:therapeutic use; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008107:Liver Diseases / Q000097:blood / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use; D011897:Random Allocation
chemical_list: D018712:Analgesics, Non-Narcotic; D009566:Nitrates; D009573:Nitrites; D020011:Protective Agents; D000082:Acetaminophen; D008315:Malondialdehyde; D006170:Gum Arabic; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione