title: Diallyl sulphide, a component of garlic, abrogates ferric nitrilotriacetate-induced oxidative stress and renal damage in rats.
abstract: Ferric nitrilotriacetate (Fe-NTA) induces tissue necrosis as a result of lipid peroxidation (LPO) and oxidative damage that leads to high incidence of renal carcinomas. The present study was undertaken to evaluate the effect of diallyl sulphide (DAS) against Fe-NTA-induced nephrotoxicity. A total of 30 healthy male rats were randomly divided into 5 groups of 6 rats each: (1) control, (2) DAS (200 mg kg(-1)), (3) Fe-NTA (9 g Fe kg(-1)), (4) DAS (100 mg kg(-1)) + Fe-NTA (9 mg Fe kg(-1)) and (5) DAS (200 mg kg(-1)) + Fe-NTA (9 mg Fe kg(-1)). Fe-NTA + DAS-treated groups were given DAS for a period of 1 week before Fe-NTA administration. The intraperitoneal administration of Fe-NTA enhanced blood urea nitrogen and creatinine levels with reduction in levels of antioxidant enzymes. However, significant restoration of depleted renal glutathione and its dependent enzymes (glutathione reductase and glutathione-S-transferase) was observed in DAS pretreated groups. DAS also attenuated Fe-NTA-induced increase in LPO, hydrogen peroxide generation and protein carbonyl formation (p < 0.05). The results indicate that DAS may be beneficial in ameliorating the Fe-NTA-induced renal oxidative damage in rats.
authors.affiliation: Department of Clinical Laboratory Sciences, College of Applied Medical Science, King Saud University, Riyadh, Saudi Arabia sansar@ksu.edu.sa.
authors.forename: S
authors.initials: S
authors.lastname: Ansar
authors.affiliation: Biotechnology Research Institute, Universiti Malaysia Sabah, Jalan UMS, Kota Kinabalu Sabah, Malaysia.
authors.forename: M
authors.initials: M
authors.lastname: Iqbal
authors.affiliation: Department of Clinical Laboratory Sciences, College of Applied Medical Science, King Saud University, Riyadh, Saudi Arabia.
authors.forename: N
authors.initials: N
authors.lastname: AlJameil
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology* / Q000627:therapeutic use*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use*; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D005290:Ferric Compounds; D005737:Garlic; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000188:drug therapy*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008861:Microsomes / Q000187:drug effects / Q000378:metabolism; D009571:Nitrilotriacetic Acid / Q000031:analogs & derivatives; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation; D017208:Rats, Wistar; D013440:Sulfides / Q000494:pharmacology* / Q000627:therapeutic use*
chemical_list: D000498:Allyl Compounds; D000975:Antioxidants; D005290:Ferric Compounds; D013440:Sulfides; C038491:allyl sulfide; D003404:Creatinine; D006861:Hydrogen Peroxide; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D009571:Nitrilotriacetic Acid; C020326:ferric nitrilotriacetate
keywords: Ferric nitrilotriacetate; diallyl sulphide; oxidative stress; renal toxicity