Ansar S, Iqbal M, AlJameil N
Department of Clinical Laboratory Sciences, College of Applied Medical Science, King Saud University, Riyadh, Saudi Arabia
Biotechnology Research Institute, Universiti Malaysia Sabah, Jalan UMS, Kota Kinabalu Sabah, Malaysia.
Hum Exp Toxicol. 2014 Dec;33(12):1209-16. doi: 10.1177/0960327114524237. Epub 2014 Mar 4.
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.
次氮基三乙酸铁（Fe-NTA）由于脂质过氧化（LPO）和氧化损伤导致肾癌高发率，从而引发组织坏死。本研究旨在评估二烯丙基硫醚（DAS）对Fe-NTA诱导的肾毒性的影响。总共30只健康雄性大鼠被随机分为5组，每组6只：（1）对照组，（2）DAS（200毫克/千克），（3）Fe-NTA（9克铁/千克），（4）DAS（100毫克/千克）+ Fe-NTA（9毫克铁/千克）和（5）DAS（200毫克/千克）+ Fe-NTA（9毫克铁/千克）。Fe-NTA + DAS处理组在给予Fe-NTA前1周给予DAS。腹腔注射Fe-NTA可提高血尿素氮和肌酐水平，同时降低抗氧化酶水平。然而，在DAS预处理组中观察到肾脏中消耗的谷胱甘肽及其相关酶（谷胱甘肽还原酶和谷胱甘肽-S-转移酶）水平显著恢复。DAS还减弱了Fe-NTA诱导的LPO增加、过氧化氢生成和蛋白质羰基形成（p < 0.05）。结果表明，DAS可能有助于改善Fe-NTA诱导的大鼠肾脏氧化损伤。
