Kilikdar Debamita, Mukherjee Debasri, Mitra Elina, Ghosh Arnab K, Basu Anjali, Chandra Ananga Mohan, Bandyoapdhyay Debasish
Oxidative Stress and Free Radical Biology Laboratory, Department of Physiology, University of Calcutta, 92, APC Road, Kolkata 700 009, India.
Indian J Exp Biol. 2011 Jul;49(7):498-510.
Effect of aqueous extract of garlic on hepatic injury due to lead-induced oxidative stress in experimental rats has been investigated. Lead acetate (LA) at a dose of 15 mg/kg body wt was administered ip to rats for 7 consecutive days to induce hepatic injury. Freshly prepared aqueous garlic extract (AGE) at a dose of 50 mg/kg body wt was fed orally to rats 1 h before LA treatment for similar period. LA treatment caused hepatic injury as evident from increased activities of serum glutamate pyruvate transaminase (SGPT) and alkaline phosphatase (ALP), increased serum bilirubin level and damage in the tissue morphology. Lead-induced oxidative stress in liver was evident from increased levels of lipid peroxidation and reduced glutathione. The decreased activity of superoxide dismutase (SOD) and an increased activity of catalase as well as an increased activity of xanthine oxidase (XO) indicate generation and possible accumulation of reactive oxygen intermediates. Furthermore, altered activities of lactate dehydrogenase (LDH), isocitrate dehydrogenase (ICDH), alpha-keto glutarate dehydrogenase (alpha-KGDH) and succinate dehydrogenase (SDH) also indicate an impaired substrate utilization and generation of oxidative stress. All these changes were found to be mitigated when the rats were pre-treated with the AGE. Results indicate that AGE has the potential to ameliorate lead-induced hepatic injury due to oxidative stress in rats. The protective effects may be due to the antioxidant properties of AGE and may have future therapeutic relevance.
研究了大蒜水提取物对实验大鼠铅诱导的氧化应激所致肝损伤的影响。以15mg/kg体重的剂量腹腔注射醋酸铅（LA）给大鼠连续7天，以诱导肝损伤。在LA处理前1小时，以50mg/kg体重的剂量给大鼠口服新鲜制备的大蒜水提取物（AGE），持续相同时间。LA处理导致肝损伤，这从血清谷丙转氨酶（SGPT）和碱性磷酸酶（ALP）活性增加、血清胆红素水平升高以及组织形态损伤可以明显看出。铅诱导的肝脏氧化应激从脂质过氧化水平升高和谷胱甘肽减少可以明显看出。超氧化物歧化酶（SOD）活性降低、过氧化氢酶活性增加以及黄嘌呤氧化酶（XO）活性增加表明活性氧中间体的产生和可能的积累。此外，乳酸脱氢酶（LDH）、异柠檬酸脱氢酶（ICDH）、α-酮戊二酸脱氢酶（α-KGDH）和琥珀酸脱氢酶（SDH）活性的改变也表明底物利用受损和氧化应激的产生。当大鼠用AGE预处理时，发现所有这些变化都得到缓解。结果表明，AGE有潜力改善大鼠因氧化应激导致的铅诱导的肝损伤。保护作用可能归因于AGE的抗氧化特性，并且可能具有未来的治疗意义。
