Manna Prasenjit, Sinha Mahua, Sil Parames C
Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata 700009, West Bengal, India.
Amino Acids. 2009 Mar;36(3):417-28. doi: 10.1007/s00726-008-0094-x. Epub 2008 Apr 15.
The present study has been carried out to investigate the role of taurine (2-aminoethanesulfonic acid), a conditionally essential amino acid, in ameliorating cadmium-induced renal dysfunctions in mice. Cadmium chloride (CdCl(2)) has been selected as the source of cadmium. Intraperitoneal administration of CdCl(2 )(at a dose of 4 mg/kg body weight for 3 days) caused significant accumulation of cadmium in renal tissues and lessened kidney weight to body weight ratio. Cadmium administration reduced intracellular ferric reducing/antioxidant power (FRAP) of renal tissues. Levels of serum marker enzymes related to renal damage, creatinine and urea nitrogen (UN) have been elevated due to cadmium toxicity. Cadmium exposure diminished the activities of enzymatic antioxidants, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PD) as well as non-enzymatic antioxidant, reduced glutathione (GSH) and total thiols. On the other hand, the levels of oxidized glutathione (GSSG), lipid peroxidation, protein carbonylation, DNA fragmentation, concentration of superoxide radicals and activities of cytochrome P450 enzymes (CYP P450s) have been found to increase due to cadmium intoxication. Treatment with taurine (at a dose of 100 mg/kg body weight for 5 days) before cadmium intoxication prevented the toxin-induced oxidative impairments in renal tissues. The beneficial role of taurine against cadmium-induced renal damage was supported from histological examination of renal segments. Vitamin C, a well-established antioxidant was used as the positive control in the study. Experimental evidence suggests that both taurine and vitamin C provide antioxidant defense against cadmium-induced renal oxidative injury. Combining all, results suggest that taurine protects murine kidneys against cadmium-induced oxidative impairments, probably via its antioxidative property.
本研究旨在探讨条件必需氨基酸牛磺酸(2-氨基乙磺酸)在改善镉诱导的小鼠肾功能障碍中的作用。已选用氯化镉(CdCl₂)作为镉的来源。腹腔注射CdCl₂(剂量为4 mg/kg体重,持续3天)导致镉在肾组织中显著蓄积,并降低了肾重与体重之比。镉的给药降低了肾组织的细胞内铁还原/抗氧化能力(FRAP)。由于镉中毒,与肾损伤相关的血清标志物酶肌酐和尿素氮(UN)水平升高。镉暴露降低了酶促抗氧化剂超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽-S-转移酶(GST)、谷胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GPx)和葡萄糖-6-磷酸脱氢酶(G6PD)以及非酶促抗氧化剂还原型谷胱甘肽(GSH)和总硫醇的活性。另一方面,发现由于镉中毒,氧化型谷胱甘肽(GSSG)水平、脂质过氧化、蛋白质羰基化、DNA片段化、超氧自由基浓度和细胞色素P450酶(CYP P450s)活性增加。在镉中毒前用牛磺酸(剂量为100 mg/kg体重,持续5天)治疗可预防毒素诱导的肾组织氧化损伤。肾段的组织学检查支持了牛磺酸对镉诱导的肾损伤的有益作用。在该研究中,公认的抗氧化剂维生素C用作阳性对照。实验证据表明,牛磺酸和维生素C均提供针对镉诱导的肾氧化损伤的抗氧化防御。综合所有结果表明,牛磺酸可能通过其抗氧化特性保护小鼠肾脏免受镉诱导的氧化损伤。