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牛磺酸对六价铬诱导的小鼠肝脏组织氧化应激的保护和解毒作用。

The protective and antidotal effects of taurine on hexavalent chromium-induced oxidative stress in mice liver tissue.

作者信息

Boşgelmez I Ipek, Söylemezoğlu Tülin, Güvendik Gülin

机构信息

Department of Toxicology, Ankara University, Tandoğan, 06100, Ankara, Turkey.

出版信息

Biol Trace Elem Res. 2008 Oct;125(1):46-58. doi: 10.1007/s12011-008-8154-3. Epub 2008 Jun 5.

Abstract

Acute exposure to hexavalent chromium [Cr(VI)] compounds can cause hepatotoxicity. Reactive intermediates and free radicals generated during reduction process may be responsible for Cr(VI) toxicity. In this study, the effects of pretreatment or posttreatment of taurine on Cr(VI)-induced oxidative stress and chromium accumulation in liver tissue of Swiss Albino mice were investigated. Single intraperitoneal (ip) potassium dichromate treatment (20 mgCr/kg), as Cr(VI) compound, significantly elevated the level of lipid peroxidation as compared with control group (p < 0.05). This was accompanied by significant decreases in nonprotein sulfhydryls (NPSHs) level, superoxide dismutase (SOD), and catalase (CAT) enzyme activities as well as a significant chromium accumulation in the tissue (p < 0.05). Taurine administration (1 g/kg, ip) before or after Cr(VI) exposure resulted in reduction of lipid peroxidation (p < 0.05) showed rebalancing effect on tissue NPSH levels either in pretreatment or in posttreatment (p < 0.05). Enzyme activities of SOD and CAT were restored by taurine pretreatment (p < 0.05), whereas posttreatment had less pronounced effects on these parameters. On the other hand, taurine treatment, before or after exposure, could exert only slight decreases in tissue Cr levels (p > 0.05). In view of the results, taurine seems to exert some beneficial effects against Cr(VI)-induced oxidative stress in liver tissue.

摘要

急性接触六价铬[Cr(VI)]化合物可导致肝毒性。还原过程中产生的反应性中间体和自由基可能是Cr(VI)毒性的原因。在本研究中,考察了牛磺酸预处理或后处理对瑞士白化小鼠肝组织中Cr(VI)诱导的氧化应激和铬蓄积的影响。作为Cr(VI)化合物,单次腹腔注射重铬酸钾(20 mgCr/kg)与对照组相比,显著提高了脂质过氧化水平(p<0.05)。同时,非蛋白巯基(NPSHs)水平、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性显著降低,组织中铬蓄积显著增加(p<0.05)。在Cr(VI)暴露之前或之后给予牛磺酸(1 g/kg,腹腔注射)可降低脂质过氧化水平(p<0.05),在预处理或后处理中均显示对组织NPSH水平有重新平衡作用(p<0.05)。牛磺酸预处理可恢复SOD和CAT的酶活性(p<0.05),而后处理对这些参数的影响较小。另一方面,暴露前后的牛磺酸处理仅能使组织铬水平略有降低(p>0.05)。鉴于这些结果,牛磺酸似乎对Cr(VI)诱导的肝组织氧化应激具有一些有益作用。

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