Renal Physiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Chem Biol Interact. 2012 Oct 25;200(1):21-7. doi: 10.1016/j.cbi.2012.08.026. Epub 2012 Sep 13.
This study examined whether caffeic acid phenethyl ester (CAPE) can protect kidney mitochondria against cadmium toxicity. Kidney mitochondria isolated from Wistar rat were exposed to cadmium and/or CAPE at various concentrations. Mitochondrial function, ultrastructure and oxidative stress status were determined. Cadmium exposure resulted in mitochondrial swelling, dissipation of membrane potential, overproduction of reactive oxygen species, and impaired ultrastructure. The injury was accompanied by an increase in mitochondrial nitric oxide and malondialdehyde levels as well as a decrease in superoxide dismutase activity and antioxidant thiols. Pretreatment with CAPE ameliorated all the changes caused by cadmium. The results suggest a promising role for CAPE as mitochondria-targeted antioxidant to combat the renal toxicity of cadmium.
本研究探讨了咖啡酸苯乙酯（CAPE）是否可以保护肾脏线粒体免受镉毒性的影响。从 Wistar 大鼠中分离出肾脏线粒体，使其在不同浓度下暴露于镉和/或 CAPE 中。测定线粒体功能、超微结构和氧化应激状态。镉暴露导致线粒体肿胀、膜电位耗散、活性氧过度产生以及超微结构受损。损伤伴随着线粒体一氧化氮和丙二醛水平的增加以及超氧化物歧化酶活性和抗氧化硫醇的减少。CAPE 的预处理改善了镉引起的所有变化。结果表明，CAPE 作为一种线粒体靶向抗氧化剂，有望对抗镉的肾毒性。
