Department of Chemistry, Federal University of Santa Maria, Santa Maria, RS, Brazil.
J Enzyme Inhib Med Chem. 2010 Aug;25(4):467-75. doi: 10.3109/14756360903257892.
We evaluated the in vitro antioxidant effect of alkyl-organotellurides A-D on lipid peroxidation and protein carbonylation in rat liver homogenates. The thiol oxidase and thiol peroxidase-like activities of compounds were investigated. delta-Aminolevulinic acid dehydratase (delta-ALA-D) activity was determined in rat liver homogenates. Compounds A-D protected against lipid peroxidation induced by Fe(2+)/EDTA and sodium nitroprusside (SNP). According to the confidence limits of the IC(50) values of compounds A-D, the IC(50) values for organotellurides followed the order: C (0.30 microM) < or = B (0.40 microM) < D (0.68 microM) < A (2.90 microM), for Fe(2+)/EDTA, and B (0.21 microM) < or = C (0.33 microM) < or = D (0.43 microM) < A (1.21 microM) for SNP-induced lipid peroxidation. Compounds A-D reduced protein carbonyl content to control levels. The results demonstrated an inverse correlation between thiol oxidase and delta-ALA-D activities. This study supports an antioxidant effect of organotellurides A-D on rat liver.
我们评估了烷基有机碲化物 A-D 在大鼠肝匀浆中对脂质过氧化和蛋白质羰基化的体外抗氧化作用。研究了化合物的硫氧还酶和硫氧还蛋白样活性。测定了大鼠肝匀浆中 δ-氨基酮戊酸脱水酶（δ-ALA-D）的活性。化合物 A-D 可防止 Fe(2+)/EDTA 和硝普酸钠（SNP）诱导的脂质过氧化。根据化合物 A-D 的 IC(50) 值置信限，有机碲化物的 IC(50) 值顺序为：C（0.30 microM）≦B（0.40 microM）≦D（0.68 microM）≦A（2.90 microM），用于 Fe(2+)/EDTA，和 B（0.21 microM）≦C（0.33 microM）≦D（0.43 microM）≦A（1.21 microM）用于 SNP 诱导的脂质过氧化。化合物 A-D 将蛋白质羰基含量降低至对照水平。结果表明，硫氧还酶和 δ-ALA-D 活性之间存在负相关。这项研究支持有机碲化物 A-D 对大鼠肝脏的抗氧化作用。
