Peroxisome proliferation induced by 2 hypolipidemic agents (clofibrate and ciprofibrate) was studied in rats by complementary approaches, ie cell fractionation, electron microscopy, marker enzyme activities, immunoblotting and nucleic acid hybridization techniques. Administration of clofibrates for 2 and 52 weeks in doses of 500 ppm and 50 ppm respectively, or ciprofibrate for 2,28 and 52 weeks in doses of 250, 25 and 25 ppm respectively, did not alter the behavior of the peroxisomes after induction as shown by ultracentrifugation profiles. The peroxisome mass was increased as shown by the purification procedure. Specific enzymes (catalase and mostly cyanide insensitive palmitoyl CoA oxidase) were induced. A mechanism of peroxisome biogenesis might have been initiated ie cytosolic factor, ligand-receptor interaction and/or post-translational modification of the import. Increase in marker enzyme activities showed that the peroxisomes are the most responsive organelles in comparison to lysosomes, mitochondria and smooth endoplasmic reticulum (except for cytochrome P-450 LA omega-hydroxylase). Peroxisomal integral membrane proteins appeared to be differently induced: some of them were virtually absent in untreated rat liver but were strongly expressed in treated liver. Induction was sustained for 52 weeks, indicating that there was no compensatory mechanism.

译文

在大鼠中,通过补充方法,即细胞分级分离,电子显微镜,标记酶活性,免疫印迹和核酸杂交技术,研究了由两种降血脂药(氯贝特和环丙贝特)诱导的过氧化物酶体增殖。如图所示,分别以500 ppm和50 ppm的剂量给予氯贝贝特2和52周,或分别以250、25和25 ppm的剂量给予环丙贝特2,28和52周,均未改变过氧化物酶体的行为。通过超速离心曲线。如纯化程序所示,过氧化物酶体质量增加。诱导了特定的酶(过氧化氢酶和大多数对氰化物不敏感的棕榈酰CoA氧化酶)。过氧化物酶体生物发生的机制可能已经开始,即胞质因子,配体-受体相互作用和/或输入的翻译后修饰。标记酶活性的增加表明,与溶酶体,线粒体和平滑的内质网(细胞色素P-450 LAω-羟化酶除外)相比,过氧化物酶体是最敏感的细胞器。过氧化物酶体整合膜蛋白似乎被不同地诱导:其中一些在未经治疗的大鼠肝脏中实际上不存在,但在经过治疗的肝脏中强烈表达。诱导持续52周,表明没有补偿机制。

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