Orellana M, Rodrigo R, Thielemann L, Jiménez P, Valdés E
ICBM, Programa de Farmacología Molecular y Clínica, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Comp Biochem Physiol B Biochem Mol Biol. 1998 Dec;121(4):407-16. doi: 10.1016/s0305-0491(98)10134-7.
The effect of acetone consumption on some microsomal and peroxisomal activities was studied in rat kidney and these results were compared with data from former investigations in liver. Acetone increased the microsomal lauric acid hydroxylation, the aminopyrine N-demethylation catalyzed by cytochrome P450 and the microsomal UDP-glucuronyltransferase activity. Also, acetone increased the peroxisomal beta-oxidation of palmitoyl CoA and catalase activities in kidney. These studies suggest that acetone is a common inducer of the microsomal and peroxisomal fatty acid oxidation, as previously shown in both starved and ethanol treated rats. Our results support the hypothesis that microsomal fatty acid omega-hydroxylation results in the generation of substrates being supplied for peroxisomal beta-oxidation. We propose that the final purpose of these linked fatty acid oxidations could be the catabolism of fatty acids or the generation of a substrate for the synthesis of glucose from fatty acids. This pathway would be triggered by acetone treatment in a similar way in liver and kidney.
研究了丙酮摄入对大鼠肾脏中一些微粒体和过氧化物酶体活性的影响,并将这些结果与之前在肝脏中的研究数据进行了比较。丙酮增加了微粒体月桂酸羟化作用、细胞色素P450催化的氨基比林N-脱甲基作用以及微粒体UDP-葡萄糖醛酸基转移酶活性。此外,丙酮增加了肾脏中过氧化物酶体棕榈酰辅酶A的β-氧化作用和过氧化氢酶活性。这些研究表明,丙酮是微粒体和过氧化物酶体脂肪酸氧化的常见诱导剂,正如之前在饥饿和乙醇处理的大鼠中所显示的那样。我们的结果支持这样的假设,即微粒体脂肪酸ω-羟化作用导致为过氧化物酶体β-氧化作用提供底物。我们提出,这些相连的脂肪酸氧化作用的最终目的可能是脂肪酸的分解代谢或为从脂肪酸合成葡萄糖生成底物。这条途径在肝脏和肾脏中会以类似的方式由丙酮处理引发。