Ghanem C, Ghisolfi C, Marabotto L, Ouviña G, Rubio M, Perazzo J, Lemberg A, Bengochea L
Catedra de Fisiopatologia y Farmacologia, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Argentina.
Arch Physiol Biochem. 1997 Oct;105(6):607-10. doi: 10.1076/apab.105.6.607.3282.
The liver is responsible for the most important metabolic pathway of non polar compounds. The aim of the present work was to study the p-nitrophenol glucuronidation and its relationship with lipidic composition of microsomal membrane in a model of hepatic portal hypertension and hepatocellular damage induced by monocrotaline. A global increment in liver microsomal phospholipids as well as changes in the phospholipid pattern (phosphatidylethanolamine and sphingomyelin increased up to 156 +/- 13 and 195 +/- 14% respectively) were detected in monocrotaline intoxicated rats when it were compared to control rats. The microsomal cholesterol content showed a decrease in monocrotaline intoxicated rats. (4.1 +/- 0.7 against 6.6 +/- 1.5 micrograms/mg of microsomal protein, in control rats). When p-nitrophenol activity was measured, Km from monocrotaline intoxicated rats was 0.137 mM, and Vmax was 2.9 nmol of p-nitrophenol/mg microsomal protein since in control group Km was 0.322 mM, and Vmax was 4.5 nmol of p-nitrophenol/mg microsomal protein. It is concluded that monocrotaline intoxicated rats showed a different behavior in the kinetics of p-nitrophenol UDP-glucuronyltransferase, as well as a different microsomal lipidic profile, when compared to control group.
肝脏负责非极性化合物最重要的代谢途径。本研究的目的是在由野百合碱诱导的肝门静脉高压和肝细胞损伤模型中，研究对硝基苯酚葡萄糖醛酸化及其与微粒体膜脂质组成的关系。与对照大鼠相比，在野百合碱中毒大鼠中检测到肝脏微粒体磷脂总体增加以及磷脂模式的变化（磷脂酰乙醇胺和鞘磷脂分别增加至156±13%和195±14%）。野百合碱中毒大鼠的微粒体胆固醇含量降低。（对照大鼠中为6.6±1.5微克/毫克微粒体蛋白，野百合碱中毒大鼠中为4.1±0.7微克/毫克微粒体蛋白）。当测量对硝基苯酚活性时，野百合碱中毒大鼠的Km为0.137毫摩尔，Vmax为2.9纳摩尔对硝基苯酚/毫克微粒体蛋白，而对照组的Km为0.322毫摩尔，Vmax为4.5纳摩尔对硝基苯酚/毫克微粒体蛋白。结论是，与对照组相比，野百合碱中毒大鼠在对硝基苯酚UDP - 葡萄糖醛酸基转移酶的动力学以及微粒体脂质谱方面表现出不同的行为。
