Portolés M T, Diaz-Laviada I, Ainaga M J, Pagani R, Municio A M
Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Universidad Complutense, Madrid, Spain.
Mol Cell Biochem. 1989 May 4;87(1):79-84. doi: 10.1007/BF00421085.
Cytotoxic lesions, induced by Gram-negative lipopolysaccharides (LPS), occur mainly in liver where the microsomal compartment of hepatocytes is involved in the detoxification mechanisms as well as in the biosynthesis of different active metabolites. The alterations induced by LPS from E. coli 0111:B4 on cytochrome b5 and its correlation with cytochrome P450, have been studied using an in vivo reversible endotoxic shock model and 24 h non-replicative hepatocyte monolayers. Results show that cytochrome b5 is directly affected by LPS that induces also a membrane damage with an active release of lactate dehydrogenase (LDH). The increase of cytochrome b5 levels may enhance the efficiency of the electron transport, thus facilitating the cytochrome P450-associate oxidations and reactions involved in the repair mechanisms of membranes.
由革兰氏阴性脂多糖(LPS)诱导的细胞毒性损伤主要发生在肝脏,肝细胞的微粒体部分参与解毒机制以及不同活性代谢物的生物合成。利用体内可逆性内毒素休克模型和24小时非复制性肝细胞单层,研究了大肠杆菌0111:B4的LPS对细胞色素b5的影响及其与细胞色素P450的相关性。结果表明,细胞色素b5直接受到LPS的影响,LPS还会诱导膜损伤并伴有乳酸脱氢酶(LDH)的活性释放。细胞色素b5水平的升高可能会提高电子传递效率,从而促进细胞色素P450相关的氧化作用以及膜修复机制中涉及的反应。