Beier K, Völkl A, Fahimi H D
Institut für Anatomie und Zellbiologie II, Universität Heidelberg, Germany.
FEBS Lett. 1992 Oct 5;310(3):273-6. doi: 10.1016/0014-5793(92)81347-o.
TNF-alpha is a potent cytokine which induces marked hyperlipidemia. Because of the important role of peroxisomes in lipid metabolism we investigated the effects of human recombinant TNF-alpha upon rat liver peroxisomal enzymes. Sixteen hours after the administration of a single dose of 25 micrograms of TNF-alpha to male rats the activity of peroxisomal fatty acyl-CoA oxidase was reduced by 50%. This was confirmed also by immunoblotting and by quantitative immunoelectron microscopy which in addition revealed substantial reduction of the trifunctional protein (hydratase-dehydrogenase-isomerase) in peroxisomes. These observations suggest that the suppression of peroxisomal beta-oxidation may contribute to the perturbation of the isomerase) in peroxisomes. These observations suggest that the suppression of peroxisomal beta-oxidation may contribute to the perturbation of the lipid metabolism induced by TNF-alpha.
肿瘤坏死因子-α（TNF-α）是一种强效细胞因子，可引发显著的高脂血症。由于过氧化物酶体在脂质代谢中发挥重要作用，我们研究了重组人TNF-α对大鼠肝脏过氧化物酶体酶的影响。给雄性大鼠单次注射25微克TNF-α后16小时，过氧化物酶体脂肪酰辅酶A氧化酶的活性降低了50%。免疫印迹法以及定量免疫电子显微镜检查也证实了这一点，此外还发现过氧化物酶体中的三功能蛋白（水化酶-脱氢酶-异构酶）大幅减少。这些观察结果表明，过氧化物酶体β氧化的抑制可能导致TNF-α诱导的脂质代谢紊乱。
