Sohlenius A K, Eriksson A M, Högström C, Kimland M, DePierre J W
Department of Biochemistry, Wallenberg Laboratory, Stockholm University, Sweden.
Pharmacol Toxicol. 1993 Feb;72(2):90-3. doi: 10.1111/j.1600-0773.1993.tb00296.x.
Perfluorooctane sulfonic acid is almost as potent as perfluorooctanoic acid in causing increases in peroxisomal fatty acid beta-oxidation, peroxisomal catalase activity, omega-hydroxylation of lauric acid, cytosolic epoxide hydrolase activity and cytosolic DT-diaphorase activity. Octane sulfonic acid was ineffective at doses used for perfluorooctane sulfonic acid and perfluorooctanoic acid. The results support the theory of co-regulation of these parameters and peroxisome proliferation. The fact that perfluorooctane sulfonic acid causes peroxisome proliferation challenges the hypothesis that the first step in this process is formation of a thioester between the proliferator (the carboxylic group) and coenzyme A.
全氟辛烷磺酸在引起过氧化物酶体脂肪酸β-氧化、过氧化物酶体过氧化氢酶活性、月桂酸ω-羟基化、胞质环氧化物水解酶活性和胞质DT-黄递酶活性增加方面,几乎与全氟辛酸一样有效。辛烷磺酸在所使用的全氟辛烷磺酸和全氟辛酸剂量下无效。这些结果支持了这些参数与过氧化物酶体增殖共同调节的理论。全氟辛烷磺酸导致过氧化物酶体增殖这一事实对以下假设提出了挑战,即该过程的第一步是增殖剂(羧基)与辅酶A之间形成硫酯。