Van den Branden C, Roels F
Biochem Pharmacol. 1985 Jun 15;34(12):2147-9. doi: 10.1016/0006-2952(85)90409-5.
The influence of sodium valproate on peroxisomal beta-oxidation was investigated in rats, by evaluating in vivo changes in hepatic H2O2 production, using a combination of the catalase inhibitor 3-amino-1,2,4-triazole, and methanol. In rats starvation causes an increased flux of fatty acids through the peroxisomal beta-oxidation pathway. Valproate inhibits the formation of 3-hydroxybutyrate but not increased H2O2 production during starvation. There is no inhibitory effect of valproate on the peroxisomal oxidase. At low valproate concentrations it is possible that peroxisomes partially take over impaired mitochondrial function.
通过联合使用过氧化氢酶抑制剂3-氨基-1,2,4-三唑和甲醇,评估肝脏过氧化氢生成的体内变化,研究了丙戊酸钠对大鼠过氧化物酶体β-氧化的影响。在大鼠中,饥饿会导致脂肪酸通过过氧化物酶体β-氧化途径的通量增加。丙戊酸盐可抑制3-羟基丁酸的形成,但不会抑制饥饿期间过氧化氢生成的增加。丙戊酸盐对过氧化物酶体氧化酶没有抑制作用。在低丙戊酸盐浓度下,过氧化物酶体有可能部分接管受损的线粒体功能。