Korsova T L, Morozova N A, Poznanskaia A A, Kurganov B I
Vopr Med Khim. 1989 Mar-Apr;35(2):97-102.
Distinct activation of lipid peroxidation, reduction in N-demethylation of dimethyl aniline and in NADPH-dependent electron transport chain were observed in liver microsomes of rabbits poisoned with phenyl hydrazine. Methylcobalamine and adenosyl-cobalamine, two coenzyme forms of vitamin B12, were firstly shown to serve as modulators of the monooxygenase system, whereas methyl-cobalamine proved to be inductor and adenosylcobalamine-repressor of the system. Administration of methylcobalamine into the poisoned rabbits stimulated much higher the activities of dimethyl aniline N-demethylase, aniline p-hydroxylase, NADPH-cytochrome P-450- and NODH-cytochrome b5 reductases as compared with normal state, while adenosylcobalamine inhibited the reduction of all the monooxygenase system patterns studied. At the same time, both these coenzymes contributed to normalization of lipid peroxidation in liver microsomes of poisoned rabbits.
在苯肼中毒的家兔肝脏微粒体中,观察到脂质过氧化的明显激活、二甲基苯胺N-去甲基化以及NADPH依赖的电子传递链的减少。维生素B12的两种辅酶形式,甲基钴胺素和腺苷钴胺素,首次被证明可作为单加氧酶系统的调节剂,而甲基钴胺素被证明是该系统的诱导剂,腺苷钴胺素是抑制剂。与正常状态相比,给中毒的家兔注射甲基钴胺素能显著提高二甲基苯胺N-去甲基酶、苯胺对羟基化酶、NADPH-细胞色素P-450和NODH-细胞色素b5还原酶的活性,而腺苷钴胺素则抑制了所有研究的单加氧酶系统模式的降低。同时,这两种辅酶都有助于中毒家兔肝脏微粒体中脂质过氧化的正常化。