四氯化碳诱导多核糖体解体。脂质过氧化作用以及在该过程中与核糖体组分结合的相对重要性。
Carbon tetrachloride induced polysome breakdown. Relative importance of lipid peroxidation and of binding to ribosomal components in the process.
作者信息
Castro J A, Gómez M I, de Castro C R, de Fenos O M, de Ferreyra E C, D'Acosta N
出版信息
Res Commun Chem Pathol Pharmacol. 1975 Jan;10(1):93-104.
In vivo, CC1-4 causes an intense polysome breakdown; CHC1-3 effect is much less intense and CH2C1-2 effect is negligible. Previous administration of either diphenyl-p-phenyelnediamine or alpha-tocopherol to the rats does not prevent CC1-4-induced polysome breakdown. Promethazine and cystamine were able to prevent to a good extent the CC1-4 induced polysome breakdown process. 14CC1-4 irreversibly binds to ribosomal proteins but not to ribosomal RNA. Several hepatocarcinogens which are effective alkylating agents and cause in vivo polysome breakdown do not induce a lipid peroxidation process.
在体内，四氯化碳会导致强烈的多核糖体解体；三氯甲烷的作用强度要小得多，而二氯甲烷的作用可忽略不计。事先给大鼠施用二苯基对苯二胺或α-生育酚并不能阻止四氯化碳诱导的多核糖体解体。异丙嗪和半胱胺能够在很大程度上阻止四氯化碳诱导的多核糖体解体过程。14C标记的四氯化碳不可逆地与核糖体蛋白结合，但不与核糖体RNA结合。几种作为有效烷化剂并在体内导致多核糖体解体的肝癌致癌物不会诱导脂质过氧化过程。
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