Castro J A, Diaz Gomez M I
Res Commun Chem Pathol Pharmacol. 1976 Apr;13(4):731-41.
CCl4 ability to cause polysome breakdown in liver is age-dependent being negligible in the 7 days old rat and abruptly changing to adult values after 14 days of age. The CCl4 induced polysome breakdown process is more intense in the phenobarbital treated than in control rats while the 3-MC prior treatment does not modify its intensity. Prior treatment with SKF 525A increases the intensity of the polysome breakdown process while Sch 5705 or Sch 5706 administration do not modify it. Aminotriazole or cycloheximide pretreatment but not pyrazole administration decrease the intensity of polysome rupture caused by CCl4. The CCl4 deleterious action on strain A/J mouse liver polysomes is as intense as is in the rat liver. Results are discussed in relation to the role of either the irreversible binding of CCl4 components to ribosomes or lipid peroxidation as reponsible for the breakdown process.
四氯化碳导致肝脏多核糖体解体的能力具有年龄依赖性,在7日龄大鼠中可忽略不计,而在14日龄后会突然转变为成年大鼠的水平。与对照大鼠相比,苯巴比妥处理的大鼠中四氯化碳诱导的多核糖体解体过程更为强烈,而3-甲基胆蒽预处理不会改变其强度。用SKF 525A预处理会增加多核糖体解体过程的强度,而给予Sch 5705或Sch 5706则不会改变。氨基三唑或环己酰亚胺预处理而非吡唑给药会降低四氯化碳引起的核糖体破裂强度。四氯化碳对A/J品系小鼠肝脏多核糖体的有害作用与对大鼠肝脏的作用一样强烈。文中讨论了四氯化碳成分与核糖体的不可逆结合或脂质过氧化作为导致解体过程的原因所起的作用。