Sazuka Y, Tanizawa H, Takino Y
School of Pharmaceutical Sciences, University of Shizuoka.
Jpn J Cancer Res. 1989 Jan;80(1):89-94. doi: 10.1111/j.1349-7006.1989.tb02250.x.
The increment of lipid peroxide in the hearts of mice treated with adriamycin (ADR) was examined in relation to the decrease in the activities of superoxide dismutase (SOD), glutathione peroxidase (GSHpx) and catalase. The natural activities of these enzymes in mouse heart are lower than those in the liver. The biggest decrease in enzyme activity observed in the heart after ADR administration was that of GSHpx. Therefore, the increment of lipid peroxide was attributable to the decrease in the activities of these enzymes, especially GSHpx. Subsequently, the effects of antioxidants on the decreases in activities of SOD, GSHpx and catalase in the hearts of mice treated with ADR were examined. However, the decrease in the activities of the enzymes were not accompanied with any increment of lipid peroxide. This result suggests that active oxygen radicals produced by ADR through the agent's redox cycling have no effect on the activities of these enzymes. Therefore, it appears that the decrease in the activities of these enzymes induced by ADR in the mouse results from inhibition of enzyme protein biosynthesis.
研究了阿霉素（ADR）处理的小鼠心脏中脂质过氧化物的增加与超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSHpx）和过氧化氢酶活性降低之间的关系。这些酶在小鼠心脏中的天然活性低于肝脏中的活性。ADR给药后在心脏中观察到的酶活性最大降幅是GSHpx的降幅。因此，脂质过氧化物的增加归因于这些酶活性的降低，尤其是GSHpx。随后，研究了抗氧化剂对ADR处理的小鼠心脏中SOD、GSHpx和过氧化氢酶活性降低的影响。然而，酶活性的降低并未伴随着脂质过氧化物的任何增加。该结果表明，ADR通过其氧化还原循环产生的活性氧自由基对这些酶的活性没有影响。因此，似乎ADR诱导的小鼠中这些酶活性的降低是由于酶蛋白生物合成受到抑制。
