Nakano E, Takeshige K, Toshima Y, Tokunaga K, Minakami S
Department of Cardiac Surgery, Kyushu University School of Medicine, Fukuoka, Japan.
Cardiovasc Res. 1989 Jun;23(6):498-504. doi: 10.1093/cvr/23.6.498.
The protective effects of the glutathione peroxidase system against functional damage induced by perfusion of isolated hearts with adriamycin, an anthracycline antibiotic, were studied. We used selenium deficient rats, in which cardiac glutathione peroxidase activity was only 3% of control rats. Both contractile tension and coronary flow decreased during perfusion with the antibiotic. The degree of decline was significantly greater in the selenium deficient hearts than in the control hearts. The increase in malondialdehyde, a product of lipid peroxidation, induced by adriamycin perfusion was more evident in selenium deficient hearts, though the level of reduced glutathione was well maintained. Isolated mitochondrial function also decreased after aerobic adriamycin perfusion and the decrease was greater in selenium deficient rats. These observations indirectly suggest that the decrease in cardiac function induced by adriamycin is protected by the glutathione peroxidase system and that the decrease may be due, at least in part, to damage to the mitochondria caused by oxygen radicals generated by adriamycin.
研究了谷胱甘肽过氧化物酶系统对阿霉素（一种蒽环类抗生素）灌注离体心脏所诱导的功能损伤的保护作用。我们使用了缺硒大鼠，其心脏谷胱甘肽过氧化物酶活性仅为对照大鼠的3%。在用抗生素灌注期间，收缩张力和冠脉血流量均下降。缺硒心脏的下降程度显著大于对照心脏。尽管还原型谷胱甘肽水平保持良好，但阿霉素灌注所诱导的脂质过氧化产物丙二醛的增加在缺硒心脏中更为明显。有氧条件下阿霉素灌注后，分离的线粒体功能也下降，且在缺硒大鼠中下降幅度更大。这些观察结果间接表明，谷胱甘肽过氧化物酶系统可保护阿霉素所诱导的心脏功能下降，且这种下降可能至少部分归因于阿霉素产生的氧自由基对线粒体的损伤。
