Muliawan H, Burkhardt A, Scheulen M E, Kappus H
J Cancer Res Clin Oncol. 1982;103(2):135-43. doi: 10.1007/BF00409644.
Bleomycin was injected i.p. in rats, and the amount of expired ethane which indicates lipid peroxidation was followed up for 78 h. Compared to controls neither 1 x 30 mg/kg and 2 x 30 mg/kg nor 1 x 70 mg/kg bleomycin led to increased ethane expiration, although body weight loss indicated toxicity. That pulmonary toxicity had been developed due to the acute bleomycin treatment could be demonstrated by histological examinations of lungs of the animals of the highest dosage group. The combined treatment of rats with bleomycin and ferrous ions neither resulted in an increase of ethane expired compared to that of the ferrous ion-treated animals. Rather a decrease was observed. Our results indicate that acute bleomycin toxicity is not associated with increased lipid peroxidation. Furthermore, our data suggest that the bleomycin-ferrous-complex does not initiate lipid peroxidation in vivo.
将博来霉素腹腔注射到大鼠体内,并对指示脂质过氧化的呼出乙烷量进行了78小时的跟踪监测。与对照组相比,无论是1×30mg/kg和2×30mg/kg的博来霉素,还是1×70mg/kg的博来霉素,均未导致乙烷呼出量增加,尽管体重减轻表明存在毒性。通过对最高剂量组动物的肺部进行组织学检查,可以证明急性博来霉素治疗已导致肺部毒性。与用亚铁离子处理的动物相比,博来霉素和亚铁离子联合处理大鼠并未导致呼出乙烷量增加。相反,观察到呼出乙烷量减少。我们的结果表明,急性博来霉素毒性与脂质过氧化增加无关。此外,我们的数据表明,博来霉素-亚铁复合物在体内不会引发脂质过氧化。