急性饥饿或单剂量阿霉素、表阿霉素或米托蒽醌对cd1小鼠心脏形态变化和过氧化氢酶活性的影响

M Crescimanno, C Flandina, L Rausa, R Sanguedolce, N D'Alessandro
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引用次数: 0

摘要

光镜下观察了急性(5天)饥饿和单剂量(15 mg/kg i.p)阿霉素、表阿霉素或米托蒽醌治疗的cd1小鼠的心脏形态。心脏过氧化氢酶也进行了测定。中度饥饿小鼠的平均体重减轻18.7%,没有出现心脏形态损伤。这些动物的心脏过氧化氢酶特异性活性略有增加(38%)。在遭受严重饥饿的动物中,体重减轻了32.2%。在这种情况下,心肌纤维丢失,过氧化氢酶显著升高(158.5%),可见严重的心脏损伤。在药物组中,治疗后5天体重减轻(约15%)。在3个药物组中观察到以肌溶解,尤其是肌细胞微空泡化为代表的中度心脏病变,且其程度相似。过氧化氢酶特异性活性在阿霉素小鼠中提高了119.9%,在表阿霉素小鼠中提高了73%,在米托蒽醌小鼠中提高了30.3%。光学显微镜使区分由饥饿引起的心脏改变和由抗菌剂引起的心脏改变成为可能。过氧化氢酶可能有助于指示心脏损伤的存在,但它与抗塑剂损伤的严重程度没有很好的相关性。心脏过氧化氢酶升高的另一个原因可能是由蒽环类药物引起的自由基产生,而不是由米托蒽醌引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morphological changes and catalase activity in the hearts of CD 1 mice following acute starvation or single doses of doxorubicin, epirubicin or mitoxantrone.

The cardiac morphology of CD 1 mice undergoing two different schedules of acute (5 day) starvation and that of animals treated with a single dose (15 mg/kg i.p.) of doxorubicin, epirubicin or mitoxantrone were studied by light microscopy. Determinations of heart catalase were also carried out. Mice subjected to moderate starvation had a mean weight reduction of 18.7% and did not show heart morphological damage. A slight increase (38%) of heart catalase specific activity occurred in these animals. In animals subjected to severe starvation the weight loss was 32.2%. In this case considerable heart damage, in the form of myofibrillar loss, and a striking increase of catalase (158.5%) were seen. In the drug groups comparable weight reductions (about 15%) occurred 5 days after the treatment. Moderate heart lesions, represented by myolysis and especially by myocytic microvacuolation, were observed and appeared to be of similar degree in the 3 drug groups. Catalase specific activity increased by 119.9% in the doxorubicin animals, by 73% in the epirubicin mice and by 30.3% in the mitoxantrone ones. Light microscopy made it possible to distinguish between cardiac alterations induced by starvation and those specifically induced by antiblastics. Catalase may be helpful to indicate the existence of heart damage but it does not correlate well with the severity of the lesions by antiblastics. An additional cause of heart catalase elevation might be the free radical generation induced by the anthracyclines but not by mitoxantrone.

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