Evaluation of oxaliplatin-induced pulmonary toxicity in rats

S. Kalemci, O. Tanrıverdi, A. Şimşek, S. Aksun, O. Celik, S. Barutça, Arife Zeybek, B. Demirci
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引用次数: 4

Abstract

Introduction The mechanism of oxaliplatin (OXA) induced pulmonary toxicity is not fully understood. Aim of the study The present study was designed to investigate the pulmonary toxicity of OXA that has been reported in previous studies. Study design: animal experiments. Material and methods A total of 40 female Wistar rats were divided into 5 groups. In group 1, 5% glucose was injected intra-peritoneally; then the rats were sacrificed on day 14. OXA was administered in groups 2, 3, 4, and 5; then the animals were sacrificed on day 7 in group 2, day 14 in group 3, day 28 in group 4 and day 48 in group 5. The groups were further categorized as short-term administration and long-term administration groups. Furthermore, tissue glutathione peroxidase (GPX) activity was measured in all rats. Results The mean GPX activities were 0.66 U/mg in the sham group, 0.74 U/mg in the short-term groups, and 0.74 U/mg in the long-term groups. We found that long-term OXA administration causes pulmonary toxicity resulting in increased intra-alveolar/interstitial macrophages and interstitial pneumonia. Similarly, we found reduced and permanent tissue GPX activity in rats that received OXA in higher doses and for a long term. Conclusions Long-term OXA therapy causes toxic changes in the lung tissue.
奥沙利铂致大鼠肺毒性的评价
奥沙利铂(OXA)引起肺毒性的机制尚不完全清楚。本研究的目的是调查在以往的研究中报道的氧化亚砷的肺毒性。研究设计:动物实验。材料与方法将40只雌性Wistar大鼠分为5组。1组腹腔注射5%葡萄糖;第14天处死大鼠。2、3、4、5组分别给予OXA;第2组第7天、第3组第14天、第4组第28天、第5组第48天处死。各组进一步分为短期给药组和长期给药组。测定各组大鼠组织谷胱甘肽过氧化物酶(GPX)活性。结果假手术组GPX平均活性为0.66 U/mg,短期治疗组为0.74 U/mg,长期治疗组为0.74 U/mg。我们发现长期给药OXA会引起肺毒性,导致肺泡内/间质巨噬细胞增加和间质性肺炎。同样地,我们发现在大鼠长期接受高剂量的OXA后,组织GPX活性降低和永久性降低。结论长期OXA治疗可引起肺组织毒性改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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