癌症恶病质诱导的多器官损伤及其发病机制。

Basic and applied histochemistry Pub Date : 1989-01-01
S Noriki, Y Imamura, T Ikeda, K Nakanishi, N Miyoshi, M Kohno, K Mitsuda, M Fukuda
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引用次数: 0

摘要

腹腔植入腹水肝癌细胞AH-130后,大鼠全身器官在2周内出现明显萎缩,导致动物死亡。通过Feulgen水解曲线分析,这些萎缩器官中单链DNA的数量和DNA的不稳定程度都增加了。随着恶病质多器官损伤(MOD)的进展,电子自旋共振(ESR)测定的过氧化脂量和超氧化物歧化酶(SOD)活性在恶病质末期腹水中升高。脂质过氧化物和SOD诱导的增加反映了活性氧特别是超氧化物的产生增加。癌症恶病质引起的明显的全身器官损伤似乎是由于活性氧对DNA的损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Multi-organ damage (MOD) induced by cancer cachexia and its pathogenesis.

The intraperitoneal implantation of the ascitic hepatoma cells, AH-130 to rats induced marked atrophy of the systemic organs within 2 weeks, resulting in the animal death. By the method of Feulgen hydrolysis curve analysis, the amount of single-stranded DNA and the degree of DNA instability were shown to be increased in these atrophic organs. In keeping pace with the progression of the cachectic multi-organ damage (MOD), the amount of lipidperoxide and the activity of superoxide dismutase (SOD) as measured by electron spin resonance (ESR) were increased in the ascites toward the end stage of chachexia. The increased lipidperoxide and SOD induction reflect the increased production of active oxygens, especially superoxide. The marked systemic organ damage induced in cancer cachexia seems to be due to DNA damage by active oxygens.

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