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缺氧及缺氧相关因素对溶酶体和线粒体的原位损伤作用

Labilization of lysosomes and mitochondria in situ by hypoxia and hypoxia-related factors.

作者信息

Wenzel D G, Acosta D

出版信息

Res Commun Chem Pathol Pharmacol. 1975 Sep;12(1):173-6.

PMID:242048
Abstract

Primary cultures of rat heart muscle and endothelioid cells were used to study the labilization of lysosomes and mitochondria by hypoxia, "hypoxia substitutes", and the in vivo-related factors of free fatty acid and pH. Subliminally-active levels tested were: hypoxia (1% O2/4 days), 5x10(-6)M sodium stearate: albumin in 6:1 ratio/30 min, KCN (1x10(-3)M/1 hr), 2 deoxy-glucose (3x10(-2)M/12 hr), acidosis (pH 6.9/30 min) and combinations. KCN plus 2-DG labilized the organelles in both cell types. Sensitivity to injury was in the order mitochondria greater than lysosomes and muscle cells greater than endothelioid cells.

摘要

利用大鼠心肌和类内皮细胞的原代培养物,研究缺氧、“缺氧替代物”以及游离脂肪酸和pH等体内相关因素对溶酶体和线粒体的损伤作用。所测试的亚活性水平包括:缺氧(1%氧气/4天)、5×10⁻⁶M硬脂酸钠:白蛋白以6:1比例/30分钟、氰化钾(1×10⁻³M/1小时)、2-脱氧葡萄糖(3×10⁻²M/12小时)、酸中毒(pH 6.9/30分钟)及其组合。氰化钾加2-脱氧葡萄糖使两种细胞类型中的细胞器均发生损伤。对损伤的敏感性顺序为线粒体大于溶酶体,且肌肉细胞大于类内皮细胞。

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