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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。

相似文献

1
Labilization of lysosomes and mitochondria in situ by hypoxia and hypoxia-related factors.缺氧及缺氧相关因素对溶酶体和线粒体的原位损伤作用
Res Commun Chem Pathol Pharmacol. 1975 Sep;12(1):173-6.
2
Clofibrate enhancement of stearate-induced permeability of lysosomes and mitochondria in cultured heart muscle and endothelioid cells.氯贝丁酯增强硬脂酸盐诱导的培养心肌细胞和内皮样细胞溶酶体及线粒体的通透性。
Res Commun Chem Pathol Pharmacol. 1974 Jan;7(1):201-4.
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Toxicity of free fatty acids for cultured rat heart muscle and endothelioid cells. I. Saturated long-chain fatty acids.游离脂肪酸对培养的大鼠心肌和内皮样细胞的毒性。I. 饱和长链脂肪酸。
Toxicology. 1978 Oct;11(2):109-17. doi: 10.1016/s0300-483x(78)90789-8.
4
Cholesterol and beta-lipoprotein on lipid inclusions and lysosomal and mitochondrial permeability of cultured heart muscle and endothelioid cells.胆固醇和β-脂蛋白对培养的心肌细胞和内皮样细胞中脂质包涵体以及溶酶体和线粒体通透性的影响。
Res Commun Chem Pathol Pharmacol. 1975 Dec;12(4):789-92.
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Injury produced by free fatty acids to lysosomes and mitochondria in cultured heart muscle and endothelial cells.游离脂肪酸对培养的心肌细胞和内皮细胞中的溶酶体和线粒体造成的损伤。
Atherosclerosis. 1974 Nov-Dec;20(3):417-26. doi: 10.1016/0021-9150(74)90023-9.
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Oxygen-induced enzyme release after irreversible myocardial injury. Effects of cyanide in perfused rat hearts.不可逆性心肌损伤后氧诱导的酶释放。氰化物对灌注大鼠心脏的影响。
Am J Pathol. 1976 Aug;84(2):327-50.
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Cytotoxicity of caffeine in cultured heart cells.咖啡因对培养心脏细胞的细胞毒性。
Toxicology. 1976 Aug-Sep;6(2):225-33. doi: 10.1016/0300-483x(76)90024-x.
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Acute mitochondrial toxicity of caffeine in cultured heart cells.咖啡因对培养的心脏细胞的急性线粒体毒性
Drug Chem Toxicol. 1977;1(1):19-24. doi: 10.3109/01480547709034424.
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Toxicity of free fatty acids for cultured rat heart muscle and endothelioid cells. II. Unsaturated long-chain fatty acids.游离脂肪酸对培养的大鼠心肌和内皮样细胞的毒性。II. 不饱和长链脂肪酸。
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[Comparison of the effect of acute hypoxia on the rat liver lysosomal apparatus against a background of adaptation to hypoxia and the administration of gutimine].[急性缺氧对适应缺氧背景下大鼠肝脏溶酶体装置的影响以及古替明给药的比较]
Farmakol Toksikol. 1979 May-Jun;42(3):294-8.

引用本文的文献

1
Reversible and irreversible damage in reoxygenated 'ischemic' ventricular myocytes in culture.培养的再灌注“缺血”心室肌细胞中的可逆性和不可逆性损伤
Mol Cell Biochem. 1996 Jul-Aug;160-161:137-41. doi: 10.1007/BF00240043.
2
Studies on oxygen and volume restriction in cultured cardiac cell: possible rearrangement of sarcolemmal lipid moieties during anoxia and ischemia-like states.培养心肌细胞中氧和容量限制的研究:缺氧和缺血样状态下肌膜脂质部分可能的重排。
Mol Cell Biochem. 1988 Jan;79(1):39-46. doi: 10.1007/BF00229396.
3
Ischemic myocardial injury in cultured heart cells: leakage of cytoplasmic enzymes from injured cells.
培养心肌细胞中的缺血性心肌损伤:受损细胞中细胞质酶的泄漏。
In Vitro. 1978 Aug;14(8):728-32. doi: 10.1007/BF02616170.
4
Ischemic myocardial injury in cultured heart cells: preliminary observations on morphology and beating activity.
In Vitro. 1977;13(12):818-23. doi: 10.1007/BF02615129.