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冷体鱼类中的线粒体生物发生。

Mitochondrial biogenesis in cold-bodied fishes.

机构信息

University of Alaska Fairbanks, Institute of Arctic Biology, PO Box 757000, Fairbanks, AK 99775, USA.

出版信息

J Exp Biol. 2011 Jan 15;214(Pt 2):275-85. doi: 10.1242/jeb.046854.

Abstract

Mitochondrial biogenesis is induced in response to cold temperature in many organisms. The effect is particularly pronounced in ectotherms such as fishes, where acclimation to cold temperature increases mitochondrial density. Some polar fishes also have exceptionally high densities of mitochondria. The net effect of increasing mitochondrial density is threefold. First, it increases the concentration of aerobic metabolic enzymes per gram of tissue, maintaining ATP production. Second, it elevates the density of mitochondrial membrane phospholipids, enhancing rates of intracellular oxygen diffusion. Third, it reduces the diffusion distance for oxygen and metabolites between capillaries and mitochondria. Although cold-induced mitochondrial biogenesis has been well documented in fishes, little is known about the molecular pathway governing it. In mammals, the co-transcriptional activator peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) is thought to coordinate the three components of mitochondrial biogenesis: the synthesis of mitochondrial proteins, the synthesis of phospholipids and the replication of mitochondrial DNA. Some components of the mitochondrial biogenic pathway are conserved between fishes and mammals, yet the pathway appears more versatile in fishes. In some tissues of cold-acclimated fishes, the synthesis of mitochondrial proteins increases in the absence of an increase in phospholipids, whereas in some polar fishes, densities of mitochondrial phospholipids increase in the absence of an increase in proteins. The ability of cold-bodied fishes to fine-tune the mitochondrial biogenic pathway may allow them to modify mitochondrial characteristics to meet the specific needs of the cell, whether it is to increase ATP production or enhance oxygen diffusion.

摘要

线粒体生物发生是许多生物对低温的反应诱导的。这种效应在鱼类等变温动物中尤为明显,鱼类适应低温会增加线粒体密度。一些极地鱼类的线粒体密度也异常高。增加线粒体密度的净效应有三个方面。首先,它增加了每克组织中需氧代谢酶的浓度,维持了 ATP 的产生。其次,它提高了线粒体膜磷脂的密度,提高了细胞内氧气扩散的速度。第三,它减少了毛细血管和线粒体之间氧气和代谢物的扩散距离。虽然低温诱导的线粒体生物发生在鱼类中已经得到了很好的证明,但对于控制它的分子途径知之甚少。在哺乳动物中,转录共激活因子过氧化物酶体增殖物激活受体γ共激活因子 1α(PGC-1α)被认为协调线粒体生物发生的三个组成部分:线粒体蛋白的合成、磷脂的合成和线粒体 DNA 的复制。鱼类和哺乳动物之间存在一些线粒体生物发生途径的保守成分,但该途径在鱼类中似乎更为多样。在低温适应鱼类的一些组织中,线粒体蛋白的合成增加而磷脂的合成没有增加,而在一些极地鱼类中,线粒体磷脂的密度增加而蛋白质的密度没有增加。冷体鱼类微调线粒体生物发生途径的能力可能使它们能够根据细胞的特定需求来改变线粒体的特征,无论是增加 ATP 的产生还是增强氧气的扩散。

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