Altered hepatic mitochondrial ribosome structure following chronic ethanol consumption.

Altered hepatic mitochondrial ribosome structure following chronic ethanol consumption.
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慢性乙醇消耗后肝线粒体核糖体结构发生改变。

DOI:
--
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发表时间:
2002
影响因子:
3.9
通讯作者:
C. Cunningham
C. Cunningham
中科院分区:
生物学3区
文献类型:
--
作者:
V. Patel;C. Cunningham

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慢性乙醇消耗减少了由肝线粒体基因组编码的所有13种多肽的合成。线粒体蛋白质合成的这种改变是由于线粒体核糖体的修饰。在目前的研究中,这些变化的性质进行了研究,通过确定一些流体动力学特性,即沉降系数,形状和线粒体核糖体的质量。乙醇消耗对线粒体核糖体翻译蛋白质的能力的影响也使用体外Poly(U)测定系统测定。大鼠喂食Lieber-DeCarli饮食31天,乙醇占总热量的36%。通过沉降速度分析测量的沉降系数在乙醇线粒体核糖体(53.2 +/- 0.5S)中略微但显著低于配对饲喂对照组(54.1 +/- 0.5S)(P = 0.04)。来自乙醇喂养动物的线粒体核糖体也有更大的倾向于解离成亚基。通过动态光散射测定的扩散系数,在来自乙醇喂养大鼠的线粒体核糖体中低于配对喂养对照组,这表明乙醇核糖体的直径(42.1 +/- 0.2 nm)显著大于来自配对喂养对照组的制剂(39.1 +/- 0.5 nm; P = 0.008)。尽管分子量没有变化,但乙醇线粒体核糖体发生了这些改变,这表明核糖体中存在显著的乙醇相关形状变化。从乙醇喂养的动物线粒体核糖体制剂的翻译能力显着降低,由于解离成轻,重亚基的单体。总之,这些观察结果表明,慢性乙醇消耗导致线粒体核糖体的显着结构和功能的改变。核糖体功能的丧失导致线粒体多肽合成受损,并且是引起线粒体核糖体结构改变的病理学的实例。
Chronic ethanol consumption decreases the synthesis of all 13 polypeptides encoded by the hepatic mitochondrial genome. This alteration in mitochondrial protein synthesis is due to modifications in mitochondrial ribosomes. In the current study, the nature of these alterations was investigated by determining some of the hydrodynamic properties, namely sedimentation coefficient, shape, and mass of mitochondrial ribosomes. The effect of ethanol consumption on the capacity for mitochondrial ribosomes to translate proteins was also determined using an in vitro Poly (U) assay system. Rats were fed the Lieber-DeCarli diet for 31 days with ethanol as 36% of total calories. The sedimentation coefficient, measured by sedimentation velocity analyses, was slightly, but significantly lower in ethanol mitochondrial ribosomes (53.2 +/- 0.5S) when compared with pair-fed controls (54.1 +/- 0.5S) (P = 0.04). Mitochondrial ribosomes from ethanol-fed animals also had a greater tendency to dissociate into subunits. The diffusion coefficient, determined by dynamic light scattering, was lower in mitochondrial ribosomes from ethanol-fed rats than pair-fed controls and this indicated a significantly greater diameter for ethanol ribosomes (42.1 +/- 0.2 nm) than for preparations from pair-fed controls (39.1 +/- 0.5 nm; P = 0.008). These alterations to ethanol mitochondrial ribosomes occurred despite no change in molecular mass, which suggested a significant ethanol-related shape change in the ribosomes. The translation capacity of mitochondrial ribosome preparations from ethanol-fed animals was markedly reduced due to dissociation of the monosome into light and heavy subunits. In summary, these observations demonstrate that chronic ethanol consumption causes significant structural and functional alterations to mitochondrial ribosomes. The loss in ribosome function leads to impaired mitochondrial polypeptide synthesis and is an example of a pathology giving rise to an alteration in the mitochondrial ribosome structure.
DOI: --
发表时间: 1981
期刊: The Journal of biological chemistry
影响因子: --
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影响因子: 3.1
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DOI: 10.1073/pnas.96.8.4301
发表时间: 1999-04-13
影响因子: 11.1
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DOI: 10.1111/j.1530-0277.2001.tb02273.x
发表时间: 2001-05-01
影响因子: 3.2
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乙醇消耗对细胞质和线粒体编码的 ATP 合酶亚基合成的不同影响。
DOI: 10.1111/j.1530-0277.1994.tb00064.x
发表时间: 1994
期刊: Alcoholism, clinical and experimental research
影响因子: --
作者:
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