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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >The effect of cysteine on the altered expression of class α and μ glutathione S-transferase genes in the rat liver during protein-calorie malnutrition
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The effect of cysteine on the altered expression of class α and μ glutathione S-transferase genes in the rat liver during protein-calorie malnutrition

机译：半胱氨酸对蛋白质热量营养不良期间大鼠肝脏α和μ型谷胱甘肽S-转移酶基因表达改变的影响

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Protein-calorie malnutrition (PCM) represents a global health problem. The breakdown rate of glutathione S-transferase (GST) subunits determines their differential contents during protein depletion. Hepatic GST expression and the underlying mechanistic basis were investigated in PCM rats. PCM caused no change in rGSTA1/2 subunit. In contrast, rGSTA3/5 subunit was 2.4-fold induced during PCM, while the levels for rGSTM1 and M2 subunits were 30% and 70% suppressed. Increased GSTA3/5 expression was significantly prevented by cysteine or methionine treatment, although such treatment failed to restore the rGSTM2 level. In contrast to differential GST protein expression, PCM caused a 5-10-fold increase in rGSTA2/A3/A5 and M1 mRNAs, whereas rGSTM2 mRNA was 70% decreased. The elevations in rGSTA2/A3/A5 and M1 mRNAs were completely abolished by cysteine or methionine treatment during PCM, although the rGSTM2 mRNA level was not restored. PCM induced oxidative stress in the liver, as evidenced by protein carbonylation. Antioxidant response element (ARE)-binding activity of nuclear extracts from PCM rats was increased, which was immunodepleted with anti-Nrf-1/2 antibodies. Activation of nuclear ARE-binding proteins was inhibited by cysteine. Data showed that hepatic GSTs were differentially expressed during PCM, that certain GST mRNAs were increased with the ARE activation, and that cysteine was active in preventing increases in GST mRNAs and ARE activation.
机译：蛋白质热量营养不良（PCM）代表全球性的健康问题。谷胱甘肽S-转移酶（GST）亚基的分解速率决定了它们在蛋白质消耗过程中的差异含量。研究了PCM大鼠肝脏GST表达及其潜在的机制基础。 PCM在rGSTA1 / 2子单元中未引起任何变化。相比之下，rGSTA3 / 5亚基在PCM期间被诱导为2.4倍，而rGSTM1和M2亚基的水平被抑制30％和70％。半胱氨酸或蛋氨酸处理可明显阻止GSTA3 / 5表达增加，尽管这种处理无法恢复rGSTM2水平。与差异GST蛋白表达相反，PCM导致rGSTA2 / A3 / A5和M1 mRNA增加5-10倍，而rGSTM2 mRNA降低70％。 PCM期间，通过半胱氨酸或蛋氨酸处理完全消除了rGSTA2 / A3 / A5和M1 mRNA的升高，尽管rGSTM2 mRNA的水平并未恢复。如蛋白羰基化所证明，PCM在肝脏中引起氧化应激。来自PCM大鼠的核提取物的抗氧化反应元件（ARE）结合活性增加，该活性被抗Nrf-1 / 2抗体免疫消耗。半胱氨酸抑制核ARE结合蛋白的激活。数据显示，肝GST在PCM期间差异表达，某些GST mRNA随着ARE激活而增加，而半胱氨酸在阻止GST mRNA和ARE激活增加方面具有活性。

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