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Aldehyde reductase gene expression by lipid peroxidation end products, MDA and HNE.

机译:脂质过氧化终产物MDA和HNE的醛还原酶基因表达。

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Membrane lipid peroxidation results in the production of a variety of aldehydic compounds that play a significant role in aging, drug toxicity and the pathogenesis of a number of human diseases, such as atherosclerosis and cancer. Increased lipid peroxidation and reduced antioxidant status may also contribute to the development of diabetic complications. This study reports that lipid peroxidation end products such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE) induce aldehyde reductase (ALR) gene expression. MDA and HNE induce an increase in intracellular peroxide levels; N-Acetyl-L-cysteine (NAC) suppressed MDA- and HNE-induced ALR gene expression. These results indicate that increased levels of intracellular peroxides by MDA and HNE might be involved in the upregulation of ALR.
机译:膜脂质过氧化作用导致产生各种醛类化合物,这些化合物在衰老,药物毒性和许多人类疾病(如动脉粥样硬化和癌症)的发病机理中起重要作用。脂质过氧化的增加和抗氧化剂状态的降低也可能导致糖尿病并发症的发展。这项研究报告脂质过氧化终产物如丙二醛(MDA)和4-羟基壬烯(HNE)诱导醛还原酶(ALR)基因表达。 MDA和HNE引起细胞内过氧化物水平增加; N-乙酰-L-半胱氨酸(NAC)抑制MDA和HNE诱导的ALR基因表达。这些结果表明MDA和HNE增加的细胞内过氧化物水平可能与ALR的上调有关。

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