Aldehyde reductase gene expression by lipid peroxidation end products, MDA and HNE
Aldehyde reductase gene expression by lipid peroxidation end products, MDA and HNE
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DOI：
10.1080/10715760000301261
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发表时间：
2000-01-01
影响因子：
3.3
通讯作者：
Taniguchi, N
中科院分区：
文献类型：
--
作者：
Koh, YH;Park, YS;Taniguchi, N
膜脂质过氧化导致产生多种在衰老、药物毒性和许多人类疾病（如动脉粥样硬化和癌症）的发病机制中起重要作用的脂质化合物。脂质过氧化增加和抗氧化状态降低也可能导致糖尿病并发症的发生。本研究报告，脂质过氧化终产物，如丙二醛（MDA）和4-羟基壬烯醛（HNE）诱导醛还原酶（ALR）基因的表达。MDA和HNE诱导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引起的细胞内过氧化物水平的增加可能参与了ALR的上调。
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.