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Lack of quinone reductase activity suggests that amyloid-beta peptide/ERAB induced lipid peroxidation is not directly related to production of reactive oxygen species by redoxcycling.
Toxicology ( IF 4.5 ) Pub Date : 2000-04-27 , DOI: 10.1016/s0300-483x(99)00203-6
S Salim 1 , C Filling , E Mårtensson , U C Oppermann
Affiliation  

Mitochondrial type II hydroxyacyl-CoA dehydrogenase (ERAB) has recently been shown to mediate amyloid-beta peptide (Abeta) induced apoptosis and neurodegeneration. The precise mechanism of cell death induction is unknown, however, Abeta inhibits ERAB activities and as a result of ERAB-Abeta interactions, enhanced formation of lipid peroxidation products occur. The possibility that ERAB mediates quinone reduction is therefore investigated, thus giving the potential of redoxcycling and production of reactive oxygen species, leading to lipid peroxidation. Recombinant human ERAB was produced in a bacterial expression system and enzymological properties were evaluated. Using several orthoquinones as substrates, no ERAB mediated quinone reductase activity was found either in the presence or absence of Abeta, suggesting that the observed in vivo lipid peroxidation is a result of other mechanisms than redoxcycling by quinones.

中文翻译:

缺乏醌还原酶活性表明淀粉样蛋白-β肽/ ERAB诱导的脂质过氧化与通过氧化还原循环产生活性氧没有直接关系。

线粒体II型羟酰基辅酶A脱氢酶(ERAB)最近已显示出介导淀粉样β肽(Abeta)诱导的细胞凋亡和神经变性。细胞死亡诱导的确切机制尚不清楚,但是,Abeta抑制ERAB活性,由于ERAB-Abeta相互作用,脂质过氧化产物的形成增强。因此,研究了ERAB介导醌还原的可能性,从而提供了氧化还原循环和产生活性氧的潜力,从而导致脂质过氧化。在细菌表达系统中产生重组人ERAB,并评估了酶学性质。使用几种邻醌作为底物,无论是否存在Abeta,均未发现ERAB介导的醌还原酶活性,
更新日期:2019-11-01
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