Lankin V Z, Sharapov M G, Goncharov R G, Tikhaze A K, Novoselov V I
National Medical Research Center of Cardiology, Ministry of Healthcare of the Russian Federation, 121552, Moscow, Russia.
Institute of Cell Biophysics, Russian Academy of Sciences, 142290, Pushchino, Moscow oblast, Russia.
Dokl Biochem Biophys. 2019 Mar;485(1):132-134. doi: 10.1134/S1607672919020157. Epub 2019 Jun 14.
It was established that recombinant human peroxiredoxins (Prx1, Prx2, Prx4, and Prx6) inhibit natural dicarbonyls formed during free radical peroxidation of unsaturated lipids (malonic dialdehyde) and oxidative transformations of glucose (glyoxal and methylglyoxal). A possible role of the decrease in the activity of peroxiredoxins under oxidative and carbonyl stress is discussed as an important factor that triggers the molecular mechanisms of vascular wall damage in atherosclerosis and diabetes mellitus.
已证实重组人过氧化物还原酶（Prx1、Prx2、Prx4和Prx6）可抑制不饱和脂质自由基过氧化过程中形成的天然二羰基化合物（丙二醛）以及葡萄糖的氧化转化产物（乙二醛和甲基乙二醛）。本文讨论了在氧化应激和羰基应激下过氧化物还原酶活性降低的可能作用，认为这是引发动脉粥样硬化和糖尿病中血管壁损伤分子机制的一个重要因素。
