Gudkov L L, Shumaev K B, Kalenikova E I, Gubkina S A, Vanin A F, Ruuge E K
Biofizika. 2007 May-Jun;52(3):503-9.
It has been shown that various nitric oxide donors and metabolites have similar effects on lipid peroxidation in rat myocardium homogenate. The formation of malondialdehyde, a secondary product of lipid peroxidation, was inhibited in a dose-dependent manner by PAPA/NONO (a synthetic nitric oxide donor), S-nitrosoglutathione, nitrite, and nitroxyl anion. The inhibition of lipid peroxidation was provided most efficiently by the administration of dinitrosyl-iron complexes with dextran and PAPA/NONO. S-nitrosoglutathione also inhibited the destruction of coenzymes Q9 and Q10 during free radical oxidation of myocardium homogenate. Low-molecular-weight dinitrosyl iron complexes with cysteine also promoted lipid peroxidation, which is probably due to iron release during the destruction dinitrosyl iron complexes. It is likely that the antioxidant action of nitric oxide derivatives is related to the reduction of ferry forms of hemoproteins and interaction of nitric oxide with lipid radicals.
已经表明，各种一氧化氮供体和代谢产物对大鼠心肌匀浆中的脂质过氧化具有相似的作用。脂质过氧化的次级产物丙二醛的形成受到PAPA/NONO（一种合成一氧化氮供体）、S-亚硝基谷胱甘肽、亚硝酸盐和硝酰阴离子的剂量依赖性抑制。通过给予与右旋糖酐的二亚硝基铁配合物和PAPA/NONO能最有效地抑制脂质过氧化。S-亚硝基谷胱甘肽也抑制心肌匀浆自由基氧化过程中辅酶Q9和Q10的破坏。与半胱氨酸的低分子量二亚硝基铁配合物也促进脂质过氧化，这可能是由于二亚硝基铁配合物破坏过程中铁的释放。一氧化氮衍生物的抗氧化作用可能与血红素蛋白的 ferry 形式的还原以及一氧化氮与脂质自由基的相互作用有关。
