Zago M P, Verstraeten S V, Oteiza P I
Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Biol Res. 2000;33(2):143-50. doi: 10.4067/s0716-97602000000200014.
In the present study we characterized the capacity of zinc to protect lipids and proteins from Fe2+-initiated oxidative damage. The effects of zinc on lipid oxidation were investigated in liposomes composed of brain phosphatidylcholine (PC) and phosphatidylserine (PS) at a molar relationship of 60:40 (PC:PS, 60:40). Lipid oxidation was evaluated as the oxidation of cis-parinaric acid or as the formation of 2-thiobarbituric acid-reactive substances (TBARS). Zinc protected liposomes from Fe2+ (2.5-50 microM)-supported lipid oxidation. However, zinc (50 microM) did not prevent the oxidative inactivation of glutamine synthetase and glucose 6-phosphate dehydrogenase when rat brain supernatants were oxidized in the presence of 5 microM Fe2+ and 0.5 mM H2O2. We also studied the interactions of zinc with epicatechin in the prevention of lipid oxidation in liposomes. The simultaneous addition of 0.5 microM epicatechin (EC) and 50 microM zinc increased the protection of liposomes from oxidation compared to that observed in the presence of zinc or EC separately. Zinc (50 microM) also protected liposomes from the stimulatory effect of aluminum on Fe2+-initiated lipid oxidation. Zinc could play an important role as an antioxidant in biological systems, replacing iron and other metals with pro-oxidant activity from binding sites and interacting with other components of the oxidant defense system.
在本研究中，我们对锌保护脂质和蛋白质免受亚铁离子引发的氧化损伤的能力进行了表征。在由脑磷脂酰胆碱（PC）和磷脂酰丝氨酸（PS）以60:40（PC:PS，60:40）的摩尔比组成的脂质体中，研究了锌对脂质氧化的影响。脂质氧化通过顺式-紫黄质酸的氧化或2-硫代巴比妥酸反应性物质（TBARS）的形成来评估。锌保护脂质体免受亚铁离子（2.5 - 50微摩尔）支持的脂质氧化。然而，当大鼠脑匀浆上清液在5微摩尔亚铁离子和0.5毫摩尔过氧化氢存在下被氧化时，锌（50微摩尔）并不能防止谷氨酰胺合成酶和葡萄糖6-磷酸脱氢酶的氧化失活。我们还研究了锌与表儿茶素在预防脂质体脂质氧化中的相互作用。与单独存在锌或表儿茶素时相比，同时添加0.5微摩尔表儿茶素（EC）和50微摩尔锌增强了脂质体对氧化的保护作用。锌（50微摩尔）还保护脂质体免受铝对亚铁离子引发的脂质氧化的刺激作用。锌作为生物系统中的抗氧化剂可能发挥重要作用，取代具有促氧化活性的铁和其他金属与结合位点结合，并与氧化防御系统的其他成分相互作用。
