Meglio L, Oteiza P I
Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Neurochem Res. 1999 Aug;24(8):1001-8. doi: 10.1023/a:1021000709082.
The present study was conducted to characterize the possible interaction of Al3+ and Fe2+ with synthetic melanin in the potentiation of lipid peroxidation in liposomes and rat caudate-putamen homogenates. Al3+ stimulated melanin-initiated lipid peroxidation as measured by the production of 2-thiobarbituric acid-reactive substances (TBARS) and conjugated dienes. The effect of A13+ was dependent on melanin (10-100 microg/ml) and A13+ (2.5-250 microM) concentrations and no synergism between Fe2+ and Al3+ was observed. The prooxidant effect of Al3+ was partially inhibited by superoxide dismutase indicating the involvement of O2*- . Ga3+ and Be2+ which can increase NADH oxidation in the presence of O2*-, also were shown to stimulate melanin-initiated TBARS production. Based on the effect of Al3+ and other non redox metals, we suggest that Al3+ does not act through either the induction of melanin free radicals, or the induction of changes in membrane physical properties. Results show that Al3+ enhances melanin-initiated lipid peroxidation in part through an interaction with O2*- generated from the autoxidation of melanin. We speculate that Al3+ contributes to neuromelanin-mediated oxidative damage in dopaminergic neurons and subsequent neuronal degeneration and death in Parkinson's disease.
本研究旨在表征Al3+和Fe2+与合成黑色素在脂质体和大鼠尾状核-壳核匀浆中脂质过氧化增强过程中可能的相互作用。通过2-硫代巴比妥酸反应性物质(TBARS)和共轭二烯的产生来衡量,Al3+刺激了黑色素引发的脂质过氧化。Al3+的作用取决于黑色素(10-100微克/毫升)和Al3+(2.5-250微摩尔)的浓度,并且未观察到Fe2+与Al3+之间的协同作用。超氧化物歧化酶部分抑制了Al3+的促氧化作用,表明O2*-参与其中。在O2*-存在下可增加NADH氧化的Ga3+和Be2+,也被证明能刺激黑色素引发的TBARS产生。基于Al3+和其他非氧化还原金属的作用,我们认为Al3+既不是通过诱导黑色素自由基,也不是通过诱导膜物理性质的变化来起作用。结果表明,Al3+部分通过与黑色素自氧化产生的O2*-相互作用来增强黑色素引发的脂质过氧化。我们推测Al3+在帕金森病中促成了神经黑色素介导的多巴胺能神经元氧化损伤以及随后的神经元变性和死亡。