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首页> 外文期刊>Journal of toxicology and environmental health, Part A >Lipid peroxidation facilitates aluminum accumulation in rat brain synaptosomes.
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Lipid peroxidation facilitates aluminum accumulation in rat brain synaptosomes.

机译:脂质过氧化促进铝在大鼠脑突触体中的积累。

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Aluminum, a metal without redox capacity in biological systems, potentiates the stimulation of lipid peroxidation induced by Fe2+. In this study the interactions between aluminum and oxidative stress induced by ascorbate (0.8 mM)/Fe2+ (2.5 microM) in synaptosomes isolated from rat brain were investigated. The amount of Al3+ in aluminum solutions was calculated according to the Zatta protocol (Zatta et al., 1995), and lipid peroxidation was measured by quantifying thiobarbituric acid-reactive substances (TBARS). In synaptosomes under oxidizing conditions the addition of 11 microM Al3+ increased the formation of TBARS. In synaptosomes incubated in the absence of oxidants no significant differences were found between the levels of lipid peroxidation of synaptosomes incubated in the absence or in the presence of aluminum. In the presence of an oxidizing system aluminum accumulation was significantly increased twofold in synaptosomes. Data suggest that the facilitation of aluminum accumulation during brain oxidative injury might contribute to aluminum neurotoxicity and neuronal cell degeneration.
机译:铝是一种在生物系统中没有氧化还原能力的金属,可增强刺激由Fe2 +引起的脂质过氧化作用。在这项研究中,研究了铝与抗坏血酸(0.8 mM)/ Fe2 +(2.5 microM)在大鼠脑突触小体中诱导的氧化应激之间的相互作用。根据Zatta协议(Zatta等,1995)计算铝溶液中Al3 +的量,并通过定量硫代巴比妥酸反应性物质(TBARS)测量脂质过氧化作用。在氧化条件下的突触小体中,添加11 microM Al3 +可增加TBARS的形成。在不存在氧化剂的情况下孵育的突触体中,在不存在或存在铝的情况下孵育的突触体的脂质过氧化水平之间未发现显着差异。在存在氧化系统的情况下,突触小体中铝的积累显着增加了两倍。数据表明,在脑部氧化损伤期间促进铝积累可能有助于铝神经毒性和神经元细胞变性。

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