Panov A V, Vavilin V A, Lyakhovich V V, Brooks B R, Bonkovsky H L
Cannon Research Center, Carolinas Medical Center, Charlotte, North Carolina, USA.
Bull Exp Biol Med. 2010 Aug;149(2):187-90. doi: 10.1007/s10517-010-0904-5.
We studied the effect of BSA (in the isolation medium) on the oxidation rate of succinate, glutamate, pyruvate, and α-ketoglutarate by mitochondria of the brain and liver from C57Bl/6g mice and Taconic Sprague Dawley rats. BSA had no effect on liver mitochondrial respiration, but increased oxidation of substrates (particularly of succinate) in brain mitochondria. Therefore, the major effect of BSA on brain mitochondria is manifested in activation of SDH. The improvement of mitochondrial properties in the brain after treatment with BSA is associated with antioxidant activity of this agent. Our results confirm the hypothesis that inhibition of SDH in brain mitochondria is not the artifact. This process serves as a mechanism protecting neurons from free oxygen radicals during succinate oxidation.
我们研究了（在分离培养基中的）牛血清白蛋白（BSA）对C57Bl/6g小鼠和塔康尼克斯普拉格-道利大鼠脑和肝线粒体氧化琥珀酸、谷氨酸、丙酮酸和α-酮戊二酸速率的影响。BSA对肝线粒体呼吸没有影响，但增加了脑线粒体中底物（尤其是琥珀酸）的氧化。因此，BSA对脑线粒体的主要作用表现为琥珀酸脱氢酶（SDH）的激活。用BSA处理后，脑中线粒体特性的改善与该试剂的抗氧化活性有关。我们的结果证实了脑线粒体中SDH的抑制不是人为现象这一假设。这一过程是琥珀酸氧化过程中保护神经元免受游离氧自由基损伤的一种机制。
