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首页> 外文期刊>Journal of biochemical and molecular toxicology >Interactions of a new 2-styrylchromone with mitochondrial oxidative phosphorylation.
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Interactions of a new 2-styrylchromone with mitochondrial oxidative phosphorylation.

机译：新的2-苯乙烯基色酮与线粒体氧化磷酸化的相互作用。

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摘要

Many chromones, especially those having 2-substituents, manifest a remarkable variety of biological activities, such as the important cytotoxicity against human leukaemia cells, antiallergic, anticancer activities; unfortunately chromones normally disturb mitochondrial bioenergetics. A new 2-styrylchromone has been synthesized by the Baker-Venkataraman method and a classical approach has been used to assess the effects of 2-styrylchromone (3'-allyl-4',5,7-trimethoxy-2-styrylchromone) on rat liver mitochondrial bioenergetic. Mitochondrial respiratory rate and transmembrane potential were measured polarographically using a Clark oxygen electrode and with a selective electrode, respectively. All the disturbance induced by 2-styrylchromone on the enzymatic activities (succinate dehydrogenase, succinate cytochrome c reductase, and cytochrome c oxidase) and in the mitochondrial osmotic volume were determined spectrophotometrically. State 4, state 3, and uncoupled (presence of carbonylcyanide p-trifluoromethoxyphenylhydrazone) respiration rates were decreased by 2-styrylchromone in a concentration-dependent manner. Depression of respiratory activity promoted by 2-styrylchromone is essentially mediated through partial inhibition of succinate cytochrome c reductase. Phosphorylation capacity was strongly depressed as a result of an inhibition on the enzymatic complex (F(0)F(1)-ATPase) and also because of a deleterious effect on the integrity of the mitochondrial membrane, which uncoupled the respiration-generated proton gradient with the proton-driven phosphorylation. The structural integrity of the outside membrane is severely affected since cytochrome c can be released. 2-Styrylchromone uncouples oxidative phosphorylation by an inhibitory action on the redox chain and ATP synthase activity. Additionally, it can release cytochrome c. Cell death can probably result due to the induction of procaspase-9 and other procaspases and by a strong decrease of the available ATP.
机译：许多色酮，特别是具有2个取代基的色酮，表现出显着的生物学活性，例如对人白血病细胞的重要细胞毒性，抗过敏，抗癌活性;等等。不幸的是，色酮通常会干扰线粒体的生物能。通过Baker-Venkataraman方法合成了一种新的2-苯乙烯基色酮，并且经典方法已用于评估2-苯乙烯基色酮（3'-烯丙基-4'，5,7-三甲氧基-2-苯乙烯基色酮）的作用。肝线粒体的生物能。分别使用克拉克氧电极和选择性电极极谱法测量线粒体呼吸速率和跨膜电位。分光光度法测定了2-苯乙烯基色酮对酶活性（琥珀酸脱氢酶，琥珀酸细胞色素C还原酶和细胞色素C氧化酶）和线粒体渗透体积的所有干扰。 2-苯乙烯基色酮以浓度依赖的方式降低了状态4，状态3和未耦合（存在羰基氰化物对三氟甲氧基苯基hydr）的呼吸速率。由2-苯乙烯基色酮促进的呼吸活动抑制基本上是通过部分抑制琥珀酸细胞色素c还原酶来介导的。磷酸化能力由于抑制酶复合物（F（0）F（1）-ATPase）以及对线粒体膜完整性的有害作用而强烈降低，该作用解耦了呼吸产生的质子梯度质子驱动的磷酸化由于可以释放细胞色素c，因此严重影响了外膜的结构完整性。 2-苯乙烯基色酮通过对氧化还原链和ATP合酶活性的抑制作用使氧化磷酸化解偶联。此外，它可以释放细胞色素c。细胞死亡可能归因于procaspase-9和其他procaspase的诱导以及有效ATP的强烈降低。

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