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线粒体解偶联蛋白4和ATP敏感性钾通道的激活共同降低昆虫线粒体中的超氧化物生成。

Activation of Mitochondrial Uncoupling Protein 4 and ATP-Sensitive Potassium Channel Cumulatively Decreases Superoxide Production in Insect Mitochondria.

作者信息

Slocińska Malgorzata, Rosinski Grzegorz, Jarmuszkiewicz Wieslawa

机构信息

Department of Animal Physiology and Development, Adam Mickiewicz University, Umultowska 89, 61-614 Poznan, Poland.

出版信息

Protein Pept Lett. 2016;23(1):63-8. doi: 10.2174/0929866523666151106121943.

Abstract

It has been evidenced that mitochondrial uncoupling protein 4 (UCP4) and ATP-regulated potassium channel (mKATP channel) of insect Gromphadorhina coqereliana mitochondria decrease superoxide anion production. We elucidated whether the two energy-dissipating systems work together on a modulation of superoxide level in cockroach mitochondria. Our data show that the simultaneous activation of UCP4 by palmitic acid and mKATP channel by pinacidil revealed a cumulative effect on weakening mitochondrial superoxide formation. The inhibition of UCP4 by GTP (and/or ATP) and mKATP channel by ATP elevated superoxide production. These results suggest a functional cooperation of both energy-dissipating systems in protection against oxidative stress in insects.

摘要

已有证据表明,昆虫马达加斯加发声蟑螂线粒体中的线粒体解偶联蛋白4(UCP4)和ATP调节钾通道(mKATP通道)可减少超氧阴离子的产生。我们阐明了这两个能量耗散系统是否共同作用于调节蟑螂线粒体中的超氧水平。我们的数据表明,棕榈酸对UCP4的同时激活以及吡那地尔对mKATP通道的激活对减弱线粒体超氧形成具有累积效应。GTP(和/或ATP)对UCP4的抑制以及ATP对mKATP通道的抑制会增加超氧的产生。这些结果表明,这两个能量耗散系统在保护昆虫免受氧化应激方面存在功能协同作用。

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