Istituto di Biomembrane, Bioenergetica e Biotecnologie Molecolari (IBIOM)-CNR, Via G. Amendola 122/O, 70126 Bari, Italy.
Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università di Bari, Via E. Orabona 4, 70126 Bari, Italy.
Int J Mol Sci. 2021 Jan 19;22(2):967. doi: 10.3390/ijms22020967.
The redox states of NAD and NADP are linked to each other in the mitochondria thanks to the enzyme nicotinamide nucleotide transhydrogenase (NNT) which, by utilizing the mitochondrial membrane potential (mΔΨ), catalyzes the transfer of redox potential between these two coenzymes, reducing one at the expense of the oxidation of the other. In order to define NNT reaction direction in CF cells, NNT activity under different redox states of cell has been investigated. Using spectrophotometric and western blotting techniques, the presence, abundance and activity level of NNT were determined. In parallel, the levels of NADPH and NADH as well as of mitochondrial and cellular ROS were also quantified. CF cells showed a 70% increase in protein expression compared to the Wt sample; however, regarding NNT activity, it was surprisingly lower in CF cells than healthy cells (about 30%). The cellular redox state, together with the low mΔΨ, pushes to drive NNT reverse reaction, at the expense of its antioxidant potential, thus consuming NADPH to support NADH production. At the same time, the reduced NNT activity prevents the NADH, produced by the reaction, from causing an explosion of ROS by the damaged respiratory chain, in accordance with the reduced level of mitochondrial ROS in NNT-loss cells. This new information on cellular bioenergetics represents an important building block for further understanding the molecular mechanisms responsible for cellular dysfunction in cystic fibrosis.
由于酶烟酰胺核苷酸转氢酶 (NNT) 的存在,NAD 和 NADP 的氧化还原状态在线粒体中相互关联,该酶利用线粒体膜电位 (mΔΨ) 催化这两种辅酶之间的氧化还原电势转移,以牺牲另一种辅酶的氧化为代价还原一种辅酶。为了确定 CF 细胞中 NNT 的反应方向,研究了细胞在不同氧化还原状态下的 NNT 活性。使用分光光度法和蛋白质印迹技术确定了 NNT 的存在、丰度和活性水平。同时,还定量了 NADPH 和 NADH 以及线粒体和细胞 ROS 的水平。与野生型 (Wt) 样本相比,CF 细胞中的 NNT 蛋白表达增加了 70%;然而,令人惊讶的是,CF 细胞中的 NNT 活性比健康细胞低(约 30%)。细胞氧化还原状态和低 mΔΨ 促使 NNT 逆反应发生,牺牲其抗氧化潜力,从而消耗 NADPH 以支持 NADH 的产生。同时,降低的 NNT 活性阻止了由反应产生的 NADH 通过受损的呼吸链引起 ROS 的爆发,这与 NNT 缺失细胞中线粒体 ROS 水平降低一致。关于细胞能量代谢的这一新信息是进一步了解囊性纤维化中细胞功能障碍的分子机制的重要组成部分。