bims-cytox1 2017-03-12 papers

Issue of 2017‒03‒12
two papers selected by
Gavin McStay
New York Institute of Technology

Biochemistry (Mosc). 2016 Dec;81(12): 1401-1405

R A Zinovkin, M V Skulachev, V P Skulachev.

The mitochondrial genome provides not only respiratory chain function, but it also ensures the impact of mitochondria on nearly all crucial metabolic processes. It is well known that mitochondria regulate aging and lifespan. However, until now there were no direct experimental data concerning the influence of various mitochondrial DNA variants on lifespan of animals with identical nuclear genome. In a recent paper of J. A. Enríquez and coworkers (Latorre-Pellicer, A., et al. (2016) Nature, 535, 561-565), it was shown that mice carrying nuclear DNA from one strain and mitochondrial DNA from another had longer median lifespan and retarded development of various aging traits. This review critically analyzes that paper and considers some aspects of the crosstalk between the nuclear and mitochondrial genomes. We also discuss new perspectives of gerontology in the light of the discovery made by Enríquez's group.

DOI: https://doi.org/10.1134/S0006297916120014

Redox Biol. 2017 Feb 24. pii: S2213-2317(17)30004-6. [Epub ahead of print]12 208-215

Mitochondrial composition and function under the control of hypoxia.

Dominik C Fuhrmann, Bernhard Brüne.

Hypoxia triggers several mechanisms to adapt cells to a low oxygen environment. Mitochondria are major consumers of oxygen and a potential source of reactive oxygen species (ROS). In response to hypoxia they exchange or modify distinct subunits of the respiratory chain and adjust their metabolism, especially lowering the citric acid cycle. Intermediates of the citric acid cycle participate in regulating hypoxia inducible factors (HIF), the key mediators of adaptation to hypoxia. Here we summarize how hypoxia conditions mitochondria with consequences for ROS-production and the HIF-pathway.

Keywords: HIF; Hypoxia; Mitochondria; ROS; Respiratory chain

DOI: https://doi.org/10.1016/j.redox.2017.02.012