G6PD protects from oxidative damage and improves healthspan in mice

Sandrina Nóbrega-Pereira, Pablo J. Fernandez-Marcos (), Thomas Brioche, Mari Carmen Gomez-Cabrera, Andrea Salvador-Pascual, Juana M. Flores, Jose Viña () and Manuel Serrano ()
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Sandrina Nóbrega-Pereira: Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO)
Pablo J. Fernandez-Marcos: Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO)
Thomas Brioche: Université de Montpellier, INRA, UMR866, Dynamique Musculaire et Métabolisme
Mari Carmen Gomez-Cabrera: Faculty of Medicine, University of Valencia and Investigaciòn Hospital Clínico Universitario (INCLIVA)
Andrea Salvador-Pascual: Faculty of Medicine, University of Valencia and Investigaciòn Hospital Clínico Universitario (INCLIVA)
Juana M. Flores: Faculty of Veterinary Sciences, Complutense University of Madrid
Jose Viña: Faculty of Medicine, University of Valencia and Investigaciòn Hospital Clínico Universitario (INCLIVA)
Manuel Serrano: Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO)

Nature Communications, 2016, vol. 7, issue 1, 1-9

Abstract: Abstract Reactive oxygen species (ROS) are constantly generated by cells and ROS-derived damage contributes to ageing. Protection against oxidative damage largely relies on the reductive power of NAPDH, whose levels are mostly determined by the enzyme glucose-6-phosphate dehydrogenase (G6PD). Here, we report a transgenic mouse model with moderate overexpression of human G6PD under its endogenous promoter. Importantly, G6PD-Tg mice have higher levels of NADPH, lower levels of ROS-derived damage, and better protection from ageing-associated functional decline, including extended median lifespan in females. The G6PD transgene has no effect on tumour development, even after combining with various tumour-prone genetic alterations. We conclude that a modest increase in G6PD activity is beneficial for healthspan through increased NADPH levels and protection from the deleterious effects of ROS.

Date: 2016
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DOI: 10.1038/ncomms10894

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