6533b822fe1ef96bd127cb18

RESEARCH PRODUCT

G6PD Overexpression Protects Mice Against Associated Oxidative Stress and Delays the Occurrence of Frailty

Mari Carmen Gomez-cabreraAndrea Salvador-pascualManuel SerranoJuana M. FloresMiriam Quintela DiazThomas BriocheSandrina Nóbrega-pereiraJose ViñaPablo J. Fernandez-marcos

subject

chemistry.chemical_classificationmedicine.medical_specialtyReactive oxygen speciesProtein CarbonylationGlutathioneDNA oxidationBiologyMalondialdehydemedicine.disease_causeBiochemistrychemistry.chemical_compoundGrip strengthEndocrinologychemistryLipid oxidationPhysiology (medical)Internal medicineImmunologymedicineOxidative stress

description

To assess the impact of lifelong overexpression of G6PD on reactive oxygen species (ROS)-derived damage and the prevention of frailty, we measured the levels of macromolecular oxidative damage in young and old mice and the we tested the neuromuscular fitness and the grip strength in old mice. Old G6PD-Tg male and female mice showed diminished accumulation of DNA oxidation (measured as 8-hydroxyguanosine or 8-OHdG) in liver and brain. Old females also showed reduced lipid oxidation (measured as malondialdehyde or MDA) in the liver. Old G6PD-Tg males, but not females, presented a small but significant increase in brain protein carbonylation. In accordance with these findings, liver from 2-year-old G6PD-Tg female mice presented an elevated reduced versus oxidized gluthatione ratio (GSH:GSSG) ratio, due to an elevation in reduced GSH.Old G6PD-Tg female mice at 1.5–2 years of age also showed a significant improvement in neuromuscular fitness (evaluated by the Rotarod test) and in the maximum and mean grip strength, both parameters related to frailty. Our data point out that G6PD overexpression in mice protects against ROS-derived damage at old age.

yearjournalcountryeditionlanguage
2016-11-01Free Radical Biology and Medicine
https://doi.org/10.1016/j.freeradbiomed.2016.10.224