Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres

Casagrande, S., Stier, A. , Monaghan, P. , Loveland, J. L., Boner, W., Lupi, S., Trevisi, R. and Hau, M. (2020) Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres. Journal of Experimental Biology, 223(15), jeb222513. (doi: 10.1242/jeb.222513) (PMID:32532864)

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Telomeres are DNA structures that protect chromosome ends. However, telomeres shorten during cell replication and at critically low lengths can reduce cell replicative potential, induce cell senescence and decrease fitness. Stress exposure, which elevates glucocorticoid hormone concentrations, can exacerbate telomere attrition. This phenomenon has been attributed to increased oxidative stress generated by glucocorticoids (‘oxidative stress hypothesis’). We recently suggested that glucocorticoids could increase telomere attrition during stressful periods by reducing the resources available for telomere maintenance through changes in the metabolic machinery (‘metabolic telomere attrition hypothesis’). Here, we tested whether experimental increases in glucocorticoid levels affected telomere length and mitochondrial function in wild great tit (Parus major) nestlings during the energy-demanding early growth period. We monitored resulting corticosterone (Cort) concentrations in plasma and red blood cells, telomere lengths and mitochondrial metabolism (metabolic rate, proton leak, oxidative phosphorylation, maximal mitochondrial capacity and mitochondrial inefficiency). We assessed oxidative damage caused by reactive oxygen species (ROS) metabolites as well as the total non-enzymatic antioxidant protection in plasma. Compared with control nestlings, Cort-nestlings had higher baseline corticosterone, shorter telomeres and higher mitochondrial metabolic rate. Importantly, Cort-nestlings showed increased mitochondrial proton leak, leading to a decreased ATP production efficiency. Treatment groups did not differ in oxidative damage or antioxidants. Hence, glucocorticoid-induced telomere attrition is associated with changes in mitochondrial metabolism, but not with ROS production. These findings support the hypothesis that shortening of telomere length during stressful periods is mediated by glucocorticoids through metabolic rearrangements.

Item Type:Articles
Additional Information:We are grateful to the Max Planck Society (Max-Planck-Gesellschaft) and the German Science Foundation (Deutsche Forschungsgemeinschaft grant CA 1789/1-1-2017) for supporting our work.
Glasgow Author(s) Enlighten ID:Monaghan, Professor Pat and Stier, Dr Antoine
Creator Roles:
Stier, A.Methodology, Validation, Writing – review and editing
Monaghan, P.Methodology, Validation, Writing – review and editing
Authors: Casagrande, S., Stier, A., Monaghan, P., Loveland, J. L., Boner, W., Lupi, S., Trevisi, R., and Hau, M.
College/School:College of Medical Veterinary and Life Sciences > School of Biodiversity, One Health & Veterinary Medicine
Journal Name:Journal of Experimental Biology
Publisher:Company of Biologists
ISSN (Online):1477-9145
Published Online:04 August 2020

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