Félix Christen, Doctorat, UQAR
Supervision : Pierre Blier (UQAR), Grant Vandenberg (U. Laval)
Voici le titre et le résumé de l’article publié par Félix dans le journal Free Radical Biology & Medecine:
Thermal tolerance and thermal sensitivity of heart mitochondria: Mitochondrial integrity and ROS production
Christen F1, Desrosiers V1, Dupont-Cyr BA1, Vandenberg GW2, Le François NR3, Tardif JC4, Dufresne F1, Lamarre SG5, Blier PU6.
1 Université du Québec à Rimouski, Département de biologie, Rimouski, Québec, Canada G5L3A1.
2 Université Laval, Département de sciences animales, Québec, Canada G1V 0A6.
3 Biodôme de Montréal, Montréal, Québec, Canada H1V 1B3.
4 Montreal Heart Institute, Université de Montréal, Montréal, Québec, Canada H1T 1C8.
5 Université de Moncton, Département de biologie, Moncton, New-Brunswick, Canada E1A 3E9.
6 Université du Québec à Rimouski, Département de biologie, Rimouski, Québec, Canada G5L3A1. Electronic address: Pierre_Blier@uqar.ca.
Free Radic Biol Med. 2018 Feb 20;116:11-18. doi: 10.1016/j.freeradbiomed.2017.12.037. Epub 2017 Dec 30.
Cardiac mitochondrial metabolism provides 90% of the ATP necessary for the contractile exertion of the heart muscle. Mitochondria are therefore assumed to play a pivotal role in heart failure (HF), cardiovascular disease and ageing. Heat stress increases energy metabolism and oxygen demand in tissues throughout the body and imposes a major challenge on the heart, which is suspected of being the first organ to fail during heat stress. The underlying mechanisms inducing heart failure are still unclear. To pinpoint the processes implicated in HF during heat stress, we measured mitochondrial respiration rates and hydrogen peroxide production of isolated Arctic char (Salvelinus alpinus) heart mitochondria at 4 temperatures: 10°C (acclimation), 15°C, 20°C and 25°C (just over critical maximum). We found that at temperature ranges causing the loss of an organism’s general homeostasis (between 20°C and 25°C) and with a substrate combination close to physiological conditions, the heat-induced increase in mitochondrial oxygen consumption levels off. More importantly, at the same state, hydrogen peroxide efflux increased by almost 50%. In addition, we found that individuals with low mitochondrial respiration rates produced more hydrogen peroxide at 10°C, 15°C and 20°C. This could indicate that individuals with cardiac mitochondria having a low respiratory capacity, have a more fragile heart and will be more prone to oxidative stress and HF, and less tolerant to temperature changes and other stressors. Our results show that, at temperatures close to the thermal limit, mitochondrial capacity is compromised and ROS production rates increase. This could potentially alter the performance of the cardiac muscle and lead to heat-induced HF underlining the important role that mitochondria play in setting thermal tolerance limits.
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