Calcium overload increases oxidative stress in old rat gastrocnemius muscle
2005
Capel, Frédéric | Demaison, Luc | Maskouri, F. | Diot, Anne | Buffière, Caroline | Patureau-Mirand, Philippe | Mosoni, Laurent | Unité de nutrition et métabolisme protéique ; Institut National de la Recherche Agronomique (INRA) | FLAveur, VIsion et Comportement du consommateur (FLAVIC) ; Etablissement National d'Enseignement Supérieur Agronomique de Dijon (ENESAD)-Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB) | Institut National de la Santé et de la Recherche Médicale (INSERM) | Université Joseph Fourier - Grenoble 1 (UJF)
International audience
显示更多 [+] 显示较少 [-]英语. In order to challenge in vivo muscle Ca2+ homeostasis and analyze consequences on mitochondrial H2O2 release (MHR) and sarcopenia, we injected Ca2+ ionophore A23187 (200 µg/kg, ip) in adult and old rats and measured gastrocnemius mass and mitochondrial Ca2+ content (MCC) using radioactive Ca2+ 48 h after injection. In a second experiment performed in old rats, we measured isocitrate dehydrogenase (ICDH) activity as an index of MCC, MHR, mitochondrial respiration, citrate synthase, COX and antioxydant enzyme activities 24 h after a 150 µg/kg injection. In adult rats, muscle mass and MCC were unchanged by A23187. In old rats, MCC increased 24 h after injection as reflected by a significant increase in ICDH activity; measured MCC tended to increase at 48 h. MHR and Mn-SOD activity were significantly increased at 24 h, and GPX activity was reduced. Muscle mass was unchanged but was negatively correlated with MCC in control and treated old rats. In conclusion, in old rats, A23187 probably induced a mitochondrial Ca2+ overload responsible for the observed increase in MHR without leading to muscle atrophy on a short term basis.
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