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Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle.
Arch Biochem Biophys. 1999 Dec 15; 372(2):315-20.AB

Abstract

In this study, oxygen consumption and H(2)O(2) release rate by succinate or pyruvate/malate supplemented mitochondria isolated from skeletal muscle of trained and untrained rats were investigated. The overall mitochondrial antioxidant capacity and the effect of preincubation of mitochondria with GDP, an inhibitor of uncoupling proteins UCP1 and UCP2, on both succinate-supported H(2)O(2) release and membrane potential were also determined. The results indicate that training does not affect mitochondrial oxygen consumption with both complex-I- and complex II-linked substrates. Succinate-supported H(2)O(2) release was lower in trained than in untrained rats both in State 4 and State 3. Even the antimycin A-stimulated release was lower in trained rats. When pyruvate/malate were used as substrates, H(2)O(2) release rate was lower in trained rats only in the presence of antimycin A. The increase of mitochondrial protein content (determined by the ratio between cytochrome oxidase activities in homogenates and mitochondria) in trained muscle was such that the succinate-supported H(2)O(2) release per g of tissue was not significantly different in trained and untrained rats, while that supported by pyruvate/malate was higher in trained than in untrained animals. The lack of training-induced changes in overall antioxidant capacity of mitochondria indicates that the decrease in mitochondrial H(2)O(2) release cannot be attributed to a greater capacity of mitochondria to scavenge the reactive oxygen intermediates derived from univalent O(2) reduction by respiratory chain components. In contrast, the above decrease seems to depend on the drop induced by training in mitochondrial membrane potential. These training effects are not due to an increased level of mitochondrial uncoupling protein, because in the presence of GDP the increase in both membrane potential and H(2)O(2) release was greater in untrained than in trained rats.

Authors+Show Affiliations

Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli, Napoli, I-80134, Italy.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10600170

Citation

Venditti, P, et al. "Effect of Training On H(2)O(2) Release By Mitochondria From Rat Skeletal Muscle." Archives of Biochemistry and Biophysics, vol. 372, no. 2, 1999, pp. 315-20.
Venditti P, Masullo P, Di Meo S. Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle. Arch Biochem Biophys. 1999;372(2):315-20.
Venditti, P., Masullo, P., & Di Meo, S. (1999). Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle. Archives of Biochemistry and Biophysics, 372(2), 315-20.
Venditti P, Masullo P, Di Meo S. Effect of Training On H(2)O(2) Release By Mitochondria From Rat Skeletal Muscle. Arch Biochem Biophys. 1999 Dec 15;372(2):315-20. PubMed PMID: 10600170.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle. AU - Venditti,P, AU - Masullo,P, AU - Di Meo,S, PY - 1999/12/22/pubmed PY - 1999/12/22/medline PY - 1999/12/22/entrez SP - 315 EP - 20 JF - Archives of biochemistry and biophysics JO - Arch Biochem Biophys VL - 372 IS - 2 N2 - In this study, oxygen consumption and H(2)O(2) release rate by succinate or pyruvate/malate supplemented mitochondria isolated from skeletal muscle of trained and untrained rats were investigated. The overall mitochondrial antioxidant capacity and the effect of preincubation of mitochondria with GDP, an inhibitor of uncoupling proteins UCP1 and UCP2, on both succinate-supported H(2)O(2) release and membrane potential were also determined. The results indicate that training does not affect mitochondrial oxygen consumption with both complex-I- and complex II-linked substrates. Succinate-supported H(2)O(2) release was lower in trained than in untrained rats both in State 4 and State 3. Even the antimycin A-stimulated release was lower in trained rats. When pyruvate/malate were used as substrates, H(2)O(2) release rate was lower in trained rats only in the presence of antimycin A. The increase of mitochondrial protein content (determined by the ratio between cytochrome oxidase activities in homogenates and mitochondria) in trained muscle was such that the succinate-supported H(2)O(2) release per g of tissue was not significantly different in trained and untrained rats, while that supported by pyruvate/malate was higher in trained than in untrained animals. The lack of training-induced changes in overall antioxidant capacity of mitochondria indicates that the decrease in mitochondrial H(2)O(2) release cannot be attributed to a greater capacity of mitochondria to scavenge the reactive oxygen intermediates derived from univalent O(2) reduction by respiratory chain components. In contrast, the above decrease seems to depend on the drop induced by training in mitochondrial membrane potential. These training effects are not due to an increased level of mitochondrial uncoupling protein, because in the presence of GDP the increase in both membrane potential and H(2)O(2) release was greater in untrained than in trained rats. SN - 0003-9861 UR - https://www.unboundmedicine.com/medline/citation/10600170/Effect_of_training_on_H_2_O_2__release_by_mitochondria_from_rat_skeletal_muscle_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0003-9861(99)91494-7 DB - PRIME DP - Unbound Medicine ER -