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Copyright of Médecine et Santé Tropicales is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

As immature and aged rats could be more sensitive to ozone (O 3 )-linked lung oxidative stress we have attempted to shed more light on age-related susceptibility to O 3 with focusing our interest on lung mitochondrial respiration, reactive oxygen species (ROS) production and lung pro/antioxidant status. For this purpose, we exposed to fresh air or O 3 (500 ppb 12 h per day, for 7 days) 3 week- (immature), 6 month- (adult) and 20 month-old rats (aged). We determined, in lung, H 2 O 2 release by mitochondria, activities of major antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT)], heat shock protein (HSP 72 ) content and 8-oxodG and dG-HNE nDNA contents, as DNA oxidative damage markers. In adult rats we did not observe alteration of pro/antioxidant status. In contrast to adults, immature rats exposed to O 3 higher nDNA 8-oxodG content and HSP 72 and without antioxidant enzymes modification. Aged rats displayed mild uncoupled lung mitochondria, increased SOD and GPx activities, and higher 8-oxodG content after O 3 exposure. Thus, in contrast to adults, immature and aged rats displayed lung oxidative stress after O 3 exposure. Higher sensitivity of immature to O 3 was partly related to ventilatory parameters and to the absence of antioxidant enzyme response. In aged rats, the increase in cytosolic SOD and GPx activities during O 3 exposure was not sufficient to prevent the impairment in mitochondrial function and accumulation in lung 8- oxodG. Finally, we showed that mitochondria seem not to be a major source of ROS under O 3 exposure. [ABSTRACT FROM AUTHOR]

Previous data have demonstrated that, to handle the oxidative stress encountered with training at high intensity, skeletal muscle relies on an increase in mitochondrial biogenesis, a reduced H2O2 production, and an enhancement of antioxidant enzymes. In the present study, we evaluated the influence of voluntary running on mitochondrial O2 consumption and H2O2 production by intermyofibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) isolated from oxidative muscles in conjunction with the determination of antioxidant capacities. When mitochondria are incubated with succinate as substrate, both maximal (state 3) and resting (state 4) O2 consumption were significantly lower in SSM than in IFM populations. Mitochondrial H2O2 release per unit of O2 consumed was 2-fold higher in SSM than in IFM. Inhibition of H2O2 formation by rotenone suggests that complex I of the electron transport chain is likely the major physiological H2O2-generating system. In Lou/C rats (an inbred strain of rats of Wistar origin), neither O2 consumption nor H2O2 release by IFM and SSM were affected by long-term, voluntary wheel training. In contrast, glutathione peroxidase and catalase activity were significantly increased despite no change in oxidative capacities with long-term, voluntary exercise. Furthermore, chronic exercise enhanced heat shock protein 72 accumulation within skeletal muscle. It is concluded that the antioxidant status of muscle can be significantly improved by prolonged wheel exercise without necessitating an increase in mitochondrial oxidative capacities. [Copyright &y& Elsevier]

Undernutrition is frequently seen in cancer and is considered as a bad prognostic factor. The mechanisms involved in this complex syndrome are not fully understood. Systemic inflammation plays an important role in the occurrence and/or development of cancer-associated undernutrition. Although it is essential to counteract cancer-associated undernutrition, modalities for nutritional treatment are still discussed. It has been shown that nutritional supplementation with n-3 polyunsaturated fatty acid could be beneficial in patients.

Objectif Etudier l’effet des dérivés des acides gras à chaîne longue (AGCL) sur l’activité de la chaîne respiratoire. Méthode La production énergétique de la chaîne respiratoire a été mesurée par oxygraphie sur des fibroblastes de patients avec déficit de b-oxydation des AGCL (LCHAD) cultivés dans diverses conditions et comparée à des fibroblastes contrôles (CTRL). Les dérivés des AGCL ont été estimés par le profil des acylcarnitines cellulaires. Résultats Les fibroblastes LCHAD avaient une accumulation d’acylcarnitines à chaîne longue par rapport aux CTRL. En condition de production d’ATP (état 3), leur consommation d’oxygène (- 48±18%, p<0.001) et de production d’ATP (-31±18%, p=0.07) étaient réduites, sans majoration de la fuite de protons (état 4) ni dysfonctionnement des complexes I à IV (état découplé), suggérant une altération du système de phosphorylation. L’ajout d’un inhibiteur de l’entrée mitochondriale des AGCL (Etomoxir) réduisait l’accumulation d’acylcarnitines et normalisait la production d’énergie. Conclusion L’accumulation de dérivés des AGCL s’accompagnait d’une altération réversible de la phosphorylation oxydative dans des fibroblastes LCHAD. Ce mécanisme pourrait jouer un rôle toxique majeur dans les décompensations des déficits de b-oxydation des AGCL. [ABSTRACT FROM AUTHOR]