NADPH oxidase activity is associated with cardiac osteopontin and pro-collagen type I expression in uremia.

International audienceCardiovascular disease is a frequent complication inducing mortality in chronic kidney disease (CKD) patients, which can be determined by both traditional risk factors and non-traditional risk factors such as malnutrition and oxidative stress. This study aimed to investigate the role of oxidative stress in uremia-induced cardiopathy in an experimental CKD model. CKD was induced in Sprague-Dawley rats by a 4-week diet supplemented in adenine, calcium and phosphorous and depleted in proteins. CKD was associated with a 3-fold increase in superoxide anion production from the NADPH oxidase in the left ventricle, but the maximal activity of mitochondrial respiratory chain complexes was not different. Although manganese mitochondrial SOD activity decreased, total SOD activity was not affected and catalase or GPx activities were increased, strengthening the major role of NADPH oxidase in superoxide anion output. Superoxide anion output was associated with enhanced expression of osteopontin (×7.7) and accumulation of pro-collagen type I (×3.7). To conclude, the increased activity of NADPH oxidase during CKD is associated with protein modifications which could activate a pathway leading to cardiac remodelling

Les cardiolipides, des phospholipides clés pour la fonction mitochondriale. Relation avec les apports lipidiques et la physiopathologie

Le cardiolipide (CL) est un phospholipide exclusivement présent dans la membrane mitochondriale et joue un rôle clé dans plusieurs processus de bioénergétique mitochondriale, ainsi que dans la stabilité et la dynamique de la membrane mitochondriale. En raison de sa richesse en acides gras polyinsaturés (en particulier en acide linoléique), le CL est très sensible à l’attaque par les radicaux libres produits par la mitochondrie. L’oxydation du CL a des conséquences majeures sur le fonctionnement de la mitochondrie, en particulier la phosphorylationoxydative et la production d’ATP. Par ailleurs, les régimes alimentaires plus ou moins riches en graisses peuvent modifier la composition lipidique de la membrane mitochondriale, y compris la teneur en CL et sa composition en acides gras, et ces modifications peuvent par la suite altérer le fonctionnement de la mitochondrie. Or, les régimes alimentaires riches en graisses sont associés à la stéatose hépatique et à l’insulino-résistance, deux problèmes majeurs de santé publique. L’objectif de cet article est de faire le point sur les connaissances actuelles concernant le rôle du CL dans les pathologies nutritionnelles liées à une surcharge en lipides

Impact of high dietary lipid intake and related metabolic disorders on the abundance and acyl composition of the unique mitochondrial phospholipid, cardiolipin

Excessive dietary lipid intake, coupled with lack of exercise, are the major causes of the development and progression of metabolic syndrome features e. g. obesity, hepatic steatosis, insulin resistance, type 2 diabetes and cardiovascular diseases. These metabolic diseases are associated with both structural and functional alterations of mitochondria. Cardiolipin (CL) is a unique phospholipid that is almost exclusively localized in the mitochondrial inner membrane. Cardiolipin is at the heart of mitochondrial metabolism playing a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics, and in many of the mitochondrial-dependent steps of apoptosis. Indeed, alterations to CL content and acyl chain profile have been associated with mitochondrial dysfunction in multiple tissues in Barth syndrome and in many other physio-pathological conditions. After a brief overview of the biological roles of CL, we highlight the consequences of lipid overload-related nutritional manipulations as well as related metabolic disorders on both CL content and its fatty acid composition in the major metabolic tissues, the heart, muscle and liver. The goal of this review is to fill a void in the CL literature concerning the effects of CL abundance and form that arise following high lipid supplementation and the related metabolic disorders

Acide docosahexaénoïque et développement rétinien

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Mitochondria function and redox status in hypertrophied myostatin-deficient muscles

International audienc

Nouveaux développements dans la connaissance du métabolisme des acides gras polyinsaturés. Utilisation des isotopes stables pour l'étude de la bioconversion des acides gras polyinsaturés (AGPI) chez l'homme. Métabolisme des AGPI et isotopes stables chez l'homme;

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Short-term assessment of toxicological aspects, oxidative and inflammatory response to dietary melon superoxide dismutase in rats

The protective effects of SODB, a gastro-resistant encapsulated melon superoxide dismutase, on haematological and biochemical parameters and inflammatory and oxidative status, were evaluated in the blood and liver tissue. The study consisted in a 28-day experiment on rats supplemented with three doses (10, 40 and 160 U SOD/day) of SODB-M, SODB-D or SODB-S, different depending on the nature of the coating (palm oil, shellac or gum Arabic respectively). No mortality, abnormal clinical signs, behavioural changes or macroscopic findings were observed whatever the groups. Haematological parameters (total red blood cell count, haemoglobin content, haematocrit, red cell indices, white blood cell count and platelets count) were not modified in SODB treated-groups. No marked change was recorded in biochemical parameters (plasma urea, creatinine, lipids, electrolytes, bilirubin, transaminases and gamma-glutamyl transferase). The liver endogenous antioxidant enzymes (copper/zinc and manganese superoxide dismutase) expressions were significantly increased in the rats receiving the highest dose of SODB (160 U SOD/day) whatever the coating. Moreover, interleukin-6, a marker of inflammation, was significantly decreased in these high dose-treated-groups

Supplementation with wine phenolic compounds increases the antioxidant capacity of plasma and vitamin E of low-density lipoprotein without changing the lipoprotein CU2+ oxidizability: possible explanation by phenolic location

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