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Dietary supplementation with the microalga Galdieria sulphuraria (Rhodophyta) reduces prolonged exercise-induced oxidative stress in rat tissues.

Carfagna S, Napolitano G, Barone D, Pinto G, Pollio A, Venditti P - Oxid Med Cell Longev (2015)

Bottom Line: Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria.G. sulphuraria supplementation reduced the above exercise-induced variations.In conclusion, G. sulphuraria ability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Naples "Federico II", Via Mezzocannone 8, 80134 Naples, Italy.

ABSTRACT
We studied the effects of ten-day 1% Galdieria sulphuraria dietary supplementation on oxidative damage and metabolic changes elicited by acute exercise (6-hour swimming) determining oxygen consumption, lipid hydroperoxides, protein bound carbonyls in rat tissue (liver, heart, and muscle) homogenates and mitochondria, tissue glutathione peroxidase and glutathione reductase activities, glutathione content, and rates of H2O2 mitochondrial release. Exercise increased oxidative damage in tissues and mitochondria and decreased tissue content of reduced glutathione. Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria. G. sulphuraria supplementation reduced the above exercise-induced variations. Conversely, alga supplementation was not able to modify the exercise-induced increase in mitochondrial release rate of hydrogen peroxide and in liver and heart antioxidant enzyme activities. The alga capacity to reduce lipid oxidative damage without reducing mitochondrial H2O2 release can be due to its high content of C-phycocyanin and glutathione, which are able to scavenge peroxyl radicals and contribute to phospholipid hydroperoxide metabolism, respectively. In conclusion, G. sulphuraria ability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

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Related in: MedlinePlus

Effect of prolonged exercise and G. sulphuraria treatment on the rates of H2O2 release by rat liver, heart, and skeletal muscle mitochondria in State 4 and State 3 of respiration, in the presence of succinate or pyruvate plus malate, as respiratory substrates. Values are mean ± S.E.M. For each value eight rats were used. Mitochondrial H2O2 release rate is expressed as pmol min−1 per mg of mitochondrial protein. S: sedentary untreated rats; SG: sedentary G. sulphuraria treated rats; E: exercised untreated rats; EG: exercised G. sulphuraria treated rats.  aSignificant difference for exercised rats versus respective sedentary controls;  bsignificant difference for G. sulphuraria treated animals versus respective untreated controls. The level of significance was chosen as P < 0.05.
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fig5: Effect of prolonged exercise and G. sulphuraria treatment on the rates of H2O2 release by rat liver, heart, and skeletal muscle mitochondria in State 4 and State 3 of respiration, in the presence of succinate or pyruvate plus malate, as respiratory substrates. Values are mean ± S.E.M. For each value eight rats were used. Mitochondrial H2O2 release rate is expressed as pmol min−1 per mg of mitochondrial protein. S: sedentary untreated rats; SG: sedentary G. sulphuraria treated rats; E: exercised untreated rats; EG: exercised G. sulphuraria treated rats.  aSignificant difference for exercised rats versus respective sedentary controls;  bsignificant difference for G. sulphuraria treated animals versus respective untreated controls. The level of significance was chosen as P < 0.05.

Mentions: The rates of mitochondrial H2O2 release are reported in Figure 5. Prolonged exercise increased the rates of both succinate and pyruvate/malate supported H2O2 release in mitochondria of liver heart and muscle, during both State 4 and State 3 respiration in alga untreated and treated rats. G. sulphuraria lowered H2O2 release in the presence of pyruvate/malate during State 3 respiration in muscle mitochondria of sedentary rats. In exercised group in the presence of succinate as respiratory substrate, the alga consumption lowered H2O2 release during State 4 in muscle mitochondria and during State 3 in liver mitochondria. In the presence of pyruvate/malate as respiratory substrates, alga lowered H2O2 release during State 4 in muscle mitochondria and during State 4 and State 3 in liver mitochondria.


Dietary supplementation with the microalga Galdieria sulphuraria (Rhodophyta) reduces prolonged exercise-induced oxidative stress in rat tissues.

Carfagna S, Napolitano G, Barone D, Pinto G, Pollio A, Venditti P - Oxid Med Cell Longev (2015)

Effect of prolonged exercise and G. sulphuraria treatment on the rates of H2O2 release by rat liver, heart, and skeletal muscle mitochondria in State 4 and State 3 of respiration, in the presence of succinate or pyruvate plus malate, as respiratory substrates. Values are mean ± S.E.M. For each value eight rats were used. Mitochondrial H2O2 release rate is expressed as pmol min−1 per mg of mitochondrial protein. S: sedentary untreated rats; SG: sedentary G. sulphuraria treated rats; E: exercised untreated rats; EG: exercised G. sulphuraria treated rats.  aSignificant difference for exercised rats versus respective sedentary controls;  bsignificant difference for G. sulphuraria treated animals versus respective untreated controls. The level of significance was chosen as P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4385680&req=5

fig5: Effect of prolonged exercise and G. sulphuraria treatment on the rates of H2O2 release by rat liver, heart, and skeletal muscle mitochondria in State 4 and State 3 of respiration, in the presence of succinate or pyruvate plus malate, as respiratory substrates. Values are mean ± S.E.M. For each value eight rats were used. Mitochondrial H2O2 release rate is expressed as pmol min−1 per mg of mitochondrial protein. S: sedentary untreated rats; SG: sedentary G. sulphuraria treated rats; E: exercised untreated rats; EG: exercised G. sulphuraria treated rats.  aSignificant difference for exercised rats versus respective sedentary controls;  bsignificant difference for G. sulphuraria treated animals versus respective untreated controls. The level of significance was chosen as P < 0.05.
Mentions: The rates of mitochondrial H2O2 release are reported in Figure 5. Prolonged exercise increased the rates of both succinate and pyruvate/malate supported H2O2 release in mitochondria of liver heart and muscle, during both State 4 and State 3 respiration in alga untreated and treated rats. G. sulphuraria lowered H2O2 release in the presence of pyruvate/malate during State 3 respiration in muscle mitochondria of sedentary rats. In exercised group in the presence of succinate as respiratory substrate, the alga consumption lowered H2O2 release during State 4 in muscle mitochondria and during State 3 in liver mitochondria. In the presence of pyruvate/malate as respiratory substrates, alga lowered H2O2 release during State 4 in muscle mitochondria and during State 4 and State 3 in liver mitochondria.

Bottom Line: Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria.G. sulphuraria supplementation reduced the above exercise-induced variations.In conclusion, G. sulphuraria ability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Naples "Federico II", Via Mezzocannone 8, 80134 Naples, Italy.

ABSTRACT
We studied the effects of ten-day 1% Galdieria sulphuraria dietary supplementation on oxidative damage and metabolic changes elicited by acute exercise (6-hour swimming) determining oxygen consumption, lipid hydroperoxides, protein bound carbonyls in rat tissue (liver, heart, and muscle) homogenates and mitochondria, tissue glutathione peroxidase and glutathione reductase activities, glutathione content, and rates of H2O2 mitochondrial release. Exercise increased oxidative damage in tissues and mitochondria and decreased tissue content of reduced glutathione. Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria. G. sulphuraria supplementation reduced the above exercise-induced variations. Conversely, alga supplementation was not able to modify the exercise-induced increase in mitochondrial release rate of hydrogen peroxide and in liver and heart antioxidant enzyme activities. The alga capacity to reduce lipid oxidative damage without reducing mitochondrial H2O2 release can be due to its high content of C-phycocyanin and glutathione, which are able to scavenge peroxyl radicals and contribute to phospholipid hydroperoxide metabolism, respectively. In conclusion, G. sulphuraria ability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

Show MeSH
Related in: MedlinePlus