1,25-Dihydroxyvitamin D3 prevents deleterious effects of homocysteine on mitochondrial function and redox status in heart slices
| Autor: | Janaína Kolling, Aline Longoni, João Paulo dos Santos, Jussemara Souza da Silva, Adriano Martimbianco de Assis, Leo Anderson Meira-Martins, Cassiana Siebert, Angela T. S. Wyse, Letícia Ferreira Pettenuzzo, Carlos Alberto Gonçalves |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Hyperhomocysteinemia Antioxidant Homocysteine Calcitriol Endocrinology Diabetes and Metabolism medicine.medical_treatment Respiratory chain medicine.disease_cause Calcitriol receptor Lipid peroxidation 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Endocrinology Internal medicine medicine Nutrition and Dietetics medicine.disease 030104 developmental biology chemistry lipids (amino acids peptides and proteins) 030217 neurology & neurosurgery Oxidative stress medicine.drug |
| Zdroj: | Nutrition Research. 38:52-63 |
| ISSN: | 0271-5317 |
| Popis: | Because homocysteine (Hcy) is a risk factor for cardiovascular disease, and vitamin D deficiency can contribute to cardiovascular pathologies. In the present study, we tested the hypothesis that Hcy could impair energy metabolism, mitochondrial function, and redox status in heart slices of Wistar rats and that 1,25-dihydroxivitamin D3 (calcitriol) treatment could prevent such effects. Heart slices were first pretreated with 3 different concentrations of calcitriol (50, 100, and 250nmol/L) for 30minutes at 37°C, after which Hcy was added to promote deleterious effects on metabolism. After 1 hour of incubation, the samples were washed, homogenized, and stored at -80°C before analysis. The results showed that Hcy caused changes in energy metabolism (respiratory chain enzymes), mitochondrial function, and cell viability. Homocysteine also induced oxidative stress, increasing lipid peroxidation, reactive oxygen species generation, and protein damage. An imbalance in antioxidant enzymes was also observed. Calcitriol (50nmol/L) reverted the effect of Hcy on the parameters tested, except for the immunocontent of catalase. Both treatments (calcitriol and Hcy) did not alter the vitamin D receptor immunocontent, which combined with the fact that our ex vivo model is acute, suggesting that the beneficial effect of calcitriol occurs directly through antioxidative mechanisms and not via gene expression. In this study, we show that Hcy impairs mitochondrial function and induces changes in the redox status in heart slices, which were reverted by calcitriol. These findings suggest that calcitriol may be a preventive/therapeutic strategy for complications caused by Hcy. |
| Databáze: | OpenAIRE |
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