Evidence for the influence of vitamin C on age- and heat exposure-dependent deterioration of biochemical function in rat's liver and kidney
Autor: | Trajce Stafilov, Vase Tanska, Suzana Dinevska-Kofkarovska, Icko Gjorgoski, D. B. Duridanova, Kiril Hristov, Mitko Mladenov, Tanja Vitkovska |
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Rok vydání: | 2008 |
Předmět: |
medicine.medical_specialty
Kidney Vitamin C Physiology Cholesterol business.industry Methylglyoxal Oxidative phosphorylation Glutathione Ascorbic acid Biochemistry chemistry.chemical_compound Endocrinology medicine.anatomical_structure chemistry Internal medicine medicine Ascorbic Acid Deficiency General Agricultural and Biological Sciences business Developmental Biology |
Zdroj: | Journal of Thermal Biology. 33:431-436 |
ISSN: | 0306-4565 |
DOI: | 10.1016/j.jtherbio.2008.07.001 |
Popis: | Molecular mechanisms responsible for age-dependent deterioration of biochemical functions have not been completely revealed as yet. We studied the role of ascorbic acid food supplementation in young and aged acute heat-exposed rats. The duration of heat exposure (40±0.5 °C) for heat-exposed Wistar rats, at the age of 35 days and 22–24 months, was approximately 2 h. In the aged heat-unexposed animals cholesterol and triglycerides were considerably high, whereas tissues ascorbic acid, glutathione and methylglyoxal were significantly low. Administration of vitamin C reverted these age-associated differences to the status comparable to young rats. The role of vitamin C supplementation was almost the same in young heat-exposed animals. In this direction in young rats suppression of LTC 4 synthesis is evident during acute heat exposure as a result of vitamin C treatment. The importance of vitamin C treatment for young heat-exposed rats is in the protection of apoptosis, if it is determined across the LTC 4 changes. In contrary, in old heat-exposed rats, vitamin C does not suppress the apoptotic processes. The results suggest that oxidative and apoptotic processes in the liver and the kidney as a result of the acute heat exposure is presumably subject of ascorbic acid deficiency. |
Databáze: | OpenAIRE |
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