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Administration of vitamin D and aerobic training: recovery of lung apoptosis markers in male rats exposed to hydrogen peroxide

Background Apoptosis is one of the indications of programmed cell death (PCD) and is known as a physiological event in multicellular organisms. This study was designed to determine the effect of aerobic training alongside vitamin D supplementation on lung cell apoptosis in male rats exposed to hydro...

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Bibliographic Details
Published in:Sport sciences for health 2019-12, Vol.15 (3), p.569-576
Main Authors: Ramezani, Somayeh, Peeri, Maghsoud, Azarbayjani, Mohammad Ali, Dehghan, Firouzeh
Format: Article
Language:English
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Summary:Background Apoptosis is one of the indications of programmed cell death (PCD) and is known as a physiological event in multicellular organisms. This study was designed to determine the effect of aerobic training alongside vitamin D supplementation on lung cell apoptosis in male rats exposed to hydrogen peroxide (H 2 O 2 ). Methods 48 male rats were assigned into six groups: H 2 O 2 , (H); H 2 O 2  + D 3 , (HD); H 2 O 2  + training, (HE); H 2 O 2  + D 3  + E, (HDE); dimethyl sulfoxide, (DMSO) and control intact. 1 mmol/kg of H 2 O 2 was injected three times per week. The exercising rats performed the program on a rodent’s treadmill for 8 weeks, 5 days a week. The HD and HDE groups received a daily dose of 0.5 µg for 8 weeks. The lung tissue was exposed and stored at − 80. Then, the RT-PCR method was employed to examine the gene expressions of BAX, BCL2, Caspase-3 and Bcl-2/Bax ratios. Results Results indicated that training, as well as a combination of training and vitamin D had a significant effect on BAX, BCL 2 and Bel 2 /Bax ratio in case of H 2 O 2 toxicity. The training and vitamin D groups both had no significant effect on Caspase-3 gene expression. Conclusion Based on the results of this research, it can be concluded that regular aerobic training alongside consumption of D 3 might result in significant alteration of the genes involved in apoptosis caused by H 2 O 2 presence in lung tissues.
ISSN:1824-7490
1825-1234
DOI:10.1007/s11332-019-00546-0