Literature DB >> 28959107

Melatonin Supplementation Ameliorates Energy Charge and Oxidative Stress Induced by Acute Exercise in Rat Heart Tissue.

Behzat Cimen1, Ali Uz1, Ihsan Cetin2, Leyla Cimen3, Aysun Cetin4.   

Abstract

BACKGROUND: Regular physical exercises may help people to be more resistant to everyday problems; however, how acute and intense exercises affect the heart tissues functioning with maximum capacity and how melatonin changes the effect of acute and intense exercises are still not obvious. We aimed to comprehend whether melatonin intravenous injection supports the oxidative/antioxidative conditions and energy charge in heart tissues of rats exposed to acute swimming exercise.
METHODS: Thirty Wistar-albino male rats were categorized into 3 groups with equal number of subjects. Control group performed no application, and acute intensive swimming exercise group were subjected to acute intensive swimming exercise for 30 minutes, and melatonin group were applied 25 mg/kg single dose melatonin administration prior to 30 minutes acute intensive swimming exercise. The levels of malondialdehyde (MDA), and superoxide dismutase, catalase and glutathione peroxidase activities were measured by spectrophotometric method; and the levels of 3-nitrotyrosine (3-NT) and energy charge were determined by a high performance liquid chromatography.
RESULTS: Tissue MDA and 3-NT levels of the acute intensive exercise group were found to be higher than the control group. It was also found that the melatonin administration increased the energy charge and antioxidant activities, while decreased tissue MDA and 3-NT levels in heart tissues. Our results provide evidence for melatonin that can exert potent protective effects on oxidative stress and energy charge for heart tissues in acute swimming exercise.
CONCLUSIONS: These findings suggest that the direct beneficial effects of melatonin could be potentially applied on prevention of oxidative stress and energy deficit.

Entities:  

Keywords:  Aerobic capacity; Cardiac pharmacology; Cardiovascular risk

Year:  2017        PMID: 28959107      PMCID: PMC5611351          DOI: 10.6515/acs20170331a

Source DB:  PubMed          Journal:  Acta Cardiol Sin        ISSN: 1011-6842            Impact factor:   2.672


  38 in total

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