Redox homeostasis in a rodent model of circadian disruption: Effect of melatonin supplementation.

Authors:
Sandeep Singh
Sandeep Singh
Birla Institute of Technology
India
Syed Ibrahim Rizvi
Syed Ibrahim Rizvi
University of Allahabad
India

Gen Comp Endocrinol 2019 Apr 16. Epub 2019 Apr 16.

Department of Biochemistry, University of Allahabad, Allahabad 211002, India. Electronic address:

Continuous light or dark photoperiods are the leading cause of disruption in the circadian rhythm of day-night cycle. The purpose of this study was to understand the cellular redox balance in a model of circadian disrupted rat model and determine the effect of melatonin supplementation. Young male Wistar rats were randomly divided into five groups (n = 4). Group (I): normal day-night (12 h:12 h) cycle, Group (II): normal rats treated with melatonin, Group (III): rats subjected to continuous light exposure (CLE), Group (IV): CLE rats treated with melatonin, and Group (V) Rats subjected to continuous dark. Melatonin (10 mg/kg) was administered orally at dusk to the Group (II) & (IV). Rats were sacrificed after 10 days of treatment and biomarkers of oxidative stress were evaluated. Results demonstrated significant (p < 0.05) increase of malondialdehyde (MDA), plasma membrane redox system (PMRS), protein carbonyl oxidation (PCO), advanced oxidation protein products (AOPPs), and advanced glycation end products (AGEs) during CLE. A significantly (p < 0.05) decreased level of reduced glutathione (GSH) and ferric reducing antioxidant potential in plasma (FRAP) was also observed during CLE. Treatment with melatonin in CLE rats showed reduced level of MDA, PMRS, PCO, AOPPs and AGEs while GSH and FRAP activity were increased. During continuous dark exposure (CDE) the biomarkers of oxidative stress were attenuated compared to control. Supplementation of melatonin could be a promising strategy to maintain redox homeostasis during prolonged condition of light exposure and other conditions of redox imbalance.

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Source
https://linkinghub.elsevier.com/retrieve/pii/S00166480193008
Publisher Site
http://dx.doi.org/10.1016/j.ygcen.2019.04.016DOI Listing
April 2019
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