Abstract
The principal goal of this study was to determine the effect of the photoperiod on oxidative damage biomarkers in rats submitted to different light/darkness patterns, in a hyperlipidemic nephropathy model (induced by adriamycin), as well as its possible relationship with melatonin and leptin secretion rhythms. To test this hypothesis, six different groups were used (N = 6 rats per group): control (12 h/12h light:dark); exposure to permanent illumination (24 h light); exposure to darkness (22 h dark); injected with adriamycin, 12h/12h light:dark; injected with adriamycin + exposure to permanent illumination and injected with adriamycin + exposure to darkness (22 h dark). The different photoperiods were begun two weeks prior to medication and were maintained up to the day of the animal's sacrifice, ten days after medication. The following parameters were analysed: i) weight evolution; ii) in plasma: urea, creatinine, uric acid, total proteins, albumen, lactate dehydrogenase, creatinine-quinase, aspartate aminotransferase, alanine aminotransferase and total cholesterol; iii) in urine: urea, creatinine, total proteins and microalbumen; iv) biomarkers of oxidative damage in kidneys, heart, liver and brain: lipoperoxides, total glutathione, reduced glutathione, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase; v) melatonin (pineal gland tissue and plasma) and leptin (plasma). From the results obtained it was concluded that the administration of adriamycin generated oxidative stress in renal, cerebral, hepatic and cardiac tissue. Additionally, in the healthy animal, but of a lesser relevance in the adriamycin animal, permanent light worsened the oxidative stress, whereas darkness improved it. This could be related to the circadian rhythm of the inverse release shown by melatonin and leptin, accentuating the release of melatonin in the darkness phase and that of leptin in the light phase. The correlation between melatonin and leptin in the healthy animal seemed to confirm the relationship between both variables and their influence on oxidative damage biomarkers.
Highlights
Light is a powerful element in circadian, neuroendocrine and neurobehavioural regulation and it has a profound influence on the health and wellbeing of all mammals, including laboratory animals [1]
The circadian release of melatonin is regulated by an oscillator, which is situated in the hypothalamic suprachiasmatic nucleus (SCN) [6,7]
The gain in weight in the untreated groups was significantly higher in photoperiod D vs. the control
Summary
Light is a powerful element in circadian, neuroendocrine and neurobehavioural regulation and it has a profound influence on the health and wellbeing of all mammals, including laboratory animals [1]. Many hormones and enzymes are fundamental to life, and these are secreted following a circadian pattern in accordance with the photoperiod. Melatonin is secreted during darkness as a hormonal message of the photoperiod [5]. The circadian release of melatonin is regulated by an oscillator, which is situated in the hypothalamic suprachiasmatic nucleus (SCN) [6,7]. This oscillator is usually entrained to a 24-h rhythm [8,9] by environmental lighting conditions, which are perceived in the retina by rods, cones and intrinsically photosensitive retinal ganglion cells [10]. Circulating levels of melatonin are high at night and low in the daytime [11]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
