Effect of melatonin treatment on oxidative stress-related parameters in REM sleep-deprived rats
Molecular and Cellular Biochemistry, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s11010-026-05686-9
- Dergi Adı: Molecular and Cellular Biochemistry
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Anahtar Kelimeler: Antioxidants, Lipid peroxidation, Melatonin, Oxidative stress, REM, Sleep deprivation
- Bursa Uludağ Üniversitesi Adresli: Evet
Özet
Rapid eye movement sleep deprivation (REM-SD) is associated with increased oxidative stress, characterized by disruption of the oxidant-antioxidant balance and accumulation of reactive oxygen species (ROS). Melatonin may act as a potential modulator of REM-SD-associated oxidative alterations through its circadian regulatory effects, direct ROS scavenging activity, and support of endogenous antioxidant defense mechanisms. This study aimed to evaluate the effects of melatonin treatment administered during the six-day REM-SD period or during the recovery period following REM-SD on oxidative stress-related parameters in 8-12-week-old male Sprague-Dawley rats (n = 84). REM-SD was induced using the modified multiple platform method (MMPM). Biochemical markers reflecting oxidative balance, including total antioxidant status (TAS), total oxidant status (TOS), the lipid peroxidation product malondialdehyde (MDA), non-enzymatic antioxidant glutathione (GSH), and enzymatic antioxidants, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels, were assessed using the enzyme-linked immunosorbent assay (ELISA). The findings demonstrated that REM-SD predominantly affected enzymatic antioxidant defense-related parameters. Melatonin modulated these responses, mainly by increasing enzymatic antioxidant levels and reducing lipid peroxidation. However, no significant change was observed in TOS, whereas the effect on TAS was limited and time-dependent. During the recovery period, several oxidative stress markers partially normalized, indicating a possible reactivation of endogenous antioxidant defenses. In conclusion, six-day MMPM-induced REM-SD appears to alter oxidative stress-related parameters, while melatonin may help attenuate some of these alterations by modulating antioxidant defense mechanisms. These effects varied according to the timing of administration and the specific parameter examined.