Abstract:Free radicals generated within subcellular compartments damage macromolecules which lead to severe structural changes and functional alterations of cellular organelles. A manifestation of free radical injury to biological membranes is the process of lipid peroxidation, an autooxidative chain reaction in which polyunsaturated fatty acids in the membrane are the substrate. There is considerable evidence that damage to polyunsaturated fatty acids tends to reduce membrane fluidity. However, adequate levels of flui… Show more
“…42 Melatonin is likely to be well absorbed in humans, 43 crosses all physiological barriers easily, for example, bloodbrain barrier, membranes of cells, and organelles, additionally, has no reproducible adverse effects in humans or animals. 44 Exogenous melatonin has a short half-life (20-60 min) in human. The apparent elimination half-life of melatonin following an intravenous dose of 3 mgkg À1 (5 mgkg À1 in rats) is reported as 19.8 min in rats.…”
We investigated the changes in the serum levels of tumor necrosis factor (TNF)-a and interleukin (IL)-6, the pro-inflammatory cytokines, and the possible effect of melatonin on the modulation of these inflammatory molecules after renal ischemia reperfusion (IR). The study was carried out in the laboratory of Department of Pharmacology. Forty-six male Wistar albino rats were divided into five groups as control (n ¼ 6), positive control (n ¼ 4), sham (n ¼ 12), renal IR (n ¼ 12), and renal IR melatonin (n ¼ 12). After 1 h renal pedicle occlusion, the blood samples were taken for the measurement of cytokine levels at second hour of the reperfusion. The rats were sacrificed after 24 h of reperfusion for histopathological evaluation. Melatonin or vehicle was administrated to IR rats. Lipopolysaccharide (LPS) was administered to the positive control group and the blood was taken at fourth hour. Serum TNF-a levels increased significantly in renal IR and LPS groups. Serum IL-6 levels were not different from control except the LPS group. There was no significant correlation between the serum TNF-a levels and the histopathological score after renal IR. Melatonin treatment reversed the increase of serum TNF-a levels and histopathological injury in renal tissue after renal IR. Melatonin may have a protective effect by reducing the serum level of TNF-a in renal IR.
“…42 Melatonin is likely to be well absorbed in humans, 43 crosses all physiological barriers easily, for example, bloodbrain barrier, membranes of cells, and organelles, additionally, has no reproducible adverse effects in humans or animals. 44 Exogenous melatonin has a short half-life (20-60 min) in human. The apparent elimination half-life of melatonin following an intravenous dose of 3 mgkg À1 (5 mgkg À1 in rats) is reported as 19.8 min in rats.…”
We investigated the changes in the serum levels of tumor necrosis factor (TNF)-a and interleukin (IL)-6, the pro-inflammatory cytokines, and the possible effect of melatonin on the modulation of these inflammatory molecules after renal ischemia reperfusion (IR). The study was carried out in the laboratory of Department of Pharmacology. Forty-six male Wistar albino rats were divided into five groups as control (n ¼ 6), positive control (n ¼ 4), sham (n ¼ 12), renal IR (n ¼ 12), and renal IR melatonin (n ¼ 12). After 1 h renal pedicle occlusion, the blood samples were taken for the measurement of cytokine levels at second hour of the reperfusion. The rats were sacrificed after 24 h of reperfusion for histopathological evaluation. Melatonin or vehicle was administrated to IR rats. Lipopolysaccharide (LPS) was administered to the positive control group and the blood was taken at fourth hour. Serum TNF-a levels increased significantly in renal IR and LPS groups. Serum IL-6 levels were not different from control except the LPS group. There was no significant correlation between the serum TNF-a levels and the histopathological score after renal IR. Melatonin treatment reversed the increase of serum TNF-a levels and histopathological injury in renal tissue after renal IR. Melatonin may have a protective effect by reducing the serum level of TNF-a in renal IR.
“…The antioxidant capacity of melatonin is derived in part because it is amphiphilic and is thus able freely to move intracellularly across membranes, including mitochondria, the organelle primarily responsible for cellular respiration and thus one of the main sites of free radical generation [62,63]. At the cellular level, endogenous melatonin has been directly linked to enhanced cell maintenance [61], mitochondrial activity [63,64] and increased antioxidant capacity of gametes in vertebrates [65,66].…”
Section: (B) Melatonin and Circadian Rhythmmentioning
confidence: 99%
“…(c) Melatonin, oxidative stress and immune function Melatonin's function as a free radical scavenger and potent antioxidant has been comparatively recently recognized but is now generally accepted [33,[59][60][61]. The antioxidant capacity of melatonin is derived in part because it is amphiphilic and is thus able freely to move intracellularly across membranes, including mitochondria, the organelle primarily responsible for cellular respiration and thus one of the main sites of free radical generation [62,63].…”
Section: (B) Melatonin and Circadian Rhythmmentioning
The mechanisms underpinning the ecological impacts of the presence of artificial night lighting remain elusive. One suspected underlying cause is that the presence of light at night (LAN) supresses nocturnal production of melatonin, a key driver of biological rhythm and a potent antioxidant with a proposed role in immune function. Here, we briefly review the evidence for melatonin as the link between LAN and changes in behaviour and physiology. We then present preliminary data supporting the potential for melatonin to act as a recovery agent mitigating the negative effects of LAN in an invertebrate. Adult crickets (
Teleogryllus commodus
), exposed to constant illumination, were provided with dietary melatonin (concentrations: 0, 10 or 100 µg ml
−1
) in their drinking water. We then compared survival, lifetime fecundity and, over a 4-week period, immune function (haemocyte concentration, lysozyme-like and phenoloxidase (PO) activity). Melatonin supplementation was able only partially to mitigate the detrimental effects of LAN: it did not improve survival or fecundity or PO activity, but it had a largely dose-dependent positive effect on haemocyte concentration and lysozyme-like activity. We discuss the implications of these relationships, as well as the usefulness of invertebrates as model species for future studies that explore the effects of LAN.
“…Melatonin has been found to protect against practically all pathological processes studied to-date [1][2][3][4]. Melatonin has been documented to prevent oxidative damage in different skin components [5,6], which suggests that the human skin is a target for the protective actions of melatonin.…”
reverses the enhanced oxidative damage to membrane lipids and improves skin biophysical characteristics in former-smokers -A study in postmenopausal women. Ann Agric Environ Med. 2017; 24(4): 659-666. doi: 10.5604/12321966.1235174 Abstract Introduction and objective. Protective antioxidative effects of melatonin have been repeatedly documented in experimental and clinical studies. One of the most spectacular exogenous prooxidative agents is cigarette smoking. The aim of the study was to evaluate the level of oxidative damage to membrane lipids (lipid peroxidation; LPO) in blood serum, and in epidermis exfoliated during microdermabrasion collected from former-smokers who were treated with melatonin. Materials and Method. The study was performed in postmenopausal women. Ninety (90) female volunteers, aged 46-67 years, were enrolled. Two major groups, i.e. never-smokers (n=44) and former-smokers (n=46), were divided into: Control, melatonin topical skin application, Restructurer (containing antioxidants) topical skin application, and melatonin oral treatment. Microdermabrasion was performed at point '0', after 2 weeks, and after 4 weeks of treatment. The following parameters were measured: LPO in blood serum, LPO in epidermis exfoliated during microdermabrasion, and skin biophysical characteristics, such as sebum, moisture, elasticity, and pigmentation. Malondialdehyde+4-hydroxyalkenals level (LPO index) was measured spectrophotometrically. Results. Melatonin oral treatment significantly reversed the increased serum LPO level in former-smokers already after 2 weeks of treatment. In a univariate regression model, LPO blood level constituted the only independent factor negatively associated with melatonin oral treatment. After 4 weeks of treatment, melatonin given orally increased skin sebum, moisture and elasticity levels, and melatonin applied topically increased sebum level. Conclusion. Exogenous melatonin reverses the enhanced oxidative damage to membrane lipids and improves skin biophysical characteristics in former-smokers.
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