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Melatonin protects against chronic intermittent hypoxia-induced cardiac hypertrophy by modulating autophagy through the 5' adenosine monophosphate-activated protein kinase pathway.

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Obstructive sleep apnea syndrome (OSAS) is usually associated with multiple cardiovascular disorders, including myocardial hypertrophy. Melatonin protects the heart from damaging conditions. However, whether melatonin alleviates heart damage induced by chronic intermittent hypoxia (CIH) is unknown.

In vitro and in vivo effects of melatonin on sister chromatid exchange in human blood lymphocytes exposed to hypoxia.

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OBJECTIVE Many studies have shown that melatonin (MLT) has an anti-genotoxic effect in various tissues and cell lines. The aim of this study was to investigate the anti-genotoxic effect of MLT on normal human peripheral lymphocytes by assessing sister chromatid exchange (SCE) in vitro and in

Melatonin, bakuchiol and ascorbyl tetraisopalmitate synergize to modulate gene expression and restore Hypoxia-Inducible Factor 1 signaling in UV-exposed skin.

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Chronic exposure to solar ultraviolet (UV) radiation induces changes to the expression of hundreds of genes in the skin and modulates cellular signaling pathways that alter its structure, function and appearance. To counter these effects, we have developed a 3-in-1 night facial serum (3-in-1 NFS)

Expression of tranferrin receptors in the pineal gland of postnatal and adult rats and its alteration in hypoxia and melatonin treatment.

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Transferrin receptors (Tfrc) are membrane bound glycoproteins which function to mediate cellular uptake of iron from transferrin. We examined expression of Tfrc in the pineal gland of rats of different ages from 1 day to 12 weeks. The mRNA and protein expression of Tfrc increased up to 6 weeks of

Chronic hypoxia modulates the function and expression of melatonin receptors in the rat carotid body.

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Melatonin modulates the carotid chemoreceptor response to chemical stimuli, and chronic hypoxia changes circadian activities and carotid body function. The purpose of this study was to test the hypothesis that chronic hypoxia alters the function and expression of melatonin receptors in the rat

Melatonin promotes proliferation and differentiation of neural stem cells subjected to hypoxia in vitro.

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Melatonin, an endogenously produced neurohormone secreted by the pineal gland, has a variety of physiological functions and neuroprotective effects. It can modulate the functions of neural stem cells (NSCs) including proliferation and differentiation in embryonic brain tissue but its effect and

Melatonin and sleep responses to normobaric hypoxia and aerobic physical exercise: A randomized controlled trial.

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This work evaluated the effects of moderate physical exercise performed under hypoxic conditions on melatonin and sleep. Forty healthy men were randomized into four groups: Normoxia (N) (n = 10); Hypoxia (H) (n = 10); Exercise under Normoxia (EN) (n = 10); and Exercise under Hypoxia (EH) (n = 10).

Role of melatonin in reducing hypoxia-induced oxidative stress and morphological changes in the liver of male mice.

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Oxygen deficiency during critical illness may cause profound changes in cellular metabolism and subsequent tissue and organ dysfunction. Thus, the present study was designed to determine the effects of hypoxia and reoxygenation on the levels of lipid peroxidation and the morphological changes in the

Effect of melatonin on the relationship between lipid peroxidation and proteolytic activity in basal nuclei of rat brain during acute hypoxia.

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We studied the effect of melatonin on the relationship between LPO intensity and proteolytic activity in basal nuclei (caudate nucleus, globus pallidus, amygdaloid complex, and nucleus accumbens septi) of rat brain during acute hypobaric hypoxia. Acute hypoxia was accompanied by LPO activation and

[Effect of melatonin and epithalamin on activity of marker enzymes in the cell membrane in the forebrain of rats under acute hypoxia].

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The effects of a single-shot intraperitoneally administration of melatonin in a dose of 1 mg per kg body weight and epithalamin in a dose of 2.5 mg per kg body weight on the activities of Na+, K(+)-ATPase and 5'-nucleotidase were investigated in the forebrain of juvenile male white rats under the

mtDNA T8993G mutation-induced F1F0-ATP synthase defect augments mitochondrial dysfunction associated with hypoxia/reoxygenation: the protective role of melatonin.

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BACKGROUND F1F0-ATP synthase (F1F0-ATPase) plays important roles in regulating mitochondrial function during hypoxia, but the effect of F1F0-ATPase defect on hypoxia/reoxygenation (H/RO) is unknown. The aim of this study was to investigate how mtDNA T8993G mutation (NARP)-induced inhibition of

[THE INFLUENCE OF THE MELATONIN ON THE CORRELATION BETWEEN THE INTENSITY OF THE ACCUMULATION OF THE OXIDATI-VE-MODIFIED PROTEINS CONTENT, ACTIVITY OF THE ANTIOXIDANT ENZYMES AND THE STATE OF PROTEOLYSIS IN THE BASAL NUCLEI OF THE BRAIN UNDER THE ACUTE HYPOXIA].

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The effect of melatonin on the correlation between the intensity of the accumulation of the oxidative-modified protein content, activity of the antioxidant enzymes and the state of proteoly-sis in the basal nuclei (the nucleus caudatus, globus pallidus, nucleus accumbens, amigdaloid complex) of the

Influence of melatonin pretreatment and preconditioning by hypobaric hypoxia on the development of cortical photothrombotic ischemic lesion.

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Photothrombotic model of ischemia (PT) is based on free radical-mediated endothelial dysfunction followed by thrombosis. Free radicals are also involved in hypoxic preconditioning. We tested the sensitivity of PT to preconditioning with hypobaric hypoxia and to pretreatment with melatonin. In adult

Neuroprotective effect of melatonin in experimentally induced hypobaric hypoxia.

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Melatonin (MEL) is an endogenous neurohormone with many biological functions, including a powerful antioxidant effect. The aim of the present study was to determine whether MEL protects the brain tissue from the oxidative stress induced by hypobaric hypoxia (HH) in vivo. This study was performed on

Melatonin reduces microvascular damage and insulin resistance in hamsters due to chronic intermittent hypoxia.

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Obstructive sleep apnea (OSA) causes intermittent hypoxia (IH) associated with hypertension, insulin resistance and a systemic inflammatory response. We evaluated the effects of melatonin on vasodilation, capillary perfusion in hamster cheek pouch and insulin resistance, hypertension, and reactive

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