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      Decreased nocturnal melatonin levels during acute myocardial infarction.

      Journal of Pineal Research

      Aged, Antioxidants, metabolism, Circadian Rhythm, physiology, Darkness, Female, Glutathione Peroxidase, blood, Humans, Light, Lipid Peroxidation, Male, Melatonin, Middle Aged, Myocardial Infarction, physiopathology, Oxidative Stress

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          Abstract

          Acute myocardial infarction is accompanied by an increase in cellular oxidative stress in the pericardial coverings of the heart. Melatonin is a highly potent and efficient radical scavenger. Little research has been carried out concerning the relationship between this antioxidant and acute myocardial infarction in humans. In this work, serum levels of melatonin and parameters of oxidative stress, such as glutathione peroxidase and lipid peroxidation levels were examined in light/dark periods in patients with acute myocardial infarction. Twenty-five patients diagnosed with acute myocardial infarction were studied and 25 patients with no evidence of coronary artery disease served as controls. Venous blood samples were obtained from the patients and control subjects to determine melatonin, glutathione peroxidase and lipid peroxidation; the samples were collected at 10:00 hr (light period) and 03:00 hr (dark period) in the first 24 hr after admission to the coronary care unit. Our results demonstrate the existence of differences between changes in melatonin levels in control subjects and acute myocardial infarction patients, revealing a reduced nocturnal elevation in the acute myocardial infarction group. Glutathione peroxidase levels were lower after acute myocardial infarction and did not show diurnal variations. In the control group, lipid peroxidation levels presented a light/dark pattern but in the acute myocardial infarction group diurnal variations of this parameter were lost. Our data show that acute myocardial infarction is associated with a nocturnal serum melatonin deficit as well as increased oxidative stress, suggesting that melatonin is, at least in part, depleted during the dark phase to reduce the free radicals formed in acute myocardial infarction.

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          Most cited references 21

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          Oxygen-derived free radicals in postischemic tissue injury.

          It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury. Although there are certainly multiple components to clinical ischemic and reperfusion injury, it appears likely that free-radical production may make a major contribution at certain stages in the progression of the injury. The primary source of superoxide in reperfused reoxygenated tissues appears to be the enzyme xanthine oxidase, released during ischemia by a calcium-triggered proteolytic attack on xanthine dehydrogenase. Reperfused tissues are protected in a variety of laboratory models by scavengers of superoxide radicals or hydroxyl radicals or by allopurinol or other inhibitors of xanthine oxidase. Dysfunction induced by free radicals may thus be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.
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            Biochemical reactivity of melatonin with reactive oxygen and nitrogen species: a review of the evidence.

            Melatonin (N-acetyl-5-methoxytryptamine), an endogenously produced indole found throughout the animal kingdom, was recently reported, using a variety of techniques, to be a scavenger of a number of reactive oxygen and reactive nitrogen species both in vitro and in vivo. Initially, melatonin was discovered to directly scavenge the high toxic hydroxyl radical (*OH). The methods used to prove the interaction of melatonin with the *OH included the generation of the radical using Fenton reagents or the ultraviolet photolysis of hydrogen peroxide (H202) with the use of spin-trapping agents, followed by electron spin resonance (ESR) spectroscopy, pulse radiolysis followed by ESR, and several spectrofluorometric and chemical (salicylate trapping in vivo) methodologies. One product of the reaction of melatonin with the *OH was identified as cyclic 3-hydroxymelatonin (3-OHM) using high-performance liquid chromatography with electrochemical (HPLC-EC) detection, electron ionization mass spectrometry (EIMS), proton nuclear magnetic resonance (1H NMR) and COSY 1H NMR. Cyclic 3-OHM appears in the urine of humans and other mammals and in rat urine its concentration increases when melatonin is given exogenously or after an imposed oxidative stress (exposure to ionizing radiation). Urinary cyclic 3-OHM levels are believed to be a biomarker (footprint molecule) of in vivo *OH production and its scavenging by melatonin. Although the data are less complete, besides the *OH, melatonin in cell-free systems has been shown to directly scavenge H2O2, singlet oxygen (1O2) and nitric oxide (NO*), with little or no ability to scavenge the superoxide anion radical (O2*-) In vitro, melatonin also directly detoxifies the peroxynitrite anion (ONOO-) and/or peroxynitrous acid (ONOOH), or the activated form of this molecule, ONOOH*; the product of the latter interaction is proposed to be 6-OHM. How these in vitro findings relate to the in vivo antioxidant actions of melatonin remains to be established. The ability of melatonin to scavenge the lipid peroxyl radical (LOO*) is debated. The weight of the evidence is that melatonin is probably not a classic chain-breaking antioxidant, since its ability to scavenge the LOO* seems weak. Its ability to reduce lipid peroxidation may stem from its function as a preventive antioxidant (scavenging initiating radicals), or yet unidentified actions. In sum, in vitro melatonin acts as a direct free radical scavenger with the ability to detoxify both reactive oxygen and reactive nitrogen species; in vivo, it is an effective pharmacological agent in reducing oxidative damage under conditions in which excessive free radical generation is believed to be involved.
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              A novel melatonin metabolite, cyclic 3-hydroxymelatonin: a biomarker of in vivo hydroxyl radical generation.

              In the current study, we characterized a urinary melatonin metabolite which could provide a safe and effective method to monitor generation of HO* in humans. Using mass spectrometry (MS), proton nuclear magnetic resonance (1H NMR), COSY 1H NMR analysis, and calculations on the relative thermodynamic stability, a novel melatonin metabolite was identified as cyclic 3-hydroxymelatonin (3-OHM). 3-OHM is the product of the reaction of melatonin with HO* which was generated in two different cell-free in vitro systems. Interestingly, this same metabolite, 3-OHM, was also identified in the urine of both rats and humans. A proposed reaction pathway suggests that 3-OHM is the footprint product that results when a melatonin molecule scavenges two HO*. When rats were challenged with ionizing radiation which results in HO* generation, urinary 3-OHM increased dramatically compared to that of controls. These results strongly indicate that the quantity of 3-OHM produced is associated with in vivo HO* generation. Since melatonin exists in virtually all animal species and has a wide intracellular distribution and 3-OHM is readily detected noninvasively in urine, we suggest that 3-OHM is a valuable biomarker that can be used to monitor in vivo HO* levels in humans and other species. The measurement of urinary 3-OHM as a biomarker of HO* generation could provide clinical benefits in the diagnosis and treatment of diseases.
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