Journal ArticleDOI
Increased levels of malondialdehyde and nitrite/nitrate in the blood of asphyxiated newborns: reduction by melatonin
Francesco Fulia,Eloisa Gitto,Salvatore Cuzzocrea,Russel J. Reiter,Laura Dugo,Placido Gitto,Salvatore Barberi,S. Cordaro,Ignazio Barberi +8 more
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TLDR
The results indicate that the melatonin may be beneficial in the treatment of newborn infants with asphyxia, and the protective actions of melatonin in this study may relate to the antioxidant properties of the indole as well as to the ability ofmelatonin to increase the efficiency of mitochondrial electron transport.Abstract:
Free radicals have been implicated in the pathogenesis of neonatal asphyxia and its complications. This study measured a product of lipid peroxidation, malondialdehyde, and the nitrite/nitrate levels in the serum of 20 asphyxiated newborns before and after treatment with the antioxidant melatonin given within the first 6 hr of life. Ten asphyxiated newborns received a total of 80 mg of melatonin (8 doses of 10 mg each separated by 2-hr intervals) orally. One blood sample was collected before melatonin administration and two additional blood samples (at 12 and 24 hr) were collected after giving melatonin. A third group of healthy newborn children served as controls. Serum malondialdehyde and nitrite+nitrate concentrations in newborns with asphyxia before treatment were significantly higher than those in infants without asphyxia. In the asphyxiated newborns given melatonin, there were significant reductions in malondialdehyde and nitrite/nitrate levels at both 12 and 24 hr. Three of the 10 asphyxiated children not given melatonin died within 72 hr after birth; none of the 10 asphyxiated newborns given melatonin died. The results indicate that the melatonin may be beneficial in the treatment of newborn infants with asphyxia. The protective actions of melatonin in this study may relate to the antioxidant properties of the indole as well as to the ability of melatonin to increase the efficiency of mitochondrial electron transport.read more
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Journal ArticleDOI
Melatonin as an antioxidant: under promises but over delivers.
Russel J. Reiter,Juan C. Mayo,Dun Xian Tan,Rosa M. Sainz,Moisés Alejandro Alatorre-Jiménez,Lilian Qin +5 more
TL;DR: It is the current feeling of the authors that, in view of the widely diverse beneficial functions that have been reported for melatonin, these may be merely epiphenomena of the more fundamental, yet‐to‐be identified basic action(s) of this ancient molecule.
Journal ArticleDOI
Chemical and physical properties and potential mechanisms: melatonin as a broad spectrum antioxidant and free radical scavenger.
Dun Xian Tan,Russel J. Reiter,Lucien C. Manchester,Mei ting Yan,Mamdouh R. El-Sawi,Rosa M. Sainz,Juan C. Mayo,Ron Kohen,Mario Allegra,Rudiger Hardeland +9 more
TL;DR: Under in vivo conditions, melatonin is often several times more potent than vitamin C and E in protecting tissues from oxidative injury when compared at an equivalent dosage (micromol/kg).
Journal ArticleDOI
The basic physiology and pathophysiology of melatonin
TL;DR: Although functions of this hormone in humans are mainly based on correlative observations, there is some evidence that melatonin stabilises and strengthens coupling of circadian rhythms, especially of core temperature and sleep-wake rhythms.
Journal ArticleDOI
The chemistry of melatonin's interaction with reactive species
TL;DR: This review focuses on the direct radical scavenging activity of melatonin and provides a summary of the mechanisms of the reactions between the indoleamine and reactive species in pure chemical solutions.
Journal ArticleDOI
Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans.
TL;DR: Melatonin's functions as an antioxidant include: a), direct free radical scavenging, b), stimulation of antioxidative enzymes, c), increasing the efficiency of mitochondrial oxidative phosphorylation and reducing electron leakage (thereby lowering free radical generation), and 3), augmenting the efficiencyof other antioxidants.
References
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Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.
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