Melatonin increases the activity of the oxidative phosphorylation enzymes and the production of ATP in rat brain and liver mitochondria

Martı́n, Miguel; Macías, M.; León, Josefa; Escames, Germaine; Khaldy, Hoda; Acuña-Castroviejo, Darı́o

doi:10.1016/s1357-2725(01)00138-8

Cited by 232 publications

(173 citation statements)

References 34 publications

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“…These data agree with he interaction between melatonin and striatal D 1 /D 2 receptors elsewhere reported with electrophysiological approaches [18]. Experiments in vivo and in vitro have shown that melatonin promotes mitochondrial phosphorylation and ATP synthesis interacting with the electron transport chain complexes I and IV [5,[37][38][39]. These effects are related to the antioxidant role of melatonin, since it scavenges hydrogen peroxide [53] and increases mitochondrial GSH levels, counteracting the oxidative stress-induced mitochondrial damage [37].…”

Section: Discussionsupporting

confidence: 87%

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Khaldy

Escames

León

et al. 2003

Neurobiology of Aging

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Previous studies showed a synergistic effect of melatonin and deprenyl against dopamine (DA) autoxidation in vitro. Since oxidative stress is implicated in Parkinson's disease (PD), we explored the effects of melatonin plus deprenyl administration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD in C57/Bl6 mice. Melatonin, but not deprenyl prevents the inhibition of mitochondrial complex I and the oxidative damage in nigrostriatal neurons induced by MPTP. With the dose used deprenyl recovers 50% DA levels and tyrosine hydroxylase activity depressed by the neurotoxin, normalizing locomotor activity of mice. Melatonin, which was unable to counteract MPTP-induced DA depletion and inhibition of tyrosine hydroxylase activity, potentiates the effect of deprenyl on catecholamine turnover and mice ambulatory activity. These results suggest a dissociation of complex I inhibition from DA depletion in this model of Parkinson's disease. The data also support that a combination of melatonin, which improves mitochondrial electron transport chain and reduces oxidative damage, and deprenyl, which promotes the specific function of the rescued neurons, i.e. DA turnover, may be a promising strategy for the treatment of PD.

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Section: Discussionsupporting

confidence: 87%

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Khaldy

Escames

León

et al. 2003

Neurobiology of Aging

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“…In these conditions, diaphragmatic mitochondria increase their ATP content, thus yielding more ATP for muscle contraction, avoiding diaphragmatic dysfunction. These findings are well supported by other data in the literature (Escames et al, 2006;Lopez et al, 2006;Martin et al, 2002).…”

Section: Accepted Manuscriptsupporting

confidence: 92%

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Rodríguez

Escames

López

et al. 2008

Experimental Gerontology

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“…Although these concentrations are similar to the physiological ones found in plasma at night, their values are not indicative of the amount of melatonin present in the cells, because high physiological values of melatonin have been found in differing tissues (even two or three orders of magnitude more than the circulating level) (Martín et al 2002).…”

Section: Introductionmentioning

confidence: 54%

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

et al. 2011

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Melatonin, a metabolic product of the amino acid tryptophan, induces a dose-dependent energy drop correlated with a decrease in the oxidative phosphorylation process in isolated rat liver mitochondria. This effect involves a gradual decrease in the respiratory control index and significant alterations in the state 4/state 3 transition of membrane potential (DW). Melatonin, alone, does not affect the insulating properties of the inner membrane but, in the presence of supraphysiological Ca 2? , induces a DW drop and colloid-osmotic mitochondrial swelling. These events are sensitive to cyclosporin A and the inhibitors of Ca 2? transport, indicative of the induction or amplification of the mitochondrial permeability transition. This phenomenon is triggered by oxidative stress induced by melatonin and Ca 2? , with the generation of hydrogen peroxide and the consequent oxidation of sulfydryl groups, glutathione and pyridine nucleotides. In addition, melatonin, again in the presence of Ca 2? , can also induce substantial release of cytochrome C and AIF (apoptosis-inducing factor), thus revealing its potential as a pro-apoptotic agent.

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Melatonin increases the activity of the oxidative phosphorylation enzymes and the production of ATP in rat brain and liver mitochondria

Cited by 232 publications

References 34 publications

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Synergistic effects of melatonin and deprenyl against MPTP-induced mitochondrial damage and DA depletion

Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice

Interactions of melatonin with mammalian mitochondria. Reducer of energy capacity and amplifier of permeability transition

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