Visualization of Melatonin's Multiple Mitochondrial Levels of Protection Against Mitochondrial Ca2+-Mediated Permeability Transition and Beyond in Rat Brain Astrocytes

Jou, Mei‐Jie; Peng, Tsung-I

doi:10.1016/j.bpj.2009.12.2038

Cited by 86 publications

(120 citation statements)

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“…Another interesting aspect of melatonin is that it is taken up by mitochondria, providing in situ protection against oxidative damage [146,147]. Several reports have shown that melatonin improves mitochondrial function, reduces mitochondrial oxidative status, and increases the activity of the respiratory chain [146,148].…”

Section: Function As a Free Radical Scavengermentioning

confidence: 99%

Melatonin-Induced Oncostasis, Mechanisms and Clinical Relevance

Cardinali¹,

Escames²,

Acuña-Castroviejo³

et al. 2016

J Integr Oncol

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Section: Function As a Free Radical Scavengermentioning

confidence: 99%

Melatonin-Induced Oncostasis, Mechanisms and Clinical Relevance

Cardinali¹,

Escames²,

Acuña-Castroviejo³

et al. 2016

J Integr Oncol

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“…As a matter of fact, previous studies indicate that melatonin is neuroprotective in streptozotocin-induced rat model of diabetic neuropathy [104] . Once again, it would appear that the quenching of free radicals by melatonin might be the central mechanism for exerting neuroprotection [105,106] , although other melatonin-induced neuroprotective mechanisms cannot be ruled out. Thus, recent evidence in an experimental model of diabetic neuropathy suggests that melatonin modulates neuroinflammation by inhibiting the NF-κB pathway and downstream mediators of inflammation, and protects against oxidative stress by upregulating the nuclear erythroid 2-related factor 2 (Nrf2) pathway, thereby contributing to melatonin's neuroprotective effect [107] .…”

Section: Melatonin Modulates Diabetes-related Alterationsmentioning

confidence: 99%

Role of melatonin on diabetes-related metabolic disorders

Espino

Pariente²,

Rodríguez³

2011

WJD

104

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Melatonin is a circulating hormone that is mainly released from the pineal gland. It is best known as a regulator of seasonal and circadian rhythms, its levels being high during the night and low during the day. Interestingly, insulin levels are also adapted to day/night changes through melatonin-dependent synchronization. This regulation may be explained by the inhibiting action of melatonin on insulin release, which is transmitted through both the pertussis-toxin-sensitive membrane receptors MT1 and MT2 and the second messengers 3',5' -cyclic adenosine monophosphate, 3',5'-cyclic guanosine monophosphate and inositol 1,4,5-trisphosphate. Melatonin may influence diabetes and associated metabolic disturbances not only by regulating insulin secretion, but also by providing protection against reactive oxygen species, since pancreatic β-cells are very susceptible to oxidative stress because they possess only low-antioxidative capacity. On the other hand, in several genetic association studies, single nucleotide polymorphysms of the human MT2 receptor have been described as being causally linked to an elevated risk of developing type 2 diabetes. This suggests that these individuals may be more sensitive to the actions of melatonin, thereby leading to impaired insulin secretion. Therefore, blocking the melatonin-induced inhibition of insulin secretion may be a novel therapeutic avenue for type 2 diabetes.

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“…Melatonin is a special class of antioxidant because when scavenging free radicals, it becomes in a series of metabolites that are also free radical scavengers (Hardeland et al 2009). Melatonin is taken up by mitochondria ), providing an in situ protection against oxidative damage (Acuna et al 2002(Acuna et al , 2011Acuna-Castroviejo et al 2007;Jou et al 2010;Lopez et al 2009;Paradies et al 2010). Under physiological and pathological conditions, the ability of melatonin to maintain mitochondrial homeostasis has been reportedly showed (Acuna et al 2011;Acuna-Castroviejo et al 2001;Escames et al 2007;Lopez et al 2006a, b).…”

Section: Mitochondrial Dna Alterations In Acute Inflammatory Diseasesmentioning

confidence: 99%

Mitochondrial DNA and inflammatory diseases

et al. 2011

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Increasing experimental evidence supports a connection between inflammation and mitochondrial dysfunction. Both acute and chronic inflammatory diseases course with elevated free radicals production that may affect mitochondrial proteins, lipids, and mtDNA. The subsequent mitochondrial impairment produces more reactive oxygen species that further reduce the ATP generation, increasing the probability of cell death. Mitochondrial impairment in now considered a key factor in inflammation because (1) there are specific pathologies directly derived from mtDNA mutations, causing chronic inflammatory diseases such as neuromuscular and neurodegenerative disorders, (2) there are neurodegenerative, metabolic, and other inflammatory diseases in which their progression is accompanied by mitochondrial dysfunction, which is directly involved in the cell death. Recently, a direct implication of mitochondrial reactive oxygen species and, particularly, mtDNA in the innate immune response has been reported. Thus, the mitochondria should be considered targets for new therapies related to the treatment of acute and chronic inflammatory diseases, including the auto-inflammatory ones.

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Visualization of Melatonin's Multiple Mitochondrial Levels of Protection Against Mitochondrial Ca2+-Mediated Permeability Transition and Beyond in Rat Brain Astrocytes

Cited by 86 publications

References 0 publications

Melatonin-Induced Oncostasis, Mechanisms and Clinical Relevance

Melatonin-Induced Oncostasis, Mechanisms and Clinical Relevance

Role of melatonin on diabetes-related metabolic disorders

Mitochondrial DNA and inflammatory diseases

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