Melatonin and nitric oxide

Aydoğan, Sami; Yerer, Mehmet; Goktas, Altan

doi:10.1007/bf03345555

Cited by 82 publications

(51 citation statements)

References 50 publications

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“…• and NOO • formation and thus prevents polyunsaturated fatty acid oxidation (Teixeira et al 2003;Aydogan et al 2006). …”

Section: Discussionmentioning

confidence: 99%

Long-term melatonin administration enhances the antioxidant potential of human plasma maintained after discontinuation of the treatment

Piechota¹,

Lipińska²,

Szemraj³

et al. 2010

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Abstract.We investigated the effect of long-term oral melatonin administration on the antioxidant capacity of plasma. The study was performed on healthy volunteers divided into two groups: the control group (without melatonin treatment) and the study group treated with 6 mg of melatonin per day for two weeks, 2 hours before bedtime. Blood samples were drawn: before melatonin administration, on the 7 th and 14 th day of melatonin treatment and on the 10 th day after the last dose of melatonin. It was shown that oral administration of melatonin increases plasma antioxidant ferric reducing ability (FRAP assay) (p < 0.05) and DPPH (1,1-diphenyl-2-picrylhydrazyl) radical scavenging (p < 0.01), and decreases thiobarbituric acid reactive substances (TBARS) (p < 0.05) and DNA damage (p < 0.001). This protective effect is maintained for at last 10 days after discontinuation of the treatment.The present work highlights that the antioxidant capacity of plasma was significantly higher on the 10 th day after the discontinuation of melatonin treatment than on the 14 th day of its administration. Our findings indicated that a long-term oral melatonin administration maintained the increased antioxidant capacity of plasma and prevented oxidative damage to DNA after hormone administration was discontinued.

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“…• and NOO • formation and thus prevents polyunsaturated fatty acid oxidation (Teixeira et al 2003;Aydogan et al 2006). …”

Section: Discussionmentioning

confidence: 99%

Long-term melatonin administration enhances the antioxidant potential of human plasma maintained after discontinuation of the treatment

Piechota¹,

Lipińska²,

Szemraj³

et al. 2010

gpb

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“…It can protect cells against hydroxyl radicals (the most frequent type of free radical following irradiation), hydrogen peroxide, nitric oxide (a product by immune cells), peroxynitrite anion, and singlet oxygen (Chetsawang et al 2006;Cagnoli et al 1995;Aydogan et al 2006). Also, melatonin ameliorates oxidative stress at different levels, such as modulation of molecular pathways and cellular functions that are explained in detail below.…”

Section: Antioxidative Effects Of Melatoninmentioning

confidence: 99%

The melatonin immunomodulatory actions in radiotherapy

et al. 2017

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Radiotherapy has a key role in cancer treatment in more than half of patients with cancer. The management of severe side effects of this treatment modality is a limiting factor to appropriate treatment. Immune system responses play a pivotal role in many of the early and late side effects of radiation. Moreover, immune cells have a significant role in tumor response to radiotherapy, such as angiogenesis and tumor growth. Melatonin as a potent antioxidant has shown appropriate immune regulatory properties that may ameliorate toxicity induced by radiation in various organs. These effects are mediated through various modulatory effects of melatonin in different levels of tissue reaction to ionizing radiation. The effects on the DNA repair system, antioxidant enzymes, immune cells, cytokines secretion, transcription factors, and protein kinases are most important. Moreover, anti-cancer properties of melatonin may increase the therapeutic ratio of radiotherapy. Clinical applications of this agent for the management of malignancies such as breast cancer have shown promising results. It seems anti-proliferative, anti-angiogenesis, and stimulation or suppression of some immune cell responses are the main anti-tumor effects of melatonin that may help to improve response of the tumor to radiotherapy. In this review, the effects of melatonin on the modulation of immune responses in both normal and tumor tissues will be discussed.

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“…Inhibition of NO production may be a further means whereby melatonin reduces oxidative damage under conditions, such as in ischemia/reperfusion and sepsis, where NO seems to be important in terms of the resulting damage [43]. Previously, we have shown that melatonin can promote neuronal differentiation [41,44].…”

Section: Role Of Melatonin In the Inhibition Of Nox Releasementioning

confidence: 99%

Role of Nitric Oxide in Neurodegeneration and Vulnerability of Neuronal Cells to Nitric Oxide Metabolites and Reactive Oxygen Species

Lahiri

Ghosh

Rogers

et al. 2010

Aging and Age-Related Disorders

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Role of nitric oxide in neurodegeneration and vulnerability of neuronal cells to nitric oxide metabolites and reactive oxygen species NO can also be released chemically from a group of compounds called NO donors, such as sodium nitroprusside (SNP). NO directly or through its metabolites is believed to be involved in several disorders, including Alzheimer's disease (AD). This chapter summarizes the role of NO and oxidative stress in neurodegeneration and describes the experimental evidence of increased vulnerability of neuronal cells to NO metabolites and other reactive oxygen species (ROS). As NO is a highly labile, unstable free gas, levels of the stable end products, such as nitrite and nitrate (NOx), were measured. When different cell types were treated with SNP, a significant level of NOx was detected in a time-and dose-dependent manner, which was more than the spontaneous release by SNP. Astrocytic, glial, and epithelial cell lines released significantly higher levels of NOx compared with neuronal cell lines after SNP treatment. Neuronal cells were more sensitive to SNP-induced cytotoxicity, as determined by lactate dehydrogenase assay. SNP-mediated toxicity is known to be due, in large part, to the accumulation of cyanide ions, and the ability of cells to protect themselves against this toxicity depends upon their levels of NO metabolites. Cell lines that generate more NOx, such as astrocytic and epithelial, are better protected against the SNP-induced toxicity than are less NOx-protecting neuronal cell lines. Our results suggest that various cell types metabolize SNP differently and that neuronal cell lines are more vulnerable than other cell types to SNP treatment. As neuronal cell lines lack an NO-generated protective mechanism, these cells are potentially primary targets for neurodegeneration by toxic agents including the free radicals and peroxynitrites.

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Melatonin and nitric oxide

Cited by 82 publications

References 50 publications

Long-term melatonin administration enhances the antioxidant potential of human plasma maintained after discontinuation of the treatment

Long-term melatonin administration enhances the antioxidant potential of human plasma maintained after discontinuation of the treatment

The melatonin immunomodulatory actions in radiotherapy

Role of Nitric Oxide in Neurodegeneration and Vulnerability of Neuronal Cells to Nitric Oxide Metabolites and Reactive Oxygen Species

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