Melatonin: a hormone, a tissue factor, an autocoid, a paracoid, and an antioxidant vitamin

Tan, Dun Xian; Manchester, Lucien C.; Hardeland, Rüdiger; López‐Burillo, Silvia; Mayo, Juan C.; Sainz, Rosa M.; Reíter, Russel J.

doi:10.1034/j.1600-079x.2003.02111.x

Cited by 483 publications

(379 citation statements)

References 35 publications

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“…Large amounts of this indoleamine are present in the luminal fluid, and a fraction seems to return to the tissue [4][5][6]. Moreover, melatonin is taken up from the food, a process which has not only been shown by feeding nutrients high in melatonin (which still might be seen as a post-prandial effect), but also by a drop in the circulating hormone by providing a low-melatonin diet [27]. Therefore, melatonin present in the food should, at least transiently, appear in the gastrointestinal tissue.…”

Section: Discussionmentioning

confidence: 99%

Chronomics affirm extending scope of lead in phase of duodenal vs. pineal circadian melatonin rhythms

Pöeggeler

Cornélissen

Huether

et al. 2005

Biomedicine & Pharmacotherapy

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In Göttingen, Germany, circadian variations in melatonin had been determined time-macroscopically in pineal glands, blood plasma and duodenum of chicken and rats. When these data were metaanalyzed, they agreed with the results from an independent survey on tissues from rats collected in a laboratory in Pécs, Hungary. In the latter study, tissues were analyzed chemically in Bratislava, Slovakia, and numerically in Minneapolis, MN, USA, all by single-and multiple-component cosinor and parameter tests. In rats and chickens, these inferential statistical procedures clearly demonstrated a lead in phase of the 24-h cosine curves best fitting all of the duodenal vs. those best fitting all of the pineal melatonin values in each species in 2 geographic (geomagnetic) locations. The 24-h cosine curve of circulating melatonin was found to be in an intermediate phase position. Mechanisms of the phase differences and the contribution of gastrointestinal melatonin to circulating hormone concentrations are discussed.

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Section: Discussionmentioning

confidence: 99%

Chronomics affirm extending scope of lead in phase of duodenal vs. pineal circadian melatonin rhythms

Pöeggeler

Cornélissen

Huether

et al. 2005

Biomedicine & Pharmacotherapy

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“…Melatonin is very attractive from this point of view as it may act as a regulator of the inflammatory cell compartment with a potent anti-oxidant potential able to reduce the oxidative environment of chronic inflammation and to regulate leukocyte function and number [6,7].…”

Section: Introductionmentioning

confidence: 99%

Melatonin: A pleiotropic molecule regulating inflammation

Radogna

Diederich

Ghibelli

2010

Biochemical Pharmacology

308

247

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Melatonin is a neurohormone produced by the pineal gland that regulates sleep and circadian functions. Melatonin also regulates inflammatory and immune processes acting as both an activator and inhibitor of these responses. Melatonin demonstrates endocrine, but also paracrine and autocrine effects in the leukocyte compartment: on one side, leukocytes respond to melatonin in a circadian fashion; on the other side, leukocytes are able to synthesize melatonin by themselves.With its endocrine and paracrine effects, melatonin differentially modulates pro-inflammatory enzymes, controls production of inflammatory mediators such as cytokines and leukotrienes and regulates the lifespan of leukocytes by interfering with apoptotic processes. Moreover, its potent anti-oxidant ability allows scavenging of oxidative stress in the inflamed tissues. The interesting timing of pro-and anti-inflammatory effects, such as those affecting lipoxygenase activity, suggests that melatonin might promote early phases of inflammation on one hand and contribute to its attenuation on the other hand, in order to avoid complications of chronic inflammation. This review aims at giving a comprehensive overview of the various inflammatory pathways regulated by this pleiotropic hormone.

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“…Upon its release stimulated by nocturnal darkness, noradrenaline couples with b-adrenergic receptors, increasing intracellular cyclic adenosine monophosphate (cAMP) levels, eventually inducing the stimulation of arylalkylamine-N-acetyl-transferase (Reiter, 2003), and the production of melatonin. The pineal release of melatonin is not restricted solely to the systemic circulation (Tan et al, 2003). There is compelling evidence to suggest that melatonin is also released via the pineal recess directly into the third ventricle, resulting in cerebrospinal fluid (CSF) melatonin levels greater than those detected in the systemic circulation (Tricoire et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Seifman

Adamides

Nguyen

et al. 2008

J Cereb Blood Flow Metab

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Oxidative stress plays a significant role in secondary damage after severe traumatic brain injury (TBI); and melatonin exhibits both direct and indirect antioxidant effects. Melatonin deficiency is deleterious in TBI animal models, and its administration confers neuroprotection, reducing cerebral oedema, and improving neurobehavioural outcome. This study aimed to measure the endogenous cerebrospinal fluid (CSF) and serum melatonin levels post-TBI in humans and to identify relationships with markers of oxidative stress via 8-isoprostaglandin-F 2a (isoprostane), brain metabolism and neurologic outcome. Cerebrospinal fluid and serum samples of 39 TBI patients were assessed for melatonin, isoprostane, and various metabolites. Cerebrospinal fluid but not serum melatonin levels were markedly elevated (7.28±0.92 versus 1.47±0.35 pg/mL, P < 0.0005). Isoprostane levels also increased in both CSF (127.62 ± 16.85 versus 18.28 ± 4.88 pg/mL, P < 0.0005) and serum (562.46±50.78 versus 126.15±40.08 pg/mL (P < 0.0005). A strong correlation between CSF melatonin and CSF isoprostane on day 1 after injury (r = 0.563, P = 0.002) suggests that melatonin production increases in conjunction with lipid peroxidation in TBI. Relationships between CSF melatonin and pyruvate (r = 0.369, P = 0.049) and glutamate (r = 0.373, P = 0.046) indicate that melatonin production increases with metabolic disarray. In conclusion, endogenous CSF melatonin levels increase after TBI, whereas serum levels do not. This elevation is likely to represent a response to oxidative stress and metabolic disarray, although further studies are required to elucidate these relationships.

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Melatonin: a hormone, a tissue factor, an autocoid, a paracoid, and an antioxidant vitamin

Cited by 483 publications

References 35 publications

Chronomics affirm extending scope of lead in phase of duodenal vs. pineal circadian melatonin rhythms

Chronomics affirm extending scope of lead in phase of duodenal vs. pineal circadian melatonin rhythms

Melatonin: A pleiotropic molecule regulating inflammation

Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

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