Both Hydroxy‐and Methoxyindoles Modify Basal Temperature in the Rat

Morton, Dougal J.

doi:10.1111/j.1600-079x.1987.tb00835.x

Cited by 13 publications

(11 citation statements)

References 18 publications

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“…During the process of oxidative stress injury, mitochondria are both a significant source of ROS and also a target of damage, with a variety of consequences. Based on the prominent role of mitochondria in oxidative stress injury, many studies have clearly shown that ROS leads to cell apoptosis via the mitochondria-dependent apoptotic pathway, which involves damage to the mitochondrial membrane, release of Cyt-C into the cytoplasm followed by caspase-3 activation, and finally hepatocyte apoptosis [30]. The morphologic changes in nuclei, the dissipation of ΔΨ m , the release of Cyt-C, and the expression of cleaved caspase-3 were employed as apoptotic biomarkers to elucidate the mechanisms underlying the antiapoptotic effects of NAS.…”

Section: Discussionmentioning

confidence: 99%

“…NAS, the immediate precursor of melatonin in the tryptophan metabolic pathway in the pineal gland, is a free radical scavenger. NAS has recently been shown to have various biologic activities, including memory-facilitating [29], hypothermic [30], analgesic [31], circadian rhythm adjustment [32], antidepressant [32], antiaging [33], lowering blood pressure [28], and antioxidative effects [28]. As described in our recent reports, NAS protects against acute hepatic I/R injury in mice by reversing the imbalance between oxidants and antioxidants and inhibiting hepatocyte apoptosis via the intrinsic apoptotic pathway [34] and offers neuroprotection through inhibiting mitochondrial death pathways in experimental models of ischemic stroke [35].…”

Section: Introductionmentioning

confidence: 99%

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N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

Jiang

et al. 2014

Oxidative Medicine and Cellular Longevity

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Oxidative stress plays an important role in the pathogenesis of liver diseases. N-Acetyl-serotonin (NAS) has been reported to protect against oxidative damage, though the mechanisms by which NAS protects hepatocytes from oxidative stress remain unknown. To determine whether pretreatment with NAS could reduce hydrogen peroxide- (H2O2-) induced oxidative stress in HepG2 cells by inhibiting the mitochondrial apoptosis pathway, we investigated the H2O2-induced oxidative damage to HepG2 cells with or without NAS using MTT, Hoechst 33342, rhodamine 123, Terminal dUTP Nick End Labeling Assay (TUNEL), dihydrodichlorofluorescein (H2DCF), Annexin V and propidium iodide (PI) double staining, immunocytochemistry, and western blot. H2O2 produced dramatic injuries in HepG2 cells, represented by classical morphological changes of apoptosis, increased levels of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), decreased activity of superoxide dismutase (SOD), and increased activities of caspase-9 and caspase-3, release of cytochrome c (Cyt-C) and apoptosis-inducing factor (AIF) from mitochondria, and loss of membrane potential (ΔΨm). NAS significantly inhibited H2O2-induced changes, indicating that it protected against H2O2-induced oxidative damage by reducing MDA levels and increasing SOD activity and that it protected the HepG2 cells from apoptosis through regulating the mitochondrial apoptosis pathway, involving inhibition of mitochondrial hyperpolarization, release of mitochondrial apoptogenic factors, and caspase activity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

Jiang

et al. 2014

Oxidative Medicine and Cellular Longevity

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“…5-Methoxytryptophol displays a property otherwise known from melatonin (1) and N-acetylserotonin (2), the ability to decrease body temperature. The indole alcohol was even reported to be more efficient in this regard than the pineal hormone [260]. In another metabolic step, 5-methoxytryptophol is transformed to O-acetyl-5-methoxytryptophol, a melatonin homolog also found in the pineal gland [37].…”

Section: Melatonin Metabolism In the Central Nervous Systemmentioning

confidence: 98%

Melatonin and Synthetic Melatonergic Agonists: Actions and Metabolism in the Central Nervous System

Hardeland¹,

Pöeggeler²

2012

CNSAMC

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The CNS is both source and target of melatonin. This methoxyindole formed in the pineal gland is also produced in other CNS regions and additionally enters the brain by uptake from the circulation as well as via the pineal recess. The mammalian circadian pacemaker, the suprachiasmatic nucleus (SCN), not only controls the pineal, but also receives a feedback information on darkness. Two G protein-coupled melatonin receptors, MT1 and MT2, are responsible for the transduction of many melatonergic actions. High receptor densities are especially found in the SCN, but their presence at lower expression levels in other areas is functionally important. Various metabolites and analogs are formed in the CNS, such as N-acetylserotonin, 5-methoxytryptamine, 5-methoxytryptophol, 5-methoxylated kynuramines, and even 6-sulfatoxymelatonin. The chronobiological effects of melatonin go beyond the resetting of a single circadian oscillator. They contribute to phase relationships between oscillatory subsets and are required for robust rhythm amplitudes. CNS effects of melatonin comprise sleep initiation, antiexcitatory, antiepileptic, antinociceptive, anxiolytic, proneurotrophic, antiinflammatory, antioxidant and other neuroprotective actions. The role as a sleep-promoting compound, which is limited by its short half-life in the circulation, has led to the development of controlled-release formulations and of various synthetic agonists, such as ramelteon, agomelatine, tasimelteon, TIK-301, UCM765 and UCM924. Their differences concerning receptor affinities, preferences for receptor subtypes, and pharmacokinetics are discussed, as well as additional antidepressive actions of agomelatine and TIK-301 based on properties as antagonists of the serotonergic 5-HT2C receptor. Indirect antidepressive effects by melatonergic drugs are largely explained by circadian readjustments.

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“…The data available indicate varied results [6]. While there are some reports suggesting a hyperthermic ac tion [8,9], there are others suggesting a hypo thermic action [10,11] of melatonin. Heldmaier et al [12] indicated that photoperiodic information which may be important in cue ing thermoregulatory adjustments is pro cessed in much the same manner as the photoperiodic information that is important in con trolling gonadal activity.…”

Section: Introductionmentioning

confidence: 99%

Thermotrophic Effect of Melatonin in Adrenalectomized and Thyroidectomized Rats

Padmavathamma¹,

Joshi²

1994

Biological Signals

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A single injection of 25 µg melatonin induced hyperthermia in rats. The mechanism(s) by which melatonin induces hyperthermia is not clear. In this study the thermotrophic effects of melatonin were studied in adrenalectomized (ADX) and thyroidectomized (TX) rats to ascertain if melatonin-induced hyperthermia is mediated through these glands, as both these glands play a significant role in mammalian thermoregulation. Melatonin (25 µg) was administered as a single subcutaneous injection at 06.00, 12.00, 18.00, and 24.00 h. Body temperatures were recorded, using an anal thermometer at hourly intervals, round the clock. In the scotophase the animals were located using dim red light and injected. Although the administration of melatonin to both intact and ADX rats resulted in a rise in body temperature, the effect was more pronounced in the former compared to the latter group. Melatonin induced hyperthemia only during the photophase of the diurnal cycle; in the scotophase the response was either poor or nil. In TX rats melatonin was ineffective in inducing hyperthermia in either the photophase or scotophase. The body temperatures of TX rats and melatonin-injected TX rats were parallel. The results indicate that in ADX rats melatonin induced minor hyperthermia, whereas in TX animals it failed to produce any hyperthermia. The findings suggest that melatonin induces hyperthermia probably through its action on thyroid activity. Other mechanisms of action cannot be ruled out, however.

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Both Hydroxy‐and Methoxyindoles Modify Basal Temperature in the Rat

Cited by 13 publications

References 18 publications

N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

N-Acetyl-Serotonin Protects HepG2 Cells from Oxidative Stress Injury Induced by Hydrogen Peroxide

Melatonin and Synthetic Melatonergic Agonists: Actions and Metabolism in the Central Nervous System

Thermotrophic Effect of Melatonin in Adrenalectomized and Thyroidectomized Rats

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