Endocrine Aspects of the Mammalian Pineal Gland:A Review

Reíter, Russel J.; Fraschini, F.

doi:10.1159/000121862

Cited by 170 publications

(51 citation statements)

References 12 publications

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“…Reiter has shown that interruption of the sympathetic innervation to the pineal gland blocks its antigonadotrophic effects (27). We interpret our finding that interruption of the sympathetic innervation causes a tremendous reduction in the night-time activity of pineal N-acetyltransferase to indicate that this procedure markedly impairs the gland's ability to convert serotonin to N-acetylserotonin.…”

Section: Discussionsupporting

confidence: 56%

Melatonin Metabolism: Neural Regulation of Pineal Serotonin: Acetyl Coenzyme A N -Acetyltransferase Activity

Klein

Weller

Moore

1971

Proc. Natl. Acad. Sci. U.S.A.

240

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There is a diurnal rhythm in the activity of serotonin N-acetyltransferase in the rat pineal gland. In the normal rat, the nocturnal enzyme activities are 15-to 30-fold greater than are daytime activities. This rhythm is abolished by decentralization or removal of the superior cervical ganglia, procedures that interrupt the only source of central neural input to the pineal gland. This effect of superior cervical sympathectomy on the N-acetyltransferase rhythm cannot be attributed to changes occurring in the denervated pineal parenchymal cells. When chronically denervated glands are placed in organ culture with norepinephrine, the neurotransmitter normally located in sympathetic terminals in the gland, N-acetyltransferase activity increases 10-to 20-fold. These data indicate that superior cervical sympathectomy abolishes the N-acetyltransferase rhythm by elimination of the input of central signals to the gland. These signals appear to regulate the N-acetyltransferase rhythm in the normal rat by regulation of the release of norepinephrine from the sympathetic terminals within the pineal gland.N-acetyltransferase transfers an acetyl group from acetyl coenzyme A to the amino group of serotonin (5-hydroxytryptamine) to form N-acetylserotonin (5-hydroxy-N-acetyltryptamine) (1). N-acetylserotonin is the precursor of melatonin (5-methoxy-N-acetyltryptamine) (2), the putative pineal hormone, which is formed primarily in the pineal gland (3). In the rat pineal gland there is a 24-hr rhythm in Nacetyltransferase activity (4). During the light period of a normal lighting schedule, N-acetyltransferase activity is low. After the onset of darkness, the activity of this enzyme increases to values that are 15-to 30-fold greater than those that occur during the light period (4). The rhythm is maintained after animals are blinded or placed in constant darkness (4, 5). Exposure to constant light suppresses the rhythm, and results in continually low activity of pineal N-acetyltransferase (4). These characteristics indicate that the N-acetyltransferase rhythm is like many other 24-hr rhythms, which are driven by an endogenous mechanism in the central nervous system and can be suppressed or shifted by environmental lighting (6).The only known pathway of central input to the pineal gland is via sympathetic nerves from the superior cervical ganglia (SCG) (7). Evidence indicates that the release of norepinephrine from sympathetic terminals regulates pineal N-acetyltransferase. First, a 10-to 20-fold increase in Nacetyltransferase results when norepinephrine is added to pineal organ cultures (8). Second, pineal norepinephrine is contained entirely in nerve processes (9-11). Serotonin, which is also located in these processes, and tryptamine cannot induce N-acetyltransferase in cultured pineal glands (4, 12). Third, there is a 24-hr rhythm in pineal norepinephrine content that is abolished by decentralization of the SCG (13).To test directly whether the SCG mediate neural control of the N-acetyltransferase rhythm, we examined the e...

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Section: Discussionsupporting

confidence: 56%

Melatonin Metabolism: Neural Regulation of Pineal Serotonin: Acetyl Coenzyme A N -Acetyltransferase Activity

Klein

Weller

Moore

1971

Proc. Natl. Acad. Sci. U.S.A.

240

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“…To the best of authors' knowledge, this is the first study to show that not only are shift workers in a high risk group for breast cancer but also women sleeping in illuminated habitats. The effect of ALAN on breast cancer development is suggested to be mediated by the night-time suppression of the typical daily rhythm of melatonin, because the pineal hormone is produced in the dark phase of the 24 h cycle [50,51].…”

Section: Artificial Light At Night As a Risk Factor For Breast Cancermentioning

confidence: 99%

“…The neuro-hormone melatonin (N-acetyl-methoxytryptamine) produced and secreted from the pineal gland under dark conditions (known as the 'hormone of darkness') is considered a 'Jack of all trades' as it is involved in many of our body functions [51,52]. Melatonin production in the pineal gland is sensitive to light and it was shown that even exposures of low intensity [53] and short duration [54] will suppress its production.…”

Section: Melatonin Suppressionmentioning

confidence: 99%

Artificial light at night: melatonin as a mediator between the environment and epigenome

Haim

Zubidat

2015

Phil. Trans. R. Soc. B

106

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The adverse effects of excessive use of artificial light at night (ALAN) are becoming increasingly evident and associated with several health problems including cancer. Results of epidemiological studies revealed that the increase in breast cancer incidents co-distribute with ALAN worldwide. There is compiling evidence that suggests that melatonin suppression is linked to ALAN-induced cancer risks, but the specific genetic mechanism linking environmental exposure and the development of disease is not well known. Here we propose a possible genetic link between environmental exposure and tumorigenesis processes. We discuss evidence related to the relationship between epigenetic remodelling and oncogene expression. In breast cancer, enhanced global hypomethylation is expected in oncogenes, whereas in tumour suppressor genes local hypermethylation is recognized in the promoter CpG chains. A putative mechanism of action involving epigenetic modifications mediated by pineal melatonin is discussed in relation to cancer prevalence. Taking into account that ALAN-induced epigenetic modifications are reversible, early detection of cancer development is of great significance in the treatment of the disease. Therefore, new biomarkers for circadian disruption need to be developed to prevent ALAN damage.

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“…Recently, Kastin et al(1972) suggested the possibility that melanocyte-stimulating hormone (MSH) released by the pituitary holds the secretion of melatonin from the pineal and MSH release-inhibiting factor from the hypothalamus under inhibitory checks in rats. A relation between the pineal and the thyroid gland has been reported (for review, see Reiter and Fraschini, 1969). Therefore, the influence of MSH and thyroid stimulating hormone should not be neglected.…”

Section: Discussionmentioning

confidence: 99%

Effect of Gonadotropins on the Reduced Excretion of a Gonadotropin-Inhibiting Substance in the Hypophysectomized Rats

Shimizu

Obara

1973

Endocrinol Japon

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Endocrine Aspects of the Mammalian Pineal Gland:A Review

Cited by 170 publications

References 12 publications

Melatonin Metabolism: Neural Regulation of Pineal Serotonin: Acetyl Coenzyme A N -Acetyltransferase Activity

Melatonin Metabolism: Neural Regulation of Pineal Serotonin: Acetyl Coenzyme A N -Acetyltransferase Activity

Artificial light at night: melatonin as a mediator between the environment and epigenome

Effect of Gonadotropins on the Reduced Excretion of a Gonadotropin-Inhibiting Substance in the Hypophysectomized Rats

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