Biomedical subjects

O Vakkuri

Publications and source records attributed to O Vakkuri.

At least 19 recordsLinked to original sources

PubMed1997

Suppression of melatonin secretion by bright light in seasonal affective disorder.

Eleven patients with winter seasonal affective disorder and 10 healthy controls were exposed to light of 3300 lux for 5 min and for 1 hour respectively on consecutive evenings at 22:00 hours during winter and summer. In the winter, the measurements were undertaken both before and after the treatment with bright light for 2 weeks. In the summer, there was no treatment. Melatonin concentration in saliva and subjective sleepiness were measured at 22:00 and 23:00 hours on each test. There was no significant difference in the suppression of melatonin in response to the light tests between the patients and the controls. Exposure to light reduced the level of subjective sleepiness more among the patients compared to the control subjects. This reduction was not associated with the change in melatonin secretion nor the improvement in depressive symptoms.

Adult↗

PubMed1996

Effects of bright light on sleepiness, melatonin, and 25-hydroxyvitamin D(3) in winter seasonal affective disorder.

Sixteen patients with winter seasonal affective disorder and 13 healthy controls were exposed to 3300 lx of cool-white fluorescent light for either 1 hour or 15 min in the morning for 2 weeks during the winter. Subjective sleepiness, melatonin concentration in saliva, and serum 25-hydroxyvitamin D(3) concentration were measured before and after the 2-week trial as well as the following summer when the patients were well. There were no significant differences in the baseline values between the patients and healthy subjects. No significant differences in the outcome measures were observed in the patients or the controls in the two groups of each after the trial. The exposure to bright light resulted in a significant decrease in subjective sleepiness early in the evening in the patients but not in the control subjects. The reduction of depressive symptoms was associated with the decrease in subjective sleepiness but not with the changes in the melatonin or vitamin D concentrations.

Adult↗

PubMed1996

Mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) reduces circulating melatonin levels in the rat.

We have previously shown that the prototype for halogenated aromatic hydrocarbons, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), diminishes serum melatonin concentration at the same dose in both the most TCDD-susceptible (Long-Evans, Turku AB; L-E) and the most TCDD-resistant (Han/Wistar, Kuopio; H/W) rat strain. The change developed within 24 h and persisted for at least 28 days after TCDD exposure; was independent of the time of day and was not associated with any morphological damage to the pineal gland. In the present study, we investigated the mechanism of this endocrine effect. Despite a 40-50% decrease in circulating melatonin levels, the pineal content of melatonin, serotonin and 5-hydroxyindole acetic acid remained unaltered and the rate-limiting enzyme of pineal melatonin biosynthesis, N-acetyltransferase, displayed only a relatively minor suppression in activity (30%) in TCDD-treated L-E rats. Likewise, TSDD did not influence the ability of pineal glands from L-E rats to synthesize and secrete melatonin in ex vivo or in vitro experiments. TCDD accelerated the disappearance of exogenous melatonin from the serum in both rat strains. This enhancement probably did not originate in the liver, because liver perfusion studies revealed that even control rat livers were capable of total melatonin clearance in spite of the fact that the melatonin concentration far exceeded physiological levels. Urine excretion of the normal main metabolite of melatonin, 6-hydroxymelatoninsulfate, was reduced by TCDD treatment in both strains. This was accompanied by an altered HPLC pattern of metabolites, especially in H/W rats. We conclude that TCDD decreases serum melatonin levels in rats by enhancing the peripheral, evidently extrahepatic, metabolism of the hormone.

Animals↗

PubMed1996

Ethanol decreases nocturnal plasma levels of thyrotropin and growth hormone but not those of thyroid hormones or prolactin in man.

Previous studies on the effects of ethanol on circulating pituitary hormones have been carried out mostly during daytime when the secretion of these hormones is generally at a nadir. Therefore, we studied the effects of ethanol on the nocturnal secretion of GH, PRL, TSH, and thyroid hormones (protocol I, nine healthy subjects, five women) and on the TSH and PRL responses to synthetic TRH (protocol II, healthy subjects, four women). Ethanol was given in doses of 0, 0.5 or 1.0 g/kg of BW(protocol I) and 0 or 1.0 g/kg (protocol II) and ingested po at 1900-1945 h. In protocol I, plasma GH rose from 0.6 +/- 0.2 microgram/L (mean +/- SE) at 2200 h to 25.0 +/- 4.3 micrograms/L at 0100 h in control subjects and was almost completely inhibited at 4.5 +/- 1.7 micrograms/L at 0100 h in subjects receiving 1.0 g/kg ethanol (P < 0.01). In subjects receiving 0.5 g/kg ethanol, the inhibition was also significant (P < 0.01), plasma GH being 8.2 +/- 2.5 micrograms/L at 0100 h. Plasma GHRH was measured after solid phase separation in RIA, but it did not show any ethanol-related changes. Plasma PRL exhibited a clear diurnal rhythm in control subjects and rose from 77 +/- 16 at 1800 h to 248 +/- 62 micrograms/L at 0700 h (P < 0.01). The plasma PRL profile was not affected by ethanol. Plasma TSH was 1.4 +/- 0.2 mU/L at 1800-2200 h and rose to 2.3-2.4 mU/L for 0100-0700 h (P < 0.001) in the control subjects. Ethanol 1.0 g/kg suppressed plasma TSH to 1.4 +/- 0.2 mU/L (P < 0.05 at 0100 h and P < 0.01 at 0200 h). According to the area under the curve analyses, the suppression in the nocturnal TSH was 32% in the 0.5 g/kg group and 45% in the 1.0 g/kg group (P < 0.05 for both cases). Circulating free or total T3 and T4 did not show any statistically significant changes that could explain the ethanol-induced inhibition in the nocturnal TSH peak. In protocol II, synthetic TRH (1 microgram/kg BW) was given intravenously, and blood samples were collected before, at 20 and 60 min. TRH significantly stimulated plasma TSH and PRL, but ethanol (1.0 g/kg BW) had no effect on these responses. In conclusion, small amounts of ethanol have unexpectedly great effects on nocturnal surges of TSH, and especially on those of GH, that are apparently mediated by suprapituitary mechanisms. On the other hand, ethanol did not affect the nocturnal PRL surge. These inhibitory effects of ethanol may have unfavorable effects on growth and metabolism in adolescent drinkers.

Adult↗

PubMed1996

Decrease in melatonin precedes follicle-stimulating hormone increase during perimenopause.

Melatonin, the hormone of the pineal gland, which in animal studies has been found to inhibit aging processes, is secreted in smaller amounts towards senescence. Menopause, an aging process in women, is known to be associated with typical changes in gonadotropin and sex steroid secretion. Our main objective was to study the possible role of melatonin in the hormonal regulation of menopause. This study focused on detailed changes in melatonin and follicle-stimulating hormone (FSH) secretion cross-sectionally in pre- to postmenopausal females. Special attention was paid to females aged around 50 years, which is the mean menopausal age. Seventy-seven healthy female volunteers aged 30-75 years were the subjects of this study. Melatonin was measured radioimmunologically from nocturnal urine collected between 20.00 and 08.00 h, and FSH and melatonin from blood samples taken at 0.900 h. Nocturnal urinary excretion of melatonin was found to decline significantly from premenopause to postmenopause. The youngest premenopausal women (age group 30-39 years) excreted the highest amounts of melatonin (21.2 +/- 2.2 pmol/h, mean +/- SEM, N = 17). In the age group 40-44 years the excretion declined by 41% (p < 0.05). The second significant decline (35%, p < 0.05) took place between the age groups 50-54 years and 55-59 years. A declining trend as a function of age was also seen in morning serum melatonin. Serum FSH rose sharply to high levels before the age of 50 (p < 0.01) and remained at a high level thereafter. Urinary melatonin correlated negatively with serum FSH (r = -0.32, p < 0.05). In conclusion, the inverse changes in melatonin and FSH secretion during the perimenopausal years, with the sharpest decline in nocturnal excretion of melatonin far before menopause, suggest that melatonin may be permissively linked to the initiation of menopause.

Adult↗

PubMed1995

Ethanol induces a paradoxical simultaneous increase in circulating concentrations of insulin-like growth factor binding protein-1 and insulin.

The aim of this study was to examine the effect of acute alcohol intake on circulating concentrations of insulin, C-peptide, insulin-like growth factor (IGF) binding protein-1 (IGFBP-1), and plasma glucose levels. We measured these parameters for 12 hours after administration of 0, 0.5, or 1.0 g ethanol/kg body weight to nine healthy volunteers between 7:00 and 7:45 PM according to a randomized, double-blind, crossover design. Following a snack at 9:00 PM, plasma insulin (P < .05) and C-peptide (P < .01) concentrations were significantly increased at 10:00 PM in the 1.0-g group as compared with the control group. C-peptide to insulin molar ratios were significantly higher (P < .05) in both ethanol groups at 10:00 PM and 2:00 AM than in the control group. No differences were observed in plasma glucose levels between the three groups. Plasma IGFBP-1 levels showed a dose-dependent increase in the ethanol groups, and remained increased from 10:00 PM for 3 hours (P < .05 or less) at the lower dose and for 6 hours (P < .05 or less) at the higher dose. These observations indicate that ethanol-induced postprandial hyperinsulinemia is due to increased insulin secretion and that alcohol may increase hepatic insulin extraction. The lack of any effect on plasma glucose levels suggests that alcohol intake must be associated with decreased insulin sensitivity. Alcohol intake results in a paradoxical increase in peripheral concentrations of IGFBP-1 despite simultaneous hyperinsulinemia. This implies that ethanol has a direct stimulatory effect on hepatic IGFBP-1 synthesis.

Adult↗

PubMed1995

Effects of exposure to morning bright light in the blind and sighted controls.

Seven blind subjects and 11 sighted controls were exposed to 3300 lux of cool-white fluorescent light for either 1 h or 15 min in the morning for 2 weeks during the winter. Serum 25-hydroxyvitamin D3 concentration, melatonin concentration in saliva, body temperature from the armpit, subjective sleepiness, and depressive symptoms were measured before and after the 2-week trial. The intervention resulted in a significant elevation in the concentration of melatonin at 21.00 hours in the healthy controls but at 23:00 hours in the blind subjects. The body temperatures measured were increased in the controls but decreased in the blind in the morning following the cessation of the intervention, and these opposite changes resulted in significant differences in the temperatures between the two groups. The decreases in the body temperature were associated with the increases in the levels of melatonin in the blind but not in the controls. Bright light administered in the morning decreased subjective sleepiness and improved mood in the healthy controls and in the blind subjects as well. The intervention had no effect on the levels of vitamin D in either of the two groups.

Adult↗

PubMed1994

Ethanol decreases nocturnal plasma levels of atrial natriuretic peptide (ANP 99-126) but not the N-terminal fragment of pro-atrial natriuretic peptide (ANP 1-98) in man.

1. The aim of this study was to elucidate the role of atrial natriuretic peptides in the regulation of water and electrolyte balance after alcohol intake. To this end we measured the plasma concentrations of ethanol, atrial natriuretic peptide 99-126 and the N-terminal fragment of pro-atrial natriuretic peptide (atrial natriuretic peptide 1-98), serum osmolality and serum sodium concentration, and urine output, urine osmolality and urinary sodium excretion for 12 h after administration of ethanol (0, 0.5 and 1.0 g body weight/kg) and placebo drinks to nine healthy subjects according to a double-blind cross-over design. 2. Intake of ethanol (at 19.00-19.45 hours) inhibited the nocturnal increase in the plasma atrial natriuretic peptide 99-126 level dose-dependently (P < 0.05), but had no effect on the plasma atrial natriuretic peptide 1-98 level. Serum osmolality and serum sodium concentration were elevated dose-dependently for 2-5 h after the ethanol intake. Urine volume increased after the higher ethanol dose (net loss of 0.6 litre of water). 3. Since the plasma atrial natriuretic peptide 1-98 level was not changed after ethanol intake, we propose that the alcohol-induced inhibition of the nocturnal rise in the plasma atrial natriuretic peptide 99-126 level is not caused by an inhibition of release, but may rather reflect an increased peripheral elimination of atrial natriuretic peptide 99-126.

Adult↗

PubMed1994

Delayed pro-opiomelanocortin activation after ethanol intake in man.

To elucidate the effect of ethanol on the secretion of ACTH and beta-endorphin (BE) as the representatives of the pro-opiomelanocortin (POMC) system, as well as cortisol as the hypophyseally regulated peripheral hormone, we measured concentrations of serum ethanol and plasma ACTH, BE, and cortisol at 1- to 4-hr intervals for 12 hr after administration of 0.5 and 1.0 g ethanol/kg of body weight and placebo drinks between 1900-1945 hr to nine healthy volunteers according to a double-blind, cross-over design. Plasma ACTH, BE, and cortisol showed an expected diurnal rhythm with the highest levels at 0700 hr. Intake of ethanol had no statistically significant effects on plasma ACTH up to 0700 hr in the morning. The higher dose caused increased levels of BE at 0100 hr and both doses at 0200 hr. Plasma cortisol at 0400 hr was higher in subjects receiving 1.0 g ethanol/kg than in those receiving placebo (p < 0.05). Our present observation that plasma ACTH was unchanged after ethanol intake, but plasma BE was increased at 0100-0200 hr may be due to the fact that our BE antiserum cross-reacts with beta-lipotropin, which has a considerably longer half-life than ACTH or BE, and also to the long sampling interval. Thus, the POMC system may have been stimulated after ethanol intake. The nocturnal rise of plasma cortisol levels at 0400 hr, 2-3 hr after the peak in plasma BE, may be caused by the increased secretion of POMC. Because the ethanol dose of 1.0 g/kg body weight stimulated the POMC system but the 0.5 g/kg body weight did not, we conclude that higher ethanol doses induce increases in stress hormone secretion.

Adrenocorticotropic Hormone↗

PubMed1993

Ethanol inhibits melatonin secretion in healthy volunteers in a dose-dependent randomized double blind cross-over study.

To elucidate the effects of alcohol on pineal rhythmicity, ethanol was administered in the evening in amounts usually consumed during social ingestion to nine healthy volunteers in a double blind, cross-over study. Plasma concentrations of melatonin, catecholamines (norepinephrine and epinephrine), and ethanol were measured by RIA, high pressure liquid chromatography, and gas chromatography before and for 12 h after the administration of 0, 0.5, and 1 g ethanol/kg wt. Plasma melatonin and catecholamines displayed expected diurnal rhythms, with peak values at 0300-0400 h for melatonin and trough values at 0100-0400 h for catecholamines. Intake of ethanol between 1900-1945 h inhibited the nocturnal melatonin secretion dose-dependently during the first half of the night, with no changes in urinary excretion of melatonin. The inhibition was 41% (P < 0.05) from the control at midnight for both ethanol doses, 33% (P < 0.05) at 0100 h, and 18% (P < 0.05) at 0200 h for the higher dose. In addition, the higher dose of ethanol increased plasma norepinephrine levels at 2000 and 2200 h (P < 0.01) until 0400 h (P < 0.05). Taking into account the involvement of melatonin in the regulation of sleep and diurnal rhythms, we suggest that ethanol-induced suppression of nocturnal melatonin secretion and an increase in noradrenergic activity may be closely associated with disturbances in sleep and performance.

Adult↗

PubMed1993

Cardiopulmonary and behavioral responses to computer-driven infusion of detomidine in standing horses.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1. (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [loge detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [loge detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). (ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1992

Noradrenergic inhibition and alpha 2-adrenergic stimulation of melatonin secretion in the pigeon.

Adrenergic regulatory mechanisms of melatonin synthesis and secretion were studied in the pigeon in vivo. Late-afternoon intraperitoneal injection of noradrenaline (NA; 1 mg/kg) resulted in a significant decrease in plasma melatonin levels in 3 h. The same effect was seen after phenylephrine treatment (1 mg/kg i.p.), indicating that an alpha 1-adrenergic mechanism may mediate the inhibition. Propranolol treatment had no effect on plasma melatonin levels, supporting this concept. Detomidine (1 mg/kg i.p.), an alpha 2-adrenergic agonist, increased melatonin levels. This stimulatory effect was blocked by yohimbine, an alpha 2-adrenergic antagonist. However, yohimbine alone had no effect on the plasma melatonin levels, suggesting that alpha 2-adrenergic transmission is not primarily responsible for the nocturnal stimulation of melatonin synthesis and secretion in the pigeon.

Animals↗

PubMed1992

Pineal muscarinic phosphoinositide responses: age-associated sensitization, agonist-induced desensitization and increase in melatonin release from cultured pineal glands.

Regulation of phosphoinositide (PI) signaling through the muscarinic cholinergic receptors (mAChRs) and their possible role were explored in the rat pineal gland. A sensitization of the PI signaling pathway was seen with advancing age. Binding of the mAChR ligand [N-methyl-3H]scopolamine to pineal sections, as detected by autoradiography, significantly decreased with advancing age and thus negatively correlated with the gland's ability to respond to cholinergic stimulus. The cholinergic agonist carbachol induced a time-dependent desensitization of the muscarinic PI signaling after 2 h of pretreatment in vitro (43 and 61% dampening of the PI response after 2 and 11 h pretreatment, respectively). This homologous desensitization was not mimicked by forskolin or phorbol esters, suggesting that proteins kinases A and C were not involved. Carbachol stimulation of the pineal glands in vitro increased melatonin release 2-fold, an effect quantitatively similar to that seen after adenylyl cyclase activation. Carbachol failed, however, to affect pineal cAMP levels. These results suggest that the PI signaling through pineal mAChRs is desensitized in young rats, possibly due to higher exposure to endogenous acetylcholine. Thus acetylcholine might play a prominent role in the developing gland. Moreover, acetylcholine could modulate melatonin release from the adult pineal gland in vivo.

Aging↗

PubMed1992

Seasonal and daily patterns in melatonin secretion in female reindeer and their calves.

Daily patterns of pineal function were studied in different seasons in 10 adult semidomesticated female reindeer and 5 prepubertal calves living in a natural arctic environment at latitude 69 degrees 10'N. Serum samples for melatonin RIA were collected every 4 h for 24 h in October (10 h of light, 14 h of darkness and 8 h of light, 16 h of darkness), December (24 h of darkness), March (13 h of light, 11 h of darkness), and June (24 h of light). A significant daily variation in serum melatonin levels was observed in the adult reindeer, with peak values (20-50 ng/liter) occurring during the night in autumn, winter, and spring, but not summer. The daytime values at 13 h (5-10 ng/liter) were constant throughout the year. Total daily amounts of melatonin, the duration of peak levels, and maximal concentrations were significantly lower in spring and summer than before the rut in autumn. The exposure of adult animals to artificial darkness from bright sunlight on August 1 and September 21 resulted in an immediate increase in serum melatonin concentrations. The 2-week-old calves had detectable serum melatonin levels, but no daily rhythm in the spring, whereas a rhythm was detectable by the first autumn, only to disappear unexpectedly during the first winter and return in the spring. At the age of 16 months, the calves had serum melatonin concentrations similar to those in the adults. Our present results show that the continuous illumination experienced during the summer abolished the normal daily melatonin rhythm. This does not seem to be related to organic changes in the pineal gland, since exposure to darkness during the summer increased melatonin levels. The highest melatonin secretion occurred in the autumn and was evidently associated with the rut. Similarly, the daily melatonin rhythm of an adult type observed in the calves at the age of 16 months may be related to the observation that most calves were in rut. Thus, a high rhythmical melatonin secretion appears to relate to puberty and the initiation of heat in female reindeer.

Animals↗

PubMed1992

Differential regulation of the rat melatonin receptors: selective age-associated decline and lack of melatonin-induced changes.

To gain some understanding of the factors regulating high affinity melatonin (MT) receptors in the rat, we conducted a series of studies using quantitative autoradiography of [2-125I]iodo-MT binding in vitro with validated assay conditions. MT receptor status and the relative protein content of the autoradiographic sections were assessed in the anterior pituitary gland, the area postrema, the caudal (tail) artery (CA), the anterior cerebral artery (ACA), and the suprachiasmatic nuclei (SCN) of 9-, 96-, and 306-day-old Wistar rats. When age-associated changes in protein content were taken into account, MT receptor expression in the area postrema and the SCN remained relatively constant between 9-306 days of age. On the contrary, a dramatic loss of MT receptors was observed in the arteries of 306-day-old rats (98% and 89% loss compared to the 9-day-old rats in the ACA and CA, respectively). In the anterior pituitary gland, MT receptors were expressed only in the 9-day-old rats. The above changes reflected major changes in binding capacity and minor changes in binding affinity. Neither removal of endogenous circulating MT (acute light exposure for 24 h, pinealectomy, or superior cervical ganglionectomy) nor MT injections (1 mg/kg for 10 days 6 h after lights on) affected MT receptor status in the ACA, CA, area postrema, or SCN. Our data suggest that MT receptor expression is differentially regulated during development and that permanent alterations in MT levels do not affect rat MT receptor status.

Age Factors↗

PubMed1990

Moclobemide, an inhibitor of MAO-A, does not increase daytime plasma melatonin levels in normal humans.

1. Plasma melatonin concentrations were determined after administration of single oral doses (100, 200 and 300 mg) of moclobemide, a reversible inhibitor of monoamine oxidase (MAO) with predominant effects on the A-type of the enzyme, to eight young, healthy male volunteers in a double-blind, random-order, placebo-controlled study. The investigation was later continued in an open fashion by giving a single 10 mg dose of the MAO-B inhibitor deprenyl to the same subjects. 2. Neither drug had any effects on plasma melatonin levels, in spite of very marked MAO-A inhibition after moclobemide (as evidenced by up to 79% average decreases in the plasma concentrations of 3,4-dihydroxyphenylglycol, a deaminated metabolite of noradrenaline) and over 90% inhibition of MAO-B activity in blood platelets after deprenyl. 3. It is concluded that daytime human plasma melatonin levels do not accurately reflect MAO-A inhibition in acute drug studies.

Adult↗

PubMed1990

Melatonin in infants and mothers at delivery and in infants during the first week of life.

To evaluate the possible effect of the extreme and permanent changes in the hormonal milieu and in the lighting conditions at birth on the pineal hormone, melatonin (MT), we measured maternal vein and umbilical artery concentrations of MT in 19 parturients, post-partum urinary concentrations of MT in 14 mothers and their infants, and daytime (0800-2000 h) and night-time (2000-0800 h) urinary concentrations of MT and 6-sulphatoxymelatonin in 22 infants during the first 8 days of life. The mean MT concentrations in maternal venous blood and umbilical arterial blood did not differ significantly from each other and there was a positive correlation between them. The same was true for postpartum urinary MT of the mothers and their infants. There was no diurnal rhythm of MT during the first week of life. MT excretion in neonates was 2-5 pmol/12 h (only 1-5% in comparison with adults) and that of 6-sulphatoxymelatonin 150-300 pmol/12 h. In reverse phase high pressure liquid chromatography (HPLC) studies, 84-100% of total MT immunoreactivity was eluted at the same position as synthetic MT, and a small amount of hydrophobic MT-like immunoreactive material was also detected in five of the 10 urine extracts studied. This material (perhaps a novel neonatal metabolite of MT) may be indicative of immaturity of neonatal metabolism of MT although 6-hydroxylation is also functional in neonates. Although infant MT immediately after delivery at least partly reflects maternal MT secretion, our results show that the pineal gland is capable of producing MT at this time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Circadian and seasonal variation in human preovulatory follicular fluid melatonin concentration.

The concentrations of melatonin in 112 preovulatory follicular fluid (FF) samples obtained from 60 women undergoing in vitro fertilization and 27 patients at laparotomy during a spontaneous cycle were measured by RIA and compared with those in peripheral serum. The circadian and seasonal variations in FF melatonin were also analyzed. The FF melatonin concentrations in stimulated (mean +/- SEM, 61.9 +/- 6.4 pmol/L) and spontaneous cycles (98.1 +/- 8.9 pmol/L) were significantly higher (P less than 0.005) than those in peripheral serum (25.4 +/- 1.2 and 38.6 +/- 1.8 pmol/L, respectively), and in the stimulated cycles there was a positive correlation between them. The FF melatonin concentration in the morning (58.9 +/- 3.8 pmol/L) was significantly higher (P less than 0.005) than that in the daytime (23.2 +/- 0.8 pmol/L), but the morning concentrations did not differ between the light and the dark seasons of the year, whereas the daytime values were higher (P less than 0.005) during the dark season (27.1 +/- 2.1 pmol/L) than during the light season (21.1 +/- 2.1 pmol/L). The FF melatonin concentration did not correlate with follicular volume, and FF and serum melatonin concentrations showed no significant correlation with the serum concentrations of estradiol, progesterone, testosterone, or PRL. There were also no differences between FF melatonin concentrations in aspirates with or without an ovum. In summary, significant circadian and circannual variations in high FF melatonin concentrations were found, which suggest that melatonin could potentially interfere with the regulation of reproduction in humans at the follicular level.

Chromatography, High Pressure Liquid↗