6-sulphatoxymelatonin Excretion Research Articles

A New Perspective on the Pathogenesis of Infantile Colic: Is Infantile Colic a Biorhythm Disorder?

In this study, we investigated the relationship between infantile colic, migraine, and biorhythm regulation, by evaluating biochemical and molecular parameters. Healthy infants with and without infantile colic were eligible for this prospective cohort study. A questionnaire was applied. Between the 6th and 8th postnatal weeks, day and night circadian histone gene H3f3b mRNA expression and spot urine excretion of serotonin, cortisol, and 6-sulphatoxymelatonin were analyzed. Among the 95 infants included, 49 were diagnosed with infantile colic. In the colic group, defecation difficulty, sensitivity to light/sound, and maternal migraine frequency increased and sleep disruption was typical. In the melatonin analysis, the difference between day and night levels was significant in the control group, indicating an established circadian rhythm ( P = 0.014). In the colic group, there was no day-night difference ( P = 0.216) in melatonin, but serotonin levels were higher at night. In the cortisol analysis, day-night values were similar in both groups. Day-night variability of H3f3b mRNA levels between the groups was significant, indicating circadian rhythm disturbance in the colic group compared to the control group ( P = 0.003). Fluctuations in circadian genes and hormones expected in healthy rhythm were revealed in the control group, but were missing in the colic group. Due to the gaps in the etipathogenesis in infantile colic, a unique effective agent has not been discovered so far. This study, which demonstrated for the first time that infantile colic is a biorhythm disorder using molecular methods, fills the gap in this regard and points to a completely different perspective in terms of treatment.

Analysis of Different Melatonin Secretion Patterns in Children With Sleep Disorders: Melatonin Secretion Patterns in Children.

The objective of this study was to analyze circadian patterns of urinary 6-sulphatoxymelatonin (aMT6s) excretion in children with primary sleep disorders in comparison with healthy controls. A total of 124 control children and 124 patients (aged 4-14 years) diagnosed with diverse primary sleep disorders were recruited. aMT6s concentrations were measured in diurnal and nocturnal urine, as well as in 24-hour urine. aMT6s levels were significantly higher and showed significantly more evident circadian variations in the control group ( P < .001). Four different melatonin (aMT) production and excretion patterns were distinguished in the group with sleep disorders: (1) standard aMT production pattern, (2) low aMT production pattern, (3) aMT production pattern with absence of circadian variation, and (4) aMT hyperproduction pattern. This study highlights the importance of analyzing specific alterations of aMT secretion in each sleep disorder and provides evidences to explain why not all children with sleep disturbances do respond to aMT treatment.

Indoor cold exposure and nocturia: a cross-sectional analysis of the HEIJO-KYO study.

To investigate the association between indoor cold exposure and the prevalence of nocturia in an elderly population. The temperature in the living rooms and bedrooms of 1 065 home-dwelling elderly volunteers (aged ≥60 years) was measured for 48 h. Nocturia (≥2 voids per night) and nocturnal urine production were determined using a urination diary and nocturnal urine collection, respectively. The mean ± sd age of participants was 71.9 ± 7.1 years, and the prevalence of nocturia was 30.8%. A 1 °C decrease in daytime indoor temperature was associated with a higher odds ratio (OR) for nocturia (1.075, 95% confidence interval [CI] 1.026-1.126; P = 0.002), independently of outdoor temperature and other potential confounders such as basic characteristics (age, gender, body mass index, alcohol intake, smoking), comorbidities (diabetes, renal dysfunction), medications (calcium channel blocker, diuretics, sleeping pills), socio-economic status (education, household income), night-time dipping of ambulatory blood pressure, daytime physical activity, objectively measured sleep efficiency, and urinary 6-sulphatoxymelatonin excretion. The association remained significant after adjustment for nocturnal urine production rate (OR 1.095 [95% CI 1.042-1.150]; P < 0.001). Indoor cold exposure during the daytime was independently associated with nocturia among elderly participants. The explanation for this association may be cold-induced detrusor overactivity. The prevalence of nocturia could be reduced by modification of the indoor thermal environment.

Preterm infants produce less melatonin than term infants at 9 and 12 months of age: A randomized controlled trial

Melatonin production is known to be delayed in preterm infants up to 6 months of age. We aimed to test the profile of melatonin production in these infants at 9–12 months of age. Twenty-three term and 23 preterm infants (gestational age: 29–34 weeks) were randomly assigned. We tested nocturnal urinary melatonin excretion, within a repeated measures design, both at 9 and 12 months of age. Nocturnal urine was extracted from diapers and urinary melatonin derivate (6-sulphatoxymelatonin) excretion was analyzed by enzyme-linked immunosorbent assay assays. Preterm infants had significantly lower urinary melatonin excretion both at 9 and 12 months of age as compared to term infants. At 9 months: 8502 ± 6215 vs. 12,735 ± 10,284 ng, and at 12 months: 8623 ± 5095 vs. 14,985 ± 10,890 ng respectively, (F [1,42]=4.276), (P

The influence of indoor lighting with low blue light dose on urine 6-sulphatoxymelatonin concentrations and sleep efficiency of healthy volunteers

Light, especially its blue component, is the main synchronizer of circadian rhythms. We investigated effects of suppressed blue band of the spectrum on melatonin production and sleep efficiency in 18 young volunteers. During control days, participants lived in their home environment, and next five days in a room lit only by daylight with windows equipped with a filter blocking the blue band of the light spectrum. Light intensity, circadian stimulus and light irradiance were monitored. No significant changes in the daily pattern and total urinary 6-sulphatoxymelatonin excretion were found between control and experimental conditions. Parameters of sleep efficiency measured by wrist actigraphy were not worsened, but neutral chronotypes exhibited shortened sleep duration under light-modified conditions. We conclude that young healthy people can compensate for negative effects of transitory-worsened lighting conditions on their daily rhythms, but chronotypes and other personal characteristics may modify biological responses and should be considered.

Dual control of seasonal time keeping in male and female juvenile European hamsters

In contrast to photoperiodic rodent species, adult circannual European hamsters (Cricetus cricetus) do not rely on melatonin as transducer of the photoperiodic message. Instead, seasonal entrainment involves a special circadian organisation which characterizes a photoperiod-sensitive phase. When days shorten a precise activity pattern (“summer pattern”) switches to a weak or arrhythmic “winter pattern”. At the very same day gonadal regression is initiated and the circannual clock is reset. In contrast to this difference in photoperiodic time measurement, the broad time span in which offspring are born and the birth-season dependent timing of puberty is similar to photoperiodic rodents. We investigated how juvenile European hamsters measure photoperiod to situate themselves at the proper position in the annual cycle. Activity and 6-sulphatoxymelatonin (aMT6s) excretion were recorded in pups of five litters born at different seasons. Pups of all litters showed an activity pattern identical with the adults' summer pattern until postnatal day 78, suggesting that the pathway known to reset the circannual clock in adults is functional. The synchronous start of reproduction in yearlings supports this. However, since puberty and gonadal regression occurred before the switch in the activity pattern, the timing of reproduction in the birth year must be controlled by other means. As in photoperiodic species melatonin might be involved, since the aMT6s excretion showed daily and seasonal rhythms from early life on.

Day and nighttime excretion of 6-sulphatoxymelatonin in adolescents and young adults with autistic disorder

Several reports indicate that nocturnal production of melatonin is reduced in autism. Our objective was to examine whether melatonin production is decreased during the whole 24-h cycle, whether the melatonin circadian rhythm is inverted, and whether the reduction in melatonin production is related to the severity of autistic behavioral impairments. Day and nighttime urinary excretion of 6-sulphatoxymelatonin (6-SM) was examined during a 24-h period in post-pubertal individuals with autism (N=43) and typically developing controls (N=26) matched for age, sex and pubertal stage. Low 6-SM excretion (mean ± SEM) was observed in autism, both at daytime (0.16 ± 0.03 vs. 0.36 ± 0.05 μg/h, p<0.01), nighttime (0.52 ± 0.07 vs. 1.14 ± 0.23 μg/h, p<0.05), and during 24h (8.26 ± 1.27 vs. 18.00 ± 3.43 μg/24-h collection, p<0.001). Intra-individual nighttime-daytime differences (delta values) in 6-SM excretion were smaller in individuals with autism than in controls (0.36 ± 0.07 vs. 0.79 ± 0.23 μg/h, p<0.05). Nocturnal excretion of 6-SM was negatively correlated with autism severity in the overall level of verbal language (Spearman ρ=-0.30, p<0.05), imitative social play (Spearman ρ=-0.42, p<0.05), and repetitive use of objects (Spearman ρ=-0.36, p<0.05). A deficit in melatonin production is present both at daytime and at nighttime in individuals with autism, particularly in the most severely affected individuals. These results highlight interest in potential therapeutic uses of melatonin in autistic disorder, especially in individuals with severe autistic impairment and/or low urinary 6-SM excretion.

Use of nocturnal melatonin concentration and urinary 6-sulfatoxymelatonin excretion to evaluate melatonin status in children with severe sepsis

The aim of this study was to evaluate whether nocturnal melatonin concentration (NMC) and urinary 6-sulphatoxymelatonin (aMT6s) excretion can predict melatonin status in patients with severe sepsis in the pediatric intensive care unit (PICU). Blood samples for the determination of NMC were obtained from each patient at 3 a.m. Urine samples for the determination of aMT6s excretion were obtained from each patient at 12 h intervals. We obtained 89 blood and 178 urine samples from 23 septic patients, and 52 blood and 104 urine samples from 13 non-septic patients. The NMC of septic patients in a state of septic shock was significantly higher than that of septic patients not in septic shock (p = 0.017) and those of non-septic patients (p = 0.019). In contrast, there was no significant difference for nocturnal (NaMT6s) and total aMT6s (TaMT6s) excretion between septic patients with and without septic shock and non-septic patients (p > 0.05). The NMC was significantly higher in septic patients in shock with and without hepatic dysfunction (HD) than in non-septic patients (p = 0.004 and p = 0.024, respectively). NaMT6s and TaMT6s excretion was significantly lower in septic patients with HD than in septic patient without HD (p = 0.040 and p = 0.029, for NaMT6s and TaMT6s, respectively). Our results showed that an elevated NMC may not reflect an increased MT production in septic patients in septic shock. It seems that, to evaluate the melatonin status of septic PICU patients, it is necessary to collect both serum and urine samples.

188 Preterm-Born Infants Produce Less Melatonin Than Term-Born Infants at 9 and 12 Months of Age: A Randomized Controlled Trial

Background: Melatonin production is known to be delayed in preterm-born infants up to 6 months of age. We aimed to test the profile of melatonin production in these infants at 9-12 months of age. Methods: Twenty three term-born and 23 preterm-born infants (gestational age: 29-34 weeks) were randomly assigned. We tested nocturnal urinary melatonin excretion, within a repeated measures design, both at 9 and 12 months of age. Nocturnal urine was extracted from diapers and urinary melatonin derivate (6-sulphatoxymelatonin) excretion was analyzed by ELISA assay. Results: Preterm-born infants had significantly lower urinary melatonin excretion both at 9 and 12 months of age as compared to term-born infants. At 9 months: 8502 ± 6215 vs 12735 ±10284 ng, and at 12 months: 8623 ± 5095 vs 14985 ± 10890 ng respectively, [F (1,42)=4.276], (p < 0.05). Conclusion: At 9 and 12 months of age, the delayed maturation of melatonin production is still persistent in preterm-born infants as compared to term-born mates. The impact of persistent decreased melatonin production in preterm-born infants up to 12 months of age on their psychomotor development is to be elucidated.

Antioxidant defence and inflammatory response in professional road cyclists during a 4-day competition

Cycling competitions represent an important physical overload even for well-trained individuals. In six professional cyclists, we studied the adaptive oxidative and anti-inflammatory response to a 4-day road cycling competition and its relationship with melatonin, an antioxidant and anti-inflammatory stress hormone. Blood and urine samples were collected before and after the competition. Plasma lipid peroxidation, cytokines (interleukin-1β, interleukin-6, and tumour necrosis factor-α), creatine kinase and other metabolic markers, melatonin, erythrocyte glutathione, and glutathione peroxidase and reductase activities were measured. Urinary excretion of 6-sulphatoxymelatonin was analysed. Lipid peroxidation increased after the competition, but the erythrocyte glutathione pool remained unchanged. Changes in both glutathione peroxidase and reductase activities probably account for the recycling of glutathione after exercise. Interleukin-6 (216%) and tumour necrosis factor-α (159%) but not interleukin-1β increased after exercise. A parallel increase in plasma melatonin concentrations was detected, whereas metabolic markers, including creatine kinase, showed minor modifications. Thus, professional cyclists display an adaptative response to the physical overloads in the competitions for which they are trained. Consequently, they seem to be able to regulate efficiently the intracellular oxidative stress, and prevent an exaggerated pro-inflammatory cytokines induction. A modulator role of melatonin in these adaptive responses is also supported.

The relationship between urinary melatonin metabolite excretion and posttraumatic symptoms following traumatic injury

Background Associations between 24-hour urinary 6-sulphatoxy melatonin excretion and symptoms of posttraumatic stress disorder were assessed 2 days, 1 month and 6 months after traumatic injury requiring hospitalisation. Methods Forty-eight participants were recruited following an admission to hospital for an acute traumatic injury. They completed assessments 48 h after the accident, 1 month and 6 months later. A 24-hour urine collection was initiated the morning before questionnaires were administered. PTSD symptoms and caseness was determined using the Impact of Event Scale (IES-R) and the Clinician Administered PTSD Scale respectively. Urinary 6-sulphatoxy melatonin was assayed by radioimmunoassay. Results Mean age of participants was 34 years (SD = 12.72) and 75% were males. Ten (27%) participants met the criteria for PTSD 1 month post trauma and 6 (21%) met the criteria for PTSD at 6 months. Four of the six (67%) participants with PTSD at 6 months were also positive for major depression. Significant negative correlations were found between 6-sulphatoxy melatonin excretion at day 2 and all subscales and total score of the IES-R at the six month assessment. Controlling for depression, every one unit decrease in 6-sulphatoxy melatonin excretion was associated with a 13% increase in PTSD risk at six months (OR = 1.13, 95% CI 1.00–1.27). However, this association was lost when self-reported pain, gender and employment was added to the model (OR = 1.11, 0.93–1.32). Conclusion This study provides preliminary data suggesting disrupted melatonin levels in the first 48 h following trauma may place individuals at increased risk of PTSD.

Urinary Excretion of 5-Hydroxyindoleacetic Acid, Serotonin and 6-Sulphatoxymelatonin in Normoserotonemic and Hyperserotonemic Autistic Individuals

Objective: A substantial proportion of individuals with autism have elevated levels of platelet serotonin (5-HT). We examined whether platelet hyperserotonemia is associated with increased gut 5-HT synthesis, altered 5-HT catabolism or altered melatonin production. Methods: Urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA) and 5-HT was compared in 10 normoserotonemic and 10 hyperserotonemic age-matched autistic individuals. The relationship of urinary 6-sulfatoxymelatonin (6-SM) excretion to platelet 5-HT, and to urinary 5-HT and 5-HIAA excretion, was also examined. Results: In the hyperserotonemic group, significant increases at trend level in urinary excretion of 5-HIAA (p = 0.061) and 5-HT (p = 0.071) and a significant decrease for 6-SM were found (p = 0.027). The urinary 5-HIAA:5-HT ratio was similar in the normo- versus the hyperserotonemic groups. Conclusions: The catabolism of 5-HT does not differ in the groups, but greater exposure of the platelet to 5-HT cannot be ruled out as a cause of the platelet hyperserotonemia of autism. Although only trend level significant, the data point to a need for larger studies to examine more thoroughly the relationships between platelet hyperserotonemia, gut 5-HT synthesis and melatonin production.

Daily Profiles of Salivary and Urinary Melatonin and Steroids in Healthy Prepubertal Boys

The aim of this study was to assess the circadian hormonal profile of two circadian markers, melatonin and cortisol, as well as other steroids in prepubertal boys (Tanner stage I). Nine volunteer healthy prepubertal boys aged 10.8 +/- 0.11 years participated in this study. Concentrations of daily salivary and urinary hormones were quantified around 24-hours, every 3 hours, in daytime samples (collected between 07.00 h +/- 30 min and 21.00 h +/- 30 min) and night-time samples (collected between 21.00 h +/- 30 min and 07.00 h +/- 30 min). Significant differences (p < 0.01) were found between day- and nighttime secretion of salivary melatonin and urinary 6-sulphatoxymelatonin, whereas no significant differences were found between day- and nighttime secretion of salivary and urinary cortisol nor between day- and nighttime secretion of 17-hydroxycorticosteroids (17-OHCS). The circadian profiles of salivary melatonin and cortisol showed large amplitude with a peak occurring at night (approximately 03.00 h) for melatonin and in the early morning (between 06.00 and 09.00 h) for cortisol. The curve patterns of the urinary 6-sulphatoxymelatonin and steroids (free cortisol and 17-OHCS) were coherent with data on saliva. The pattern of salivary androstenedione and testosterone were undetectable due to the very low concentrations of these steroids in the saliva of the prepubertal children. A strong significant positive correlation was observed between the daily salivary melatonin levels and the daily urinary 6-sulphatoxymelatonin excretion (R = 0.968, p < 0.001), and between free urinary cortisol and urinary 17-OHCS (R = 0.733, p = 0.025). The salivary and urinary hormones studied were independent of body mass index. This study shows the relevance of salivary cortisol and melatonin, although lower than in plasma, in testing adrenal and pineal function as markers of circadian rhythms. The data are of interest for the diagnosis and treatment of chronobiological disorders in prepubertal children.

Influence of sympathectomy in humans on the rhythmicity of 6-sulphatoxymelatonin urinary excretion

The amount of 6-sulphatoxymelatonin, the chief metabolite of melatonin, in the urine was measured in nine patients, who were subjected to bilateral sympathectomy at the second thoracic ganglionic level for treatment of hyperhidrosis of the palms. All patients showed before surgery a normal 6-sulphatoxymelatonin excretion with a peak in the excretion during the night time. After the sympathectomy, the high night time excretion was clearly abolished in five patients but remained high in four patients. This indicates that the segmental locations of the preganglionic sympathetic perikarya in the spinal cord, stimulating the melatonin secretion in the pineal gland in humans, vary between individuals. An increase in daytime melatonin excretion was observed in the patients responding to the sympathectomy with an abolished 6-sulphatoxymelatonin rhythm. This increase could indicate that the final sympathetic neurons innervating the pineal gland might have a both stimulatory and inhibitory function.

Circadian phase-shifting effects of a laboratory environment: a clinical trial with bright and dim light.

BackgroundOur aims were to examine the influence of different bright light schedules on mood, sleep, and circadian organization in older adults (n = 60, ages 60–79 years) with insomnia and/or depression, contrasting with responses of young, healthy controls (n = 30, ages 20–40 years).MethodsVolunteers were assessed for one week in their home environments. Urine was collected over two 24-hour periods to establish baseline acrophase of 6-sulphatoxymelatonin (aMT6s) excretion. Immediately following home recording, volunteers spent five nights and four days in the laboratory. Sleep periods were fixed at eight hours in darkness, consistent with the volunteers' usual sleep periods. Volunteers were randomly assigned to one of three light treatments (four hours per day) within the wake period: (A) two hours of 3,000 lux at 1–3 hours and 13–15 hours after arising; (B) four hours of 3,000 lux at 6–10 hours after arising; (C) four hours of dim placebo light at 6–10 hours after arising. Lighting was 50 lux during the remainder of wakefulness. The resulting aMT6s acrophase was determined during the final 30 hours in the laboratory.ResultsNeither mood nor total melatonin excretion differed significantly by treatment. For the three light treatments, significant and similar phase-response plots were found, indicating that the shift in aMT6s acrophase was dependent upon the circadian time of treatment. The changes in circadian timing were not significantly correlated to changes in sleep or mood.ConclusionThe trial failed to demonstrate photoperiodic effects. The results suggest that even low levels of illumination and/or fixed timing of behavior had significant phase-shifting effects.

Seasonal variations in circadian rhythms coincide with a phase of sensitivity to short photoperiods in the European hamster

European hamsters (Cricetus cricetus) show pronounced seasonal changes in their physiology and behavior. The present study provides a detailed analysis of the temporal relationship between seasonal cycles of reproduction and body mass and seasonal changes of two circadian parameters, i.e., locomotor activity and 6-sulphatoxymelatonin (aMT6s) excretion, in individual animals kept under natural light conditions. Our results demonstrate a characteristic pattern of locomotor activity and aMT6s excretion observed around the summer solstice, i.e., from mid-May to mid-July. During this time, locomotor activity was characterized by a high level of activity and an early activity onset, while the nightly elevation of melatonin was reduced to baseline levels. These seasonal changes in aMT6s excretion and locomotor activity were only loosely related to changes in the reproductive status of the animals, but correlated well with a period of the annual cycle during which the animals were sensitive to short days. They may therefore reflect a specific state of the circadian pacemaker system within the SCN and can thus be a valuable tool to further characterize molecular and physiological mechanisms of photoperiodic time measurements in European hamsters.

Nocturnal excretion of 6-sulphatoxymelatonin in children and adolescents with autistic disorder

Many studies in autistic disorder report sleep problems and altered circadian rhythms, suggesting abnormalities in melatonin physiology. Additionally, melatonin, a pineal gland hormone produced from serotonin, is of special interest in autistic disorder given reported alterations in central and peripheral serotonin neurobiology. Nocturnal urinary excretion of 6-sulphatoxymelatonin was measured by radioimmunoassay in groups of children and adolescents with autistic disorder (n = 49) and normal control individuals (n = 88) matched on age, sex, and Tanner stage of puberty. Nocturnal 6-sulphatoxymelatonin excretion rate was significantly and substantially lower in patients with autism than in normal controls (mean +/- SEM, .75 +/- .11 vs. 1.80 +/- .17 microg/hr, p =.0001), and was significantly negatively correlated with severity of autistic impairments in verbal communication and play (p < .05). These findings indicate clearly that nocturnal production of melatonin is reduced in autism. Further research is warranted in order to understand the mechanisms underlying the lower melatonin production, to assess the impact of altered melatonin on the pathophysiology and behavioral expression of autistic disorder, and to determine the utility of melatonin administration in individuals with autism.

Efficacy of Enhanced Evening Light for Advanced Sleep Phase Syndrome

This study tested whether a newly designed enhanced evening light therapy was well tolerated and effective in relieving symptoms of Advanced Sleep Phase Syndrome (ASPS). Participants with self-reported ASPS symptoms were 47 older adults (21 men and 26 women, age 60-86). After baseline, participants underwent 28 consecutive days of either dim or enhanced intensity light treatment for 2-3 hr in the evening. Enhanced evening light (~265 lux) exposure was no more effective than a placebo dim light (~2 lux) at alleviating advanced sleep phase as measured by actigraphically recorded sleep and urinary 6-sulphatoxymelatonin (aMT6s) excretion patterns. Participants receiving the enhanced light reported subjective benefit and a significant delay in sleep onset as compared to the placebo. Although compliance was good and the new enhanced evening light therapy design was well tolerated, the benefits were statistically equivocal.

Melatonin and jet lag syndrome: experimental model and clinical implications.

What is the effect of melatonin on jet lag syndrome? Jet lag desynchronizes the internal sleep-wakefulness cycle with the environmental light/dark cycle. Advance (but not delay) of light onset is known to abolish pineal N-acetyltransferase activity and urine excretion of 6-sulphatoxymelatonin. Measurements of pineal serotonin, the substrate of melatonin biosynthesis; N-acetylserotonin (NAS), the immediate melatonin precursor; and melatonin (high-performance liquid chromatography-fluorimetric method) in the animal (rat) model of jet lag revealed that prolonged delay of dark-phase onset disrupted the rhytms in comparable ways as the advance of light-phase onset. Advance of dark phase onset resulted in less severe disturbances of rhythms as compared with the advance of light phase onset. Melatonin, but not NAS, injections at the beginning of a new dark period accelerated recovery of NAS and melatonin, but not serotonin, rhythms. Spontaneously hypertensive rats were more sensitive to advance of light onset and less responsive to melatonin injections than normotensive rats. NAS and methylene blue, an inhibitor of monoamine oxidase A, attenuated light-induced disruption of NAS but not melatonin rhythms. We draw the following conclusions from our data: the beginning of the dark period may be preferable to the beginning of light period as the arrival time on eastward flights; the efficacy of melatonin in alleviating jet lag may be enhanced by administering it before, during and after rapid transition through time zones; and hypertension may exaggerate jet lag syndrome.

One week of exposure to 50 Hz, vertical magnetic field does not reduce urinary 6-sulphatoxymelatonin excretion of male wistar rats.

The effect of exposure to 100 or 50 microT, 50 Hz, vertical magnetic field on the excretion of 6-sulphatoxymelatonin (6SM) in the nocturnal urine of rats was studied. Twelve male Wistar rats were kept under 12:12 hr light:dark conditions. The nocturnal urine of animals was collected in metabolic cages over 4 consecutive weeks. The concentration of 6SM in the rat urine was measured by 125I radioimmunoassay and normalized to creatinine concentration. After the first week of urine collection, 6 rats were exposed to 100 microT or 50 microT flux density magnetic fields (MF) for 8 hr daily for 1 week. It was found that the excretion of the primary metabolite of melatonin in the urine, 6SM, did not show statistically significant changes during and after magnetic field exposure.