Decreased Melatonin Production Research Articles

Influence of melatonin on the development of obesity

In recent years, increasing attention of researchers has been paid to the role of melatonin in the regulation of body weight. When analyzing literature data, the problem of the mechanism of action of melatonin on the body and its use in the correction of metabolic disorders is considered. Disruption of circadian rhythms caused by the use of artificial light at night leads to decreased melatonin secretion. This helps increase appetite and reduce energy costs. In addition, melatonin plays a major role in modulating the secretion of adipokines by influencing lipid metabolism. Decreased melatonin production causes insulin resistance and metabolic circadian disorganization, leading to obesity. Assessing the role of melatonin in the development of obesity and its accompanying pathologies is a promising area of scientific research in the field of diagnosis, prevention and treatment of endocrine and cardiovascular pathologies.

A Narrative Review of the Carcinogenic Effect of Night Shift and the Potential Protective Role of Melatonin.

Since the IARC (International Agency for Research on Cancer) announcement in 2007 indicating the possibility of night-shift work carrying carcinogenesis risk, multiple studies on a global level have been conducted to investigate the correlation between night-shift work and cancer development. Circadian rhythm disruption and decreased melatonin production have been postulated as potential contributing factors. There is also growing evidence that night-shift workers tend to adopt unhealthier lifestyles which contribute to poorer health and increase the risk of developing diseases such as cancer. No experimental study has been specifically dedicated to testing specific methods that could decrease cancer risk in night-shift workers. While there are a few studies that investigate melatonin's concurrent use with chemotherapy in cancer patients, there is yet to be seen for studies that investigate melatonin specifically as a cancer prevention method. This narrative review aims to examine current evidence of healthcare night-shift work's risk in cancer incidence, potential pathogenesis, and its significance in clinical practice.

Effect of iron on rat serum melatonin levels under different light/dark cycle patterns

Exposure to constant light or darkness for long periods has diverse effects on circadian physiology. Iron (Fe) overloading promotes oxidative stress and causes alterations in cellular structure and function in animals and humans. The aim of this study is to evaluate the interactions among serum melatonin (ML), photoperiod manipulation, and Fe overloading in rats. The results showed that constant darkness exposure for 15 days significantly increased serum ML levels (up to 22%) while the constant light exposure failed to reduce the serum ML level compared to the normal light/dark cycle treated rats. The lost serum ML level usually from the pineal gland under the long term of constant light exposure may be compensated by ML generated by other organs which adapted to the situation. Also, Fe overloading decreased ML production due to this molecule being consumed to scavenge the free radicals induced by the Fe overloading. In addition, we observed interactions among constant light or darkness exposure, Fe overloading and serum ML level. Overall, our results support the hypothesis of ML as scavenging molecule; it may be an effective therapeutic tool in iron-induced oxidative stress.

Cancro da Mama associado ao Trabalho

Introduction/framework/objectives There are work circumstances that can increase the oncological risk and Breast Cancer is no exception to this situation. However, knowledge on this subject is not particularly abundant among workers and/or Occupational Health and Safety teams professionals. This review was intended to mitigate this issue. Methodology This is a Bibliographic Review, initiated through a search carried out in January 2022 in the databases: “CINALH plus with full text, Medline with full text, Database of Abstracts of Reviews of Effects, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, Cochrane Methodology Register, Nursing and Allied Health Collection: comprehensive, MedicLatina and RCAAP”. Content Night shifts are chronodisruptive, probably due to decreased melatonin production. Other researchers add that night work and/or nocturnal exposure to light disturbs the circadian rhythm and hormone secretion (with emphasis also on prolactin, glucocorticoids, adrenocorticotropic hormone, corticoliberin and serotonin). However, there is no consensus that night shifts imply lower levels of prolactin secretion and that this is associated with Breast Cancer. Some studies may be biased due to having studied night shifts versus exposure to light during these shifts (the latter being the situation that presents evidence of moderately increasing the risk of this Cancer). In addition, more recent investigations consider more possibly biasing variables. It is believed that nocturnal exposure to light implies changes in the production of melatonin and vitamin D. However, others consider that these data are not supported by robust scientific evidence or free of controversy, even due to the difference between the different types of night shifts. In 2007, the IARC published some data on this possible relationship- namely that night shifts were probably carcinogenic to humans (group 2A), and/or that there was evidence of an association between oncological processes and night shifts, probably for Breast Cancer in particular, based on sufficient evidence in animals and limited evidence in humans. Discussion and Conclusions Most of the bibliography on the subject emphasizes night shifts and/or exposure to light during them as a work etiology, although without full consensus between causality and/or pathophysiology. Pesticides, solvents and products included in kitchen fumes (polycyclic aromatic hydrocarbons), aldehydes and polycyclic aromatic amines) are also mentioned. It would be an asset for some Occupational Health and Safety professionals, with adequate logistical capacity, to investigate the area, subsequently disclosing the conclusions covered. Keywords: breast cancer, occupational health, occupational medicine and occupational safety.

Astrocyte Dysregulation and Calcium Ion Imbalance May Link the Development of Osteoporosis and Alzheimer's Disease.

The typical symptoms of patients with Alzheimer's disease (AD) are amyloid-β (Aβ) plaques and tau hyperphosphorylation. However, recent studies show that these symptoms are not the cause of the disease but are generated after the pathogenesis. Compared with other types of dementia, AD has the obvious features of pineal gland calcification and decreased melatonin production. The pineal gland is mainly composed of pinealocytes that release melatonin and astrocytes. Astrocytes function to maintain a balanced concentration of calcium ions, provide nerve cell nutrients, and migrate nutrients in vivo. Calcium ions are among the most important neurotransmitters. Once triggered, a calcium wave can be formed between astrocytes to activate other astrocytes to transmit information. Most calcium is stored in the skeleton. Bone tissue is composed mainly of osteocytes, osteoblasts, and osteoclasts. Of these, osteocyte is a kind of astrocyte which regulates the activity of osteoclasts and osteoblasts. The pineal gland is composed mainly of astrocytes; osteocytes are also a kind of astrocyte. Therefore, we conclude that when astrocytes are gradually disabled, calcium may be lost from the bones, prompting osteoporosis. The calcium ions then released into the blood may accumulate and cause ectopic calcification in the pineal gland, which promotes the occurrence of AD. Finally, this study used aspects of drugs and hormones (bone and calcium metabolism hormones and melatonin) to infer the hypothesis, which proposes that astrocyte dysregulation promotes the long-term imbalance of calcium ions in vivo and leads to osteoporosis and AD.

Depression in the context of shift work schedule: a systematic review

The circadian rhythm deregulation can result in an alteration in the sleep-wake cycle, causing sleep disturbances and promoting mental and mood disorders development. Conditions that can disrupt this rhythm, such as shift work schedule (SWS) can unbalance neural functioning and favors those professional classes may have a greater tendency to develop depression. In this context, this study aims to carry out a systematic review to understand the relationship between SWS and the risk of depression, so 1,001 articles were selected for eligibility analysis for the study. After an evaluation sequence starting from the title, abstract and complete work, 31 works that responded to the proposed theme were included. Depression was found to be higher in JTT workers such as nurses, company employees, physicians, residents, and firefighters compared to other professionals. The main explanations involve decreased melatonin production, stressful conditions linked to professional activity and lifestyle habits. Thus, it is important to delineate new therapeutic forms, control, prevention, and health promotion for these workers, since the SWS is strongly associated with depression.

Prolonging photoperiod promotes testosterone synthesis of Leydig cells by directly targeting local melatonin system in rooster testes†.

The study investigated the effects of prolonging photoperiod on the synthesis of testosterone and melatonin in roosters, and the effect of melatonin on testosterone synthesis in rooster Leydig cells as well as its molecular mechanisms. We randomly divided one hundred and twenty 20-week-old roosters into three groups and provided 6, 12.5 and 16h light, respectively. The results showed that prolonging photoperiod promoted testosterone synthesis, decreased melatonin production, and inhibited the expression of melatonin membrane receptors MEL1A, MEL1B, MEL1C, and aralkylamine N-acetyltransferase (AANAT) in rooster testes. Subsequently, rooster Leydig cells were isolated and treated with 0, 0.1, 1, 10, and 100ng/mL melatonin for 36h. The results suggested that melatonin inhibited testosterone synthesis in rooster Leydig cells, and silencing MEL1A and MEL1B relieved the inhibition of melatonin on testosterone synthesis. Additionally, melatonin reduced the intracellular cyclic adenosine monophosphate (cAMP) level and the phosphorylation level of cAMP-response element binding protein (CREB), and CREB overexpression alleviated the inhibition of melatonin on testosterone synthesis. Furthermore, pretreatment with cAMP activator forskolin or protein kinase A (PKA) activator 8-bromo-cAMP blocked the inhibition of melatonin on CREB phosphorylation and testosterone synthesis. These results indicated that prolonging photoperiod promoted testosterone synthesis associated with the decrease in melatonin production and membrane receptors and biosynthetic enzyme of melatonin in rooster testes, and melatonin inhibited testosterone synthesis of rooster Leydig cells by inhibiting the cAMP/PKA/CREB pathway via MEL1A and MEL1B. This may be evidence that prolonging photoperiod could promote testosterone synthesis through the inhibition of the local melatonin pathway in rooster testes.

Mitochondria and the Gut as crucial hubs for the interactions of melatonin with sirtuins, inflammation, butyrate, tryptophan metabolites, and alpha 7 nicotinic receptor across a host of medical conditions.

Two important hubs have emerged as cutting edge areas of research across a diverse array of medical conditions, the gut microbiome and mitochondria. This article highlights the role of melatonin in modulating changes in both the gut and mitochondria. The gut microbiome, especially via its production of the small chain fatty acid, butyate, can have a significant impact on immune inflammatory processes. Lower levels of butyrate producing bacteria can increase gut permeability, thereby increasing immune-inflammatory activity. Butyrate may also modulate immune and other cells via the regulation of the content of exosomes from intestinal epithelial cells. Butyrate also induces N-acetylserotonin and melatonin synthesis in the gut, suggesting that some of the effects of butyrate may be mediated via its induction of the melatonergic pathway. The induction of melatonin by butyrate may feed back on the microbiome via melatonin increasing gut bacteria swarming, as well as melatonin optimizing gut barrier and mitochondria functioning. As butyrate readily crosses into the circulation it is likely that the immune- and glia-dampening effects of butyrate also involve the induction of melatonin in these reactive cells. Butyrate also positively modulates mitochondria functioning, suggesting that butyrate, both directly and via melatonin, will have significant impacts on gut, immune, glia and other cells, via mitochondria regulation. Other factors that act to regulate melatonin, including dietary factors and stress, will therefore act to modulate many of butyrate's effects. The regulation of melatonin at these two important hubs has significant treatment and classification implications across a wide array of medical conditions. Overall, gut dysbiosis has a significant impact on central and systemic homeostasis, via decreased butyrate and melatonin driving suboptimal mitochondria functioning. This has implications for the pathoetiology and pathophysiology of a host of medical conditions associated with gut dysbiosis and decreased melatonin production.

Premature leaf senescence 3, encoding a methyltransferase, is required for melatonin biosynthesis in rice

Premature leaf senescence in rice is one of the most common factors affecting the plant's development and yield. Although methyltransferases are involved in diverse biological functions, their roles in rice leaf senescence have not been previously reported. In this study, we identified the premature leaf senescence 3 (pls3) mutant in rice, which led to early leaf senescence and early heading date. Further investigations revealed that premature leaf senescence was triggered by the accumulation of reactive oxygen species. Using physiological analysis, we found that chlorophyll content was reduced in the pls3 mutant leaves, while hydrogen peroxide (H2 O2 ) and malondialdehyde levels were elevated. Consistent with these findings, the pls3 mutant exhibited hypersensitivity to exogenous hydrogen peroxide. The expression of other senescence-associated genes such as Osh36 and RCCR1 was increased in the pls3 mutant. Positional cloning indicated the pls3 phenotype was the result of a mutation in OsMTS1, which encodes an O-methyltransferase in the melatonin biosynthetic pathway. Functional complementation of OsMTS1 in pls3 completely restored the wild-type phenotype. We found leaf melatonin content to be dramatically reduced in pls3, and that exogenous application of melatonin recovered the pls3 mutant's leaf senescence phenotype to levels comparable to that of wild-type rice. Moreover, overexpression of OsMTS1 in the wild-type plant increased the grain yield by 15.9%. Our results demonstrate that disruption of OsMTS1, which codes for a methyltransferase, can trigger leaf senescence as a result of decreased melatonin production.

Effect of exposure to extremely low frequency magnetic fields on melatonin levels in calves is seasonally dependent.

The question of health effects of extremely low frequency (50/60 Hz) magnetic fields (ELFMF) has been widely discussed, but the mechanisms of interaction of these fields with biological systems for intensities relevant to human and animal exposure are still under question. The melatonin (MLT) hypothesis suggests that exposure to ELFMF might decrease MLT production thereby promoting cancerogenesis. So far, most studies of MLT secretion under exposure to ELFMF reported negative or inconsistent results. Here, we measured salivary MLT in 1–2 months old cattle calves exposed to 50 Hz-MF in the hundreds of nT-range. We found an inhibitory effect of the ELFMF upon MLT secretion in winter (in accordance with the MLT hypothesis). In contrast, in summer, MLT concentration was increased by ELFMF exposure (contrary to the MLT hypothesis). The inhibitory effect in winter was much stronger than the positive effect in summer. We hypothesize that this season-dependent effect upon MLT synthesis might by mediated by an effect of ELFMF upon the serotonin metabolism and conclude that future tests of ELFMF effects should also measure serotonin levels and consider association with the seasonal effects (photoperiod or temperature) during the exposure.

Association between ELF and RF electromagnetic field and Leukemia

Extremely low frequency (ELF) electromagnetic field (ELF-EMFs) are widely employed in electrical appliances and different equipment such as television sets, ELF-EMFs can affect biological systems by increasing production ROS. The altered balance between ROS generation and elimination plays a critical role in a variety of pathologic conditions. ROS levels have been observed in several hematopoietic malignancies including acute and chronic myeloid leukemia. ELF-EMFs exposure significantly decreased Nitric oxide synthase (iNOS) protein expression Lower levels of NO have been demonstrated to exert a protective function in leukemic and melanoma cells and to inhibit effector caspases by S-nitrosylation. Also ELF-EMFs can decrease melatonin production by effects on N-acetyltransferase. Melatonin is an antioxidant, effective in protecting nuclear DNA. Transmitters emitting radio frequency electromagnetic fields (RF-EMFs) are usually not located in populated areas but some epidemiology studies showed association distance transmitters from residential area and leukemia.

Progressive decrease of melatonin production over consecutive days of simulated night work

Decreased melatonin production, due to nighttime exposure to light, has been proposed as one of the physiological mechanisms increasing cancer risk in night workers. However, few studies measured melatonin production in night workers, and most of these studies did not measure melatonin over 24 h. One study compared total melatonin production between day and night shifts in rotating night workers and did not find significant differences. However, without baseline measures, it was not possible to exclude that melatonin production was reduced during both day and night work. Here, we used data collected in a simulation study of night work to determine the effect of night work on both nighttime and 24-h melatonin production, during three consecutive days of simulated night work. Thirty-eight healthy subjects (15 men, 23 women; 26.6 ± 4.2 years) participated in a 6-d laboratory study. Circadian phase assessments were made with salivary dim light melatonin onset (DLMO) on the first and last days. Simulated day work (09:00–17:00 h) occurred on the second day, followed by three consecutive days of simulated night work (00:00–08:00 h). Light intensity at eye level was set at 50 lux during both simulated day and night work. The subjects were divided into three matched groups exposed to specific daytime light profiles that produced various degrees of circadian phase delays and phase advances. Melatonin production was estimated with the excretion of urinary 6-sulfatoxymelatonin (aMT6s). For the entire protocol, urine was collected every 2 h, except for the sleep episodes when the interval was 8 h. The aMT6s concentration in each sample was multiplied by the urine volume and then added to obtain total aMT6s excretion during nighttime (00:00–08:00 h) and during each 24-h day (00:00–00:00 h). The results showed that melatonin production progressively decreased over consecutive days of simulated night work, both during nighttime and over the 24 h. This decrease was larger in women using oral contraceptives. There was no difference between the three groups, and the magnitude of the decrease in melatonin production for nighttime and for the 24 h was not associated with the magnitude of the absolute circadian phase shift. As light intensity was relatively low and because the decrease in melatonin production was progressive, direct suppression by nighttime light exposure was probably not a significant factor. However, according to previous experimental observations, the decrease in melatonin production most likely reflects the circadian disruption associated with the process of re-entrainment. It remains to be determined whether reduced melatonin production can be harmful by itself, but long-term and repeated circadian disruption most probably is.

A Working Threshold for Acute Nocturnal Melatonin Suppression from “White” Light Sources used in Architectural Applications

Retinal light exposures can decrease melatonin production at night. Since nocturnal melatonin suppression by light has been implicated as an endocrine disruptor and linked to certain diseases, such as diabetes, obesity and cancer, it is important to be able to estimate a threshold light level needed to reliably suppress melatonin. The present study was designed to develop a working threshold for melatonin suppression from “white” light that might be experienced by people in their living environments. Twenty-eight subjects participated in two studies. In addition to dark, control nights, subjects were exposed to 8, 22, and 60 lux at the cornea (study 1, n=14) and to 60, 200, and 720 lux (study 2, n=14) of a “warm white” light source (correlated color temperature of 2670 K). These corneal illuminance levels translate to modeled melatonin suppression levels of 1%, 2%, 6%, 19%, and 42%. In both studies, participants came to the laboratory for four nights, separated by one week. One blood sample was drawn in dim light at midnight and another blood sample was drawn after 60-minute exposure to each light condition (including dark). Using an orthodox statistical criterion for a Type I error of α?< 0.05, only the 200 lux and the 720 lux exposures produced significant suppression levels (19% and 37%, respectively). Based upon a criterion modeled suppression level of 5% for a “cool white” light (6500 K), a corneal light exposure of 30 lux for 30 minutes from “white” light sources used in most architectural lighting applications is proposed as a conservative hypothesized working threshold for nocturnal melatonin suppression.

The effects of extremely low-frequency magnetic fields on melatonin and cortisol, two marker rhythms of the circadian system

In the past 30 years the concern that daily exposure to extremely low-frequency magnetic fields (ELF-EMF) (1 to 300 Hz) might be harmful to human health (cancer, neurobehavioral disturbances, etc) has been the object of debate, and has become a public health concern. This has resulted in the classification of ELF-EMF into category 2B, ie, agents that are "possibly carcinogenic to humans" by the International Agency for Research on Cancer. Since melatonin, a neurohormone secreted by the pineal gland, has been shown to possess oncostatic properties, a "melatonin hypothesis" has been raised, stating that exposure to EMF might decrease melatonin production and therefore might promote the development of breast cancer in humans. Data from the literature reviewed here are contradictory. In addition, we have demonstrated a lack of effect of ELF-EMF on melatonin secretion in humans exposed to EMF (up to 20 years' exposure) which rebuts the melatonin hypothesis. Currently, the debate concerns the effects of ELF-EMF on the risk of childhood leukemia in children chronically exposed to more than 0.4 μT. Further research is thus needed to obtain more definite answers regarding the potential deleterious effects of ELF-EMF.

Melatonin Production and Light Exposure of Rotating Night Workers

Decreased melatonin production, due to acute suppression of pineal melatonin secretion by light exposure during night work, has been suggested to underlie higher cancer risks associated with prolonged experience of night work. However, the association between light exposure and melatonin production has never been measured in the field. In this study, 24-h melatonin production and ambulatory light exposure were assessed during both night-shift and day/evening-shift periods in 13 full-time rotating shiftworkers. Melatonin production was estimated with the excretion of urinary 6-sulfatoxymelatonin (aMT6s), and light exposure was measured with an ambulatory photometer. There was no difference in total 24-h aMT6s excretion between the two work periods. The night-shift period was characterized by a desynchrony between melatonin and sleep-wake rhythms, as shown by higher melatonin production during work and lower melatonin production during sleep when working night shifts than when working day/evening shifts. Light exposure during night work showed no correlation with aMT6s excreted during the night of work (p > .5), or with the difference in 24-h aMT6s excretion between the two work periods (p > .1). However, light exposure during night work was negatively correlated with total 24-h aMT6s excretion over the entire night-shift period (p < .01). In conclusion, there was no evidence of direct melatonin suppression during night work in this population. However, higher levels of light exposure during night work may have decreased total melatonin production, possibly by initiating re-entrainment and causing internal desynchrony. This interpretation is consistent with the proposition that circadian disruption, of which decreased melatonin production is only one of the adverse consequences, could be the mediator between night shiftwork and cancer risks. (Author correspondence: marie.dumont@umontreal.ca)

Melatonin in autism spectrum disorders: a systematic review and meta‐analysis

The aim of this study was to investigate melatonin-related findings in autism spectrum disorders (ASD), including autistic disorder, Asperger syndrome, Rett syndrome, and pervasive developmental disorders, not otherwise specified. Comprehensive searches were conducted in the PubMed, Google Scholar, CINAHL, EMBASE, Scopus, and ERIC databases from their inception to October 2010. Two reviewers independently assessed 35 studies that met the inclusion criteria. Of these, meta-analysis was performed on five randomized double-blind, placebo-controlled studies, and the quality of these trials was assessed using the Downs and Black checklist. Nine studies measured melatonin or melatonin metabolites in ASD and all reported at least one abnormality, including an abnormal melatonin circadian rhythm in four studies, below average physiological levels of melatonin and/or melatonin derivates in seven studies, and a positive correlation between these levels and autistic behaviors in four studies. Five studies reported gene abnormalities that could contribute to decreased melatonin production or adversely affect melatonin receptor function in a small percentage of children with ASD. Six studies reported improved daytime behavior with melatonin use. Eighteen studies on melatonin treatment in ASD were identified; these studies reported improvements in sleep duration, sleep onset latency, and night-time awakenings. Five of these studies were randomized double-blind, placebo-controlled crossover studies; two of the studies contained blended samples of children with ASD and other developmental disorders, but only data for children with ASD were used in the meta-analysis. The meta-analysis found significant improvements with large effect sizes in sleep duration (73 min compared with baseline, Hedge's g 1.97 [95% confidence interval {CI} CI 1.10-2.84], Glass's Δ 1.54 [95% CI 0.64-2.44]; 44 min compared with placebo, Hedge's g 1.07 [95% CI 0.49-1.65], Glass's Δ 0.93 [95% CI 0.33-1.53]) and sleep onset latency (66 min compared with baseline, Hedge's g-2.42 [95% CI -1.67 to -3.17], Glass's Δ-2.18 [95% CI -1.58 to -2.76]; 39 min compared with placebo, Hedge's g-2.46 [95% CI -1.96 to -2.98], Glass's Δ-1.28 [95% CI -0.67 to -1.89]) but not in night-time awakenings. The effect size varied significantly across studies but funnel plots did not indicate publication bias. The reported side effects of melatonin were minimal to none. Some studies were affected by limitations, including small sample sizes and variability in the protocols that measured changes in sleep parameters. Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects. Additional studies of melatonin would be helpful to confirm and expand on these findings.

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.

Evaluation of melatonin levels in saliva in periodontal health and disease: A clinico-biochemical study

Background: Melatonin, a secretory product of the vertebrate pineal gland, activates several elements of the immune system that reduce tissue destruction during the inflammatory response, either directly by scavenging free radical, reactive oxygen species and reactive nitrogen species or indirectly by modulating the action of agents such as cytokines and adhesion molecules, which contribute to the advance of cell damage. Aim: The aim of this study was to evaluate melatonin levels in saliva in periodontal health and disease. Materials and Methods: This study was conducted on a total of 20 patients with healthy periodontium and 20 patients each with mild, moderate and severe periodontitis who were patients in the Department of Periodontics, Rural Dental College and Hospital, Loni. The salivary levels of melatonin were assayed using ELISA, a competitive immunoassay using a capture antibody technique. Results: We observed that the periodontitis sufferers had a significantly lower melatonin level than the healthy subjects. Conclusion: Consequently, the reduction in the saliva production with higher age and the decreased melatonin production in older adults reflected in low salivary melatonin levels predispose these individuals to an increased risk of developing oral and periodontal disease.

Prevention of melatonin suppression by nocturnal lighting: relevance to cancer

The decreased melatonin production in humans and animals caused by environmental lighting, especially short wavelength lighting (between 470 and 525 nm) has been shown to be associated with an increased risk of cancer. The purpose of this study was to investigate whether blocking light in this wavelength range under bright light may prevent the suppression of melatonin, which could help to prevent cancer. Optical filter lenses were designed, allowing selective exclusion of all wavelengths below 530 nm. Salivary melatonin levels were measured under dim light (<5 lux), bright light (800 lux) and filtered light (800 lux) at hourly intervals between 2000 and 0800 h in 11 healthy young male participants (mean age 23.5+/-1.5 years). The measurements were taken during three nonconsecutive nights over a 2-week period. The Dim Light Melatonin Onset test was used as a marker of circadian phase. Nine of the 11 participants demonstrated preserved melatonin levels in filtered light similar to their dim light secretion profile. With filtered light, the participants had a mean relative amount of melatonin of 91.2 (P>0.05 between dim light and experimental condition). Unfiltered bright light drastically suppressed melatonin production with a mean relative amount of melatonin of 25.4 (P<0.05 between dim light and experimental condition). Preventing melatonin deficiencies using lenses that block light of low wavelength from reaching the retina presents a cost-effective, practical solution to the problem of increased malignancy rates in shift workers.

Melatonin synthesis under calcium constraint in gilthead sea bream ( Sparus auratus L.)

Brain or blood plasma melatonin was analysed as a measure for pineal melatonin production in sea bream. Access to calcium was limited by diluting the seawater to 2.5‰ and removing calcium from the diet or by prolonged feeding of vitamin D-deficient diet. Interactions/relations between melatonin and calcium balance and the hypercalcemic endocrines PTHrP and calcitriol were assessed. Restricting calcium availability in both water and diet had no effect on plasma melatonin, but when calcium was low in the water or absent from food, increased and decreased plasma melatonin was observed, respectively. Fish on a vitamin D-deficient diet (D− fish) showed decreased plasma calcitriol levels and remained normocalcemic. Decreased brain melatonin was found at all sampling times (10–22 weeks) in the D− fish compared to the controls. A positive correlation between plasma Ca 2+ and plasma melatonin was found ( R 2 = 0.19; N = 41; P < 0.01) and brain melatonin was negatively correlated with plasma PTHrP ( R 2 = 0.78; N = 4; P < 0.05). The positive correlation between plasma levels of melatonin and Ca 2+ provides evidence that melatonin synthesis is influenced by plasma Ca 2+. The decreased melatonin production in the D− fish points to direct or indirect involvement of calcitriol in melatonin synthesis by the pineal organ in teleosts. The hypercalcemic factors PTHrP and calcitriol appeared to be negatively correlated with melatonin and this substantiates an involvement of melatonin in modulating the endocrine response to cope with hypocalcemia. It further points to the importance of Ca 2+ in melatonin physiology.