Melatonin (MT) and selenium (Se) application known to decrease heavy metal uptake and toxicity in plants. By mixing the Se in MT medium a new complex MT-Se nanoparticles (MT-Se NPs) was synthesized and we investigated the role of MT-Se NPs on B. napus growth and tolerance against As stress. The MT-Se particles significantly enhanced the plant growth and other associated physiological attributes under As stress. The As treatment at 80 μM was more phytotoxic, however MT-Se NPs application resulted in a substantial increase in leaf chlorophyll fluorescence, biomass accumulation, and decreased ROS relative to As stressed plants. The use of MT-Se NPs to As stressed plants reduced photosynthetic inhibition and oxidative stress and attenuated the increase in MDA and H₂O₂ contents. The application of MT-Se NPs also boosted the antioxidant enzymes activities such as SOD, POD and CAT as well as the APX, GR and GSH activates under As stress. The results also showed MT-Se NPs treatments alleviated the growth inhibition induced by As and reduced the accumulation of As in leaves and roots of B. napus seedlings. Moreover, treatment with MT-Se NPs improved the plant growth more successfully than treatment of MT and Se alone. This study explored the mechanism of melatonin and selenium efficiency in the composition can be jointly encouraged to exert synergistic effects and boost plant enzymatic activities.

Melatonin (M) is a pleiotropic molecule that improves plant growth and increases heavy metal tolerance. The role of M for improving plant growth and tolerance under cadmium (Cd) stress, and mitigation of Cd-induced toxicity has not yet been sufficiently examined. Therefore, here we conducted a glasshouse experiment to explore the influence of various M dosages on Cd detoxification and stress-tolerance responses of Brassica napus under high Cd content (30 mg kg⁻¹). The effects of M on the modulation of Cd tolerance in B. napus plants have been investigated using various growth attributes, Cd accumulation and tolerance indices, and secondary metabolic parameters. We found that Cd stress inhibited root growth (by 11.9%) as well as triggered reactive oxygen species accumulation (by 31.2%) and MDA levels (by 18.7%); however, exogenous M substantially alleviated the adverse effect of oxidative stress by decreasing levels of H₂O₂ (by 38.7%), MDA (by 13.8%) and EL (by 1.8%) in the Cd-stressed plants, as compared to the M-untreated plants (control). Interestingly, exogenous M reduced Cd accumulation in roots (∼48.2–58.3-fold), stem (∼2.9–5.0-fold) and leaves (∼4.7–6.6-fold) compared to control plants, which might be due to an M-induced defense and/or detoxification response involving a battery of antioxidants. Overall, addition of the exogenous M to the Cd-stressed plants profoundly enhanced Cd tolerance in B. napus relative to control plants. These results suggested the biostimulatory role (at the physiological and molecular level) of M in improving growth, Cd tolerance, and Cd detoxification in B. napus, which indicate the potentiality of M for green remediation of Cd contaminated soils. This green trial would provide a reference for producing renewable bioenergy crops under Cd stress in contaminated soils. However, these recommendations should be verified under field conditions and the potential mechanisms for the interaction between Cd and M should be explicitly explored.

This study investigated the role of nocturnal melatonin secretion in the cognitive performance of diurnal animals. An initial experiment measured the cognitive performance in Indian house crows treated for 11 days with 12 h light at 1.426 W/m² (∼150 lux) coupled with 12 h of 0.058 W/m² (∼6-lux) dim light at night (dLAN) or with absolute darkness (0 lux dark night, LD). dLAN treatment significantly decreased midnight melatonin levels and negatively impacted cognitive performance. Subsequently, the role of exogenous melatonin (50 μg; administered intraperitoneally half an hour before the night began) was assessed on the regulation of cognitive performance in two separate experimental cohorts of crows kept under dLAN; LD controls received vehicle. Exogenous melatonin restored its mid-night levels under dLAN at par with those under LD controls, and improved the cognitive performance, as measured in the innovative problem-solving, and spatial and pattern learning-memory efficiency tests in dLAN-treated crows. There were concurrent molecular changes in the cognition-associated brain areas, namely the hippocampus, nidopallium caudolaterale and midbrain. In particular, the expression levels of genes involved in neurogenesis and synaptic plasticity (bdnf, dcx, egr1, creb), and dopamine synthesis and signalling (th, drd1, drd2, darpp32, taar1) were restored to LD control levels in crows treated with illuminated nights and received melatonin. These results demonstrate that the maintenance of nocturnal melatonin levels is crucial for an optimal higher-order brain function in diurnal animals in the face of an environmental threat, such as light pollution.

This study aimed to examine whether and how third-hand smoke (THS) exposure would influence serum melatonin level. 1083 participants with or without exposure to THS were enrolled. Serum ROS, SOD, GSH-Px, and melatonin were measured by ELISA. Methylation microarrays detection and WGCNA were performed to identify hub methylated-sites. The methylation levels of hub-sites were validated in addtional samples. Moreover, mice were exposed to THS for 6 months mimicking exposure of human and the serum, liver, and pineal were collected. Oxidative stress-related indicators in serum, pineal, and liver were measured by ELISA. The expressions of mRNA and protein and methylation levels of hub-gene discovered in human data were further explored by RT-PCR, western-blot, and TBS. The results showed the participants exposed to THS had lower melatonin-level. 820 differentially methylated sites associated with THS were identified. And the hub-site located on the CYP1A2 promoter was identified, which mediated the association between THS and decreased melatonin-level. Decreased peak of serum melatonin, increased ROS and reduced SOD and GSH-Px in pineal and liver, and elevated CYP1A2 expression in liver was also found in the THS-exposed mice. Hypo-methylation of 7 CPG sites on the CYP1A2 promoter was identified, which accelerated the catabolism of melatonin. Overall, THS exposure is associated with abnormal melatonin catabolism through hypo-methylation of CYP1A2-promoter.

Artificial light is transforming the nighttime environment and quickly becoming one of the most pervasive pollutants on earth. Across taxa, light entrains endogenous circadian clocks that function to synchronize behavioral and physiological rhythms with natural photoperiod. Artificial light at night (ALAN) disrupts these photoperiodic cues and has consequences for humans and wildlife including sleep disruption, physiological stress and increased risk of cardiovascular disease. However, the mechanisms underlying organismal responses to dim ALAN, resembling light pollution, remain elusive. Light pollution exists in the environment at lower levels (<5 lux) than tested in many laboratory studies that link ALAN to circadian rhythm disruption. Few studies have linked dim ALAN to both the upstream regulators of circadian rhythms and downstream behavioral and physiological consequences. We exposed zebra finches (Taeniopygia gutatta) to dim ALAN (1.5 lux) and measured circadian expression of five pacemaker genes in central and peripheral tissues, plasma melatonin, locomotor activity, and biomarkers of cardiovascular health. ALAN caused an increase in nighttime activity and, for males, cardiac hypertrophy. Moreover, downstream effects were detectable after just short duration exposure (10 days) and at dim levels that mimic the intensity of environmental light pollution. However, ALAN did not affect circulating melatonin nor oscillations of circadian gene expression in the central clock (brain) or liver. These findings suggest that dim ALAN can alter behavior and physiology without strong shifts in the rhythmic expression of molecular circadian pacemakers. Approaches that focus on ecologically-relevant ALAN and link complex biological pathways are necessary to understand the mechanisms underlying vertebrate responses to light pollution.

Present study demonstrates permethrin induced oxidative damage in fish brain and explores effectiveness of melatonin to ameliorate brain function. Adult female Notopterus notopterus were exposed to nominal permethrin concentrations at 1/20th (0.34 μg/l) and 1/10th (0.68 μg/l) of LC₅₀ for 15 days. The measured permethrin concentrations using gas chromatography (GC-ECD) were 0.28 μg/l and 0.57 μg/l, respectively. Some fish were sacrificed to collect brain tissue after 15 days of exposure. Remaining fish from both groups were administered exogenous melatonin (50 μg/kg, 100 μg/kg body weight) for 7 days and brain tissues were collected. Brain enzymes, ntioxidant factors, HSP70, HSP90, nuclear factor-kappa binding (NFkB), melatonin receptor (MT1R) proteins were measured. Permethrin treatment significantly (P < 0.05) decreased the levels of glutathione and brain enzymes. Malondialdehyde (MDA), xanthine oxidase (XO), HSPs increased at each concentration of permethrin. However, superoxide dismutase, glutathione s-transferase levels increased at low permethrin concentration followed by sharp decrease at higher concentration. Expression of NFkB and MT1R increased significantly (P < 0.05). Melatonin administration reinstated activity of brain enzymes, reduced MDA, XO levels and modulated HSPs. Melatonin also increased expression of NFkB and MT1R. Exogenous melatonin improves oxidative status in permethrin stressed fish brain. Melatonin modulates expression of HSPs that enables brain to become stress tolerant and survive by initiating NFkB translocation. Melatonin could act through melatonin receptor protein to induce synthesis of antioxidant proteins. Therefore the study successfully evaluates the potential of melatonin application for better culture and management of fish against pesticide toxicity.

Increasing urbanisation is altering the physiology of wild animals and the mechanisms involved are largely unknown. We hypothesised that altering the physiology of urban organisms is due to the effect of extra light at night on the circadian clock by modulating the expression of pineal machinery and clock genes. Two experiments were performed. In Experiment 1, immediately after being procured from their respective sites (urban and rural sites), birds were released individually in LLdᵢₘ light conditions. Circadian rhythm period, activity duration, and total activity count were calculated and did not differ between urban and rural birds. In Experiment 2, birds (from urban and rural habitats) were sampled at six time points at regular 4-h intervals, beginning 1 h after sunrise. We measured daily variations in plasma melatonin levels. We also analysed the expression levels of Aanat, Mel1A and Mel1B as an indicator of melatonin biosynthesis and action machinery. Clock and clock-controlled genes (Bmal1, Clock, Per2, Per3, Cry1 and Npas2) were studied in the hypothalamus, the pineal gland, and retina to investigate the effects of urban habitats on the circadian clock. Our results show that there is a lower expression of Aanat in the pineal gland and relatively low plasma melatonin levels in urban birds. Further, clock genes are also differentially expressed in all three central tissues of urban birds. We propose that alterations in the melatonin biosynthesis machinery and the expression of clock genes could result in miscalculations in the internal timing of the organism, with environmental timings leading to altered physiology in urban wild animals.

Chronic ambient fine particulate matter (PM₂.₅) exposure correlates with various adverse health outcomes. Its impact on the circulating metabolome−a comprehensive functional readout of the interaction between an organism's genome and environment−has not however been fully understood. This study thus performed metabolomics analyses using a chronic PM₂.₅ exposure mouse model. C57Bl/6J mice (female) were subjected to inhalational concentrated ambient PM₂.₅ (CAP) or filtered air (FA) exposure for 10 months. Their sera were then analyzed by liquid chromatography-mass spectrometry (LC-MS) and gas chromatography-mass spectrometry (GC-MS). These analyses identified 2570 metabolites in total, and 148 of them were significantly different between FA- and CAP-exposed mice. The orthogonal partial least-squares discriminant analysis (OPLS-DA) and heatmap analyses displayed evident clustering of FA- and CAP-exposed samples. Pathway analyses identified 6 perturbed metabolic pathways related to amino acid metabolism. In contrast, biological characterization revealed that 71 differential metabolites were related to lipid metabolism. Furthermore, our results showed that CAP exposure increased stress hormone metabolites, 18-oxocortisol and 5a-tetrahydrocortisol, and altered the levels of circadian rhythm biomarkers including melatonin, retinal and 5-methoxytryptophol.

Cadmium (Cd) is a toxic heavy metal and harmful to human health due to its ability to accumulate in organs. Previous studies have shown that Cd can induce DNA damage and autophagy. Autophagy can stabilize genetic material and DNA integrity. The aim of the present study was to determine the exact mechanism and role of autophagy induced by Cd in spermatozoa cells. Mouse spermatocyte-derived cells (GC-2) were treated with 20 μM Cd chloride for 24 h. The level of reactive oxygen species (ROS), DNA damage, autophagy and the expression of the molecular signaling pathway ATM/AMP-activated protein kinase (AMPK)/mTOR were determined. The results showed that Cd induced autophagy and DNA damage in GC-2 cells via ROS generation, and the autophagy signal pathway AMPK/mTOR was activated by ATM which is a DNA damage sensor. Melatonin, a well-known antioxidant, ameliorated DNA damage, and inhibited autophagy via the AMPK/mTOR signal pathway. Furthermore, after inhibition of autophagy by knockdown of AMPKα, increased DNA damage by Cd treatment was observed in GC-2 cells. These findings demonstrated the protective role of autophagy in DNA damage and suggested that the mechanism of autophagy induced by Cd was through the ATM/AMPK/mTOR signal pathway in spermatozoa cells.

Decabromodiphenyl ethane (DBDPE) is a novel flame retardant that is widely used in plastics, electronic products, building materials and textiles. Our previous studies have revealed the oocyte toxicity of DBDPE, but the effect of DBDPE on preimplantation embryo development has not been reported. Here, we investigated whether and how DBDPE exposure affects preimplantation embryo development. Adult female mice were orally exposed to DBDPE (0, 5, 50, 500 μg/kg bw/day) for 14 days. First, we found that after DBDPE exposure, mice showed obvious circadian rhythm disorder. Moreover, the development of preimplantation embryos was inhibited in DBDPE-exposed mice after pregnancy. Then, we further explored and revealed that DBDPE exposure reduced the endogenous melatonin (MLT) level during pregnancy, thereby inhibiting the development of preimplantation embryos. Furthermore, we discovered that exogenous MLT supplementation (15 mg/kg bw/day) rescued the inhibition of preimplantation embryo development induced by DBDPE, and a mechanistic study demonstrated that exogenous MLT inhibited the overexpression of ROS and DNA methylation at the 5-position of cytosine (5-mC) in DBDPE-exposed preimplantation embryos. Simultaneously, MLT ameliorated the DBDPE-induced mitochondrial dysfunction by increasing the mitochondrial membrane potential (MMP), ATP, and Trp1 expression. Additionally, MLT restored DBDPE-induced changes in zona pellucida (ZP) hardness and trophectoderm (TE) cortical tension. Finally, the protective effect of MLT on embryos ameliorated the adverse reproductive outcomes (dead fetus, fetus with abnormal liver, fetal weight loss) induced by DBDPE. Collectively, DBDPE induced preimplantation embryo damage leading to adverse reproductive outcomes, and MLT has emerged as a potential tool to rescue adverse reproductive outcomes induced by DBDPE.