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.

The increasing use of artificial light at night (ALAN) has led to exposure of freshwater ecosystems to light pollution worldwide. Simultaneously, the spectral composition of nocturnal illumination is changing, following the current shift in outdoor lighting technologies from traditional light sources to light emitting diodes (LED). LEDs emit broad-spectrum white light, with a significant amount of photosynthetically active radiation, and typically a high content of blue light that regulates circadian rhythms in many organisms. While effects of the shift to LED have been investigated in nocturnal animals, its impact on primary producers is unknown. We performed three field experiments in a lowland agricultural drainage ditch to assess the impacts of a transition from high-pressure sodium (HPS) to white LED illumination (color temperature 4000 K) on primary producers in periphyton. In all experiments, we compared biomass and pigment composition of periphyton grown under a natural light regime to that of periphyton exposed to nocturnal HPS or, consecutively, LED light of intensities commonly found in urban waters (approximately 20 lux). Periphyton was collected in time series (1–13 weeks). We found no effect of HPS light on periphyton biomass; however, following a shift to LED the biomass decreased up to 62%. Neither light source had a substantial effect on pigment composition. The contrasting effects of the two light sources on biomass may be explained by differences in their spectral composition, and in particular the blue content. Our results suggest that spectral composition of the light source plays a role in determining the impacts of ALAN on periphyton and that the ongoing transition to LED may increase the ecological impacts of artificial lighting on aquatic primary producers. Reduced biomass in the base of the food web can impact ecosystem functions such as productivity and food supply for higher trophic levels in nocturnally-lit ecosystems.

The aim of this study was to determine the impact of the fludioxonil (fdx) fungicide on the diurnal fluctuation in grapevine photosynthesis. Therefore, fdx treatment was performed at the end of flowering, at 8 am, 12 am or 7 pm. The study was performed in experimental field and several photosynthesis parameters were followed one day after treatment. Morning fdx treatment induced (i) a significant and simultaneous drop of both photosynthesis (Pn) and stomatal conductance between 8 am and 4 pm and (ii) an increase of intercellular CO2 concentration when compared to control plants. On the contrary, evening fdx treatment did not affect Pn whereas midday treatment caused Pn increase after 4 pm. These data suggest that (i) morning fdx treatment results in a non-stomatal limitation of Pn, (ii) midday treatment is more suitable to treat grapevine with fdx and (iii) a phenomenon of gating was noticed. The period of fdx spraying was an important parameter in stress response: the midday fdx treatment is more suitable to treat grapevine with fdx.

Most available exposure–response relationships for assessing crop loss due to elevated ozone (O3) have been established using data from chamber and open-top chamber experiments, using a simulated constant O3 concentration exposure (square wave), which is not consistent with the diurnal variation of O3 concentration that occurs in nature. We investigated the response of oilseed rape (Brassica napus L.) to O3 as affected by two exposure regimes: one with a diurnal variation (CF100D) and another with a constant concentration (CF100). Although the two exposure regimes have the same mean O3 concentration and accumulated O3 concentration above 40 ppb (AOT40), our results show that O3 at CF100D reduced biomass and number of pods/plant more than O3 at CF100. Both O3 exposures resulted in larger seed weights/100 pods compared to CF. Numbers of seeds/100 pods were reduced by CF100, while numbers of seeds/100 pods in the CF100D chambers were comparable to those in CF. Our results suggest that chamber experiments that use a constant O3 exposure may underestimate O3 effects on biomass and yields. Diurnal variation of O3 concentration should be considered when designing O3 exposure experiment.

Irregular or unnatural artificial light causes severe environmental stress on the survival and health of organisms, which is rapidly becoming a widespread new type of environmental pollution. A series of disruptive behaviors to body homeostasis brought about by light pollution, including metabolic abnormalities, are likely to be the result of circadian rhythm disturbances. Recently, the proposed role of light pollution in metabolic dysregulation has accelerated it into an emerging field. Hence, the regulatory role of light pollution in mammalian metabolic homeostasis is reviewed in this contribution. Light at night is the most widely affected type of light pollution, which disrupts metabolic homeostasis largely due to its disruption of daily food intake patterns, alterations of hormone levels such as melatonin and glucocorticoids, and changes in the rhythm of inflammatory factor production. Besides, light pollution impairs mammalian metabolic processes in an intensity-, photoperiod-, and wavelength-dependent manner, and is also affected by species, gender, and diets. Nevertheless, metabolic disorders triggered by light pollution are not irreversible to some extent. Potential interventions such as melatonin supplementation, recovery to the LD cycle, time-restricted feeding, voluntary exercise, wearing blue light-shied goggles, and bright morning light therapy open a bright avenue to prevent light pollution. This work will help strengthen the relationship between light information and metabolic homeostasis and provide new insights for the better prevention of metabolic disorders and light pollution.

Artificial light at night (ALAN) changes the natural rhythm of light and darkness and can impair the biorhythms of animals, for example the nocturnal melatonin production of vertebrates, which serves as a proxy for daily physiological rhythms. Freshwater fish are exposed to ALAN in large urban and suburban areas in the form of direct light or in the form of skyglow, a diffuse brightening of the night sky through the scattered light reflected by clouds, atmospheric molecules, and particles in the air. However, investigations on the sensitivity of melatonin production of fish towards low intensities of ALAN in the range of typical skyglow are rare. Therefore, we exposed Eurasian perch (Perca fluviatilis) to nocturnal illumination levels of 0.01 lx, 0.1 lx and 1 lx and a control group with dark nights and daylight intensities of 2900 lx in all groups. After ten days of exposure to the experimental conditions, tank water was non-invasively sampled every 3 h over a 24 h period and melatonin was measured by ELISA. Melatonin was gradually reduced in all treatments with increasing intensity of ALAN whereas rhythmicity was maintained in all treatment groups although at 1 lx not all evaluated parameters confirmed rhythmicity. These results show a high sensitivity of Eurasian perch towards ALAN indicating that low light intensities of 0.01 lx and 0.1 lx as they occur in urban and suburban areas in the form of skyglow can affect the physiology of Eurasian perch. Furthermore, we highlight how this may impact perch in their sensitivity towards lunar rhythms and the role of skyglow for biorhythms of temperate freshwater fish.

Nighttime lighting is an increasingly important anthropogenic environmental stress on plants and animals. Exposure to unnatural lighting environments may disrupt the circadian rhythm of organisms. However, the sample size of relevant studies, e.g. disruption of the molecular circadian clock by light pollution, was small (<10), which led to low statistical power and difficulties in replicating prior results. Here, we developed a power-calibrated statistical approach to overcome these weaknesses. The results showed that the effect size of 2.48 in clock genes expression induced by artificial light would ensure the reproducibility of the results as high as 80%. Long-wavelength light (560–660 nm) entrained expressions of the positive core clock genes (e.g. cClock) and negative core clock genes (e.g. cCry1, cPer2) in robust circadian rhythmicity, whereas those clock genes were arrhythmic in short-wavelength light (380–480 nm). Further, we found artificial light could entrain the transcriptional-translational feedback loop of the molecular clock in a wavelength-dependent manner. The expression of the positive core clock genes (cBmal1, cBmal2 and cClock), cAanat gene and melatonin were the highest in short-wavelength light and lowest in long-wavelength light. For the negative regulators of the molecular clock (cCry1, cCry2, cPer2 and cPer3), the expression of which was the highest in long-wavelength light and lowest in short-wavelength light. Our statistical approach opens new opportunities to understand and strengthen conclusions, comparing with the studies with small sample sizes. We also provide comprehensive insight into the effect of wavelength-specific artificial light on the circadian rhythm of the molecular clock in avian species. Especially, the global lighting is shifting from “yellow” sodium lamps, which is more like the long-wavelength light, toward short-wavelength light (blue light)-enriched “white” light-emitting diodes (LEDs).

Emerging evidence has shown that exposure to ambient fine particulate matter (PM₂.₅) is associated with hepatic lipid accumulation. However, the underlying mechanism is not fully characterized yet. Autonomous circadian clock in the liver plays a fundamental role in maintaining lipid metabolism homeostasis. In this study, we evaluated the effects of ambient PM₂.₅ exposure on the expression of hepatic circadian clock genes and expression rhythm of genes associated with lipid metabolism in mice liver. Male C57BL/6 mice were randomly assigned to ambient PM₂.₅ or filtered air for 10 weeks via a whole body exposure system. We found that the liver mass was reduced significantly at zeitgeber time (ZT) 8 in mice exposed to PM₂.₅ but not levels or circadian rhythm of hepatic triglycerides or free fatty acid (FFA). In addition, exposure to PM₂.₅ led to enhanced expression of bmal1 at ZT0/24, cry1 at ZT16 and rev-erbα at ZT4 and ZT8. Furthermore, the expression of pparα was enhanced in mice liver at ZT4 and ZT8 after PM₂.₅ exposure, with upregulation of pparα-mediated genes responsible for fatty acid transport and oxidation. Finally, the expression of rate-limiting enzymes for lipid synthesis was all significantly increased in the liver of PM₂.₅ exposed mice at ZT12. Therefore, the present study provides new perspectives for revealing the etiology of hepatic lipid metabolism abnormality from PM₂.₅-induced circadian rhythm disorder.

Circadian rhythm is believed to play important roles in atherosclerosis. The gut microbiota is found to be closely related to atherogenesis, and shows compositional and functional circadian oscillation. However, it's still unclarified whether circadian clock and intestinal microbiota are involved in the progression of atherosclerosis induced by environmental pollutant acrolein. Herein, patients with atherosclerosis showed higher MMP9, a promising biomarker for atherosclerosis, and lower Bmal1 and Clock expression in the plasma. Interestingly, acrolein exposure contributed to the increased MMP9, decreased Clock and Bmal1, and activated MAPK pathways in human umbilical vein endothelial cells (HUVECs). We found that knockdown of Clock or Bmal1 lead to upregulation of MMP9 in HUVECs, and that Clock and Bmal1 expression was elevated while MAPK pathways were blocked. Atherosclerotic apolipoproteinE-deficient mice consumed a high-fat diet were used and treated with acrolein (3 mg/kg/day) in the drinking water for 12 weeks. Upregulation of MMP9, and downregulation of Clock and Bmal1 were also observed in plasma of the mice. Besides, acrolein feeding altered gut microbiota composition at a phylum level especially for an increased Firmicutes and a decreased Bacteroidetes. Additionally, gut microbiota showed correlation with atherosclerotic plaque, MMP9 and Bmal1 levels. Therefore, our findings indicated that acrolein increased the expression of MMP9 through MAPK regulating circadian clock, which was associated with gut microbiota regulation in atherosclerosis. Circadian rhythms and gut microbiota might be promising targets in the prevention of cardiovascular disease caused by environmental pollutants.

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.