Artificial light at night (ALAN) exposes us to prolonged illumination, that adversely affects female reproduction. However, it remains to be clarified how prolonged light exposure affects oocyte meiotic maturation and quality. To this end, we exposed female mice to a constant light (CL) of 250 lux for different durations. Our findings showed that CL exposure for 7 weeks reduced the oocyte maturation rate. Meanwhile, CL exposure caused greater abnormalities in spindle assembly and chromosome alignment and a higher rate of oocyte aneuploidy than the regular light dark cycle. CL exposure also induced oxidative stress and caused mitochondrial dysfunction, which resulted in oocyte apoptosis and autophagy. Notably, our results showed that CL exposure reduced the levels of α-tubulin acetylation, DNA methylation at 5 mC, RNA methylation at m⁶A and histone methylation at H3K4me2 but increased the levels of histone methylation at H3K27me2 in oocytes. In summary, our findings demonstrate that constant bright light exposure causes oocyte meiotic defects and reduces cytoplasmic quality. These results extend the current understanding of ALAN-mediated defects in female reproduction.

Potassium (K⁺) is the most abundant cation in phytoplankton cells, but its impact on Microcystis aeruginosa (M. aeruginosa) has not been fully documented. This study presents evidence of how K⁺ availability affects the growth, oxidative stress and microcystin (MC) production of M. aeruginosa. The iTRAQ-based proteomic analysis revealed that during K⁺ deficiency, serious oxidative damage occurred and the photosynthesis-associated and ABC transporter-related proteins in M. aeruginosa were substantially downregulated. In the absence of K⁺, a 69.26% reduction in cell density was shown, and both the photosynthesis and iron uptake were depressed, which triggered a declined production of ATP and expression of MC synthetases genes (mcyA, B and D), and MC exporters (mcyH). Through the impairment of both the MC biosynthesis and MC transportation out of cells, K⁺ depletion caused an 85.89% reduction of extracellular MC content at the end of the study. However, with increasing in the available K⁺ concentrations, photosynthesis efficiency, the expression of ABC-transporter proteins, and the transcription of mcy genes displayed slight differences compared with those in the control group. This work represents evidence that K⁺ availability can regulate the physiological metabolic activity of M. aeruginosa and K⁺ deficiency leads to depressed growth and MC production in M. aeruginosa.

In this paper, the acute toxicity of monobutyl phthalate (MBP), the main hydrolysis product of dibutyl phthalate, on adult zebrafish liver antioxidant system was studied. Compared the toxicity effect of MBP and DBP by histopathology and apoptosis experiments, we speculated that the toxic effects of DBP on animals may be caused by its metabolite MBP. The results indicated that the antioxidant Nrf2-Keap1 pathway was insufficient to resist MBP-induced hepatotoxicity and led to an imbalance of membrane ion homeostasis and liver damage. Decreased cell viability, significant tissue lesions and early hepatocyte apoptosis were observed in the zebrafish liver in MBP exposure at high concentration (10 mg/L). The activities of antioxidant enzymes and ATPases in zebrafish liver were inhibited with increased malondialdehyde (MDA) content and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Integrated biomarker response (IBR) calculation results indicated that MBP mainly inhibited catalase (CAT) activity. Simultaneously, the expression of antioxidant-related genes (SOD, CAT, GPx, Nrf2, HO-1) was down-regulated, while apoptosis-related genes (p53, bax, cas3) were significantly up-regulated.

Neonicotinoid insecticides have posed a great threat to non-target organisms, yet the mechanisms underlying their toxicity are not well characterized. Major modes of action (MoAs) of imidacloprid were analyzed in an aquatic insect Chironomus dilutus. Lethal and sublethal outcomes were assessed in the midges after 96-h exposure to imidacloprid. Global transcriptomic profiles were determined using de novo RNA-sequencing to more holistically identify toxicity pathways. Transcriptional 10% biological potency values derived from ranked KEGG pathways and GO terms were 0.02 (0.01–0.08) (mean (95% confidence interval) and 0.05 (0.04–0.06) μg L⁻¹, respectively, which were more sensitive than those from phenotypic traits (10% lethal concentration: 0.44 (0.23–0.79) μg L⁻¹; 10% burrowing behavior concentration: 0.30 (0.22–0.43) μg L⁻¹). Major MoAs of imidacloprid in aquatic species were identified as follows: the activation of nicotinic acetylcholine receptors (nAChRs) induced by imidacloprid impaired organisms’ nerve system through calcium ion homeostasis imbalance and mitochondrial dysfunction, which posed oxidative stress and DNA damage and eventually caused death of organisms. The current investigation highlighted that imidacloprid affected C. dilutus at environmentally relevant concentrations, and elucidated toxicity pathways derived from gene alteration to individual outcomes, calling for more attention to toxicity of neonicotinoids to aquatic organisms.

Previous in vitro studies have indicated that 2,3,3′,4,4′,5-hexachlorobiphenyl (PCB 156) may be a new contributor to metabolic disruption and may further cause the occurrence of nonalcoholic fatty liver disease (NAFLD). However, no study has clarified the specific contributions of PCB 156 to NAFLD progression by constructing an in vivo model. Herein, we evaluated the effects of PCB 156 treatment (55 mg/kg, i.p.) on the livers of C57BL/6 mice fed a control diet (CD) or a high-fat diet (HFD). The results showed that PCB 156 administration increased intra-abdominal fat mass, hepatic lipid levels and dyslipidemia in the CD-fed group and aggravated NAFLD in HFD-fed group. By using transcriptomics studies and biological methods, we found that the genes expression involved in lipid metabolism pathways, such as lipogenesis, lipid accumulation and lipid β-oxidation, was greatly altered in liver tissues exposed to PCB 156. In addition, the cytochrome P450 pathway, peroxisome proliferator-activated receptors (PPARs) and the glutathione metabolism pathway were significantly activated following exposure to PCB 156. Furthermore, PCB 156 exposure increased serum transaminase levels and lipid peroxidation, and the redox-related genes were significantly dysregulated in liver tissue. In conclusion, our data suggested that PCB 156 could promote NAFLD development by altering the expression of genes related to lipid metabolism and inducing oxidative stress.

Heavy metal accumulation in agricultural land causes crop production losses worldwide. Metal homeostasis within cells is tightly regulated. However, homeostasis breakdown leads to accumulation of reactive oxygen species (ROS). Overall plant fitness under stressful environment is determined by coordination between roots and shoots. But little is known about organ specific responses to heavy metals, whether it depends on the metal category (redox or non-redox reactive) and if these responses are associated with heavy metal accumulation in each organ or there are driven by other signals. Maize seedlings were subjected to sub-lethal concentrations of four metals (Zn, Ni, Cd and Cu) individually, and were quantified for growth, ABA level, and redox alterations in roots, mature leaves (L1,2) and young leaves (L3,4) at 14 and 21 days after sowing (DAS). The treatments caused significant increase in endogenous metal levels in all organs but to different degrees, where roots showed the highest levels. Biomass was significantly reduced under heavy metal stress. Although old leaves accumulated less heavy metal content than root, the reduction in their biomass (FW) was more pronounced. Metal exposure triggered ABA accumulation and stomatal closure mainly in older leaves, which consequently reduced photosynthesis. Heavy metals induced oxidative stress in the maize organs, but to different degrees. Tocopherols, polyphenols and flavonoids increased specifically in the shoot under Zn, Ni and Cu, while under Cd treatment they played a minor role. Under Cu and Cd stress, superoxide dismutase (SOD) and dehydroascorbate reductase (DHAR) activities were induced in the roots, however ascorbate peroxidase (APX) activity was only increased in the older leaves. Overall, it can be concluded that root and shoot organs specific responses to heavy metal toxicity are not only associated with heavy metal accumulation and they are specialized at the level of antioxidants to cope with.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O₃, PM₂.₅, NO₂, and SO₂ exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O₃ exposures and significantly but positively associated with 2-week O₃ exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO₂ exposures, respectively. However, we did not find clear associations of PM₂.₅ and SO₂ exposure with proinflammatory cytokines and with MDA. The removal of an O₃-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O₃ for different time durations may affect systemic inflammatory responses in different ways.

Pharmacologically active compounds found in reclaimed wastewater irrigation or animal manure fertilizers pose potential risks for agriculture. The mechanism underlying the effects of ketoprofen on rice (Oryza sativa L.) seedlings was investigated. The results showed that low concentrations (0.5 mg L⁻¹) of ketoprofen slightly stimulate growth of rice seedlings, while high concentrations can significantly inhibit growth by reducing biomass and causing damage to roots. Ketoprofen affects photosynthetic pigment content (Chla, Chlb, and carotenoids) and chlorophyll synthesis gene (HEMA, HEMG, CHLD, CHLG, CHLM, and CAO) expression. Fluorescence parameters such as minimum fluorescence (F₀), maximum fluorescence (Fₘ), variable fluorescence (Fᵥ), potential photosynthetic capacity (Fᵥ/F₀), maximum quantum efficiency of PSII photochemistry (Fᵥ/Fₘ), electron transfer rate (ETR), and Y(II), Y(NPQ), Y(NO) values were affected, showing photosynthetic electron transfer was blocked. Active oxygen radical (O₂•−and H₂O₂), malondialdehyde and proline content increased. Superoxide dismutase, catalase and ascorbate peroxidase activities, glutathione content and antioxidant-related gene (FSD1, MSD1, CSD1, CSD2, CAT1, CAT2, CAT3, APX1, APX2) expression were induced. Higher integrated biomarker response values of eight oxidative stress response indexes were obtained at higher ketoprofen concentrations. Ultrastructure observation showed that ketoprofen causes cell structure damage, chloroplast swelling, increase in starch granules, and reduction in organelles. This study provides some suggested toxicological mechanisms and biological response indicators in rice due to stress from pharmacologically active compounds.

Metalaxyl is a broad-spectrum chiral fungicide that used for the protection of plants, however extensive use of metalaxyl resulted in serious environmental problems. Thus, a study on the detoxification mechanism in algae/cyanobacteria and their ability for phycoremediation is highly recommended. Here, we investigated the physiological and biochemical responses of two cyanobacterial species; Anabaena laxa and Nostoc muscorum to R-metalaxyl toxicity as well as their ability as phycoremediators. Two different levels of R-metalaxyl, at mild (10 mg/L) and high dose (25 mg/L), were applied for one-week. We found that A. laxa absorbed and accumulated more intracellular R-metalaxyl compared to N. muscorum. R-metalaxyl, which triggered a dose-based reduction in cell growth, photosynthetic pigment content, and photosynthetic key enzymes’ activities i.e., phosphoenolpyruvate carboxylase (PEPC) and ribulose‒1,5‒bisphosphate carboxylase/oxygenase (RuBisCo). These decreases were significantly less pronounced in A. laxa. On the other hand, R-metalaxyl significantly induced oxidative damage markers, e.g., H₂O₂ levels, lipid peroxidation (MDA), protein oxidation and NADPH oxidase activity. However, these increases were also lower in A. laxa compared to N. muscorum. To alleviate R-metalaxyl toxicity, A. laxa induced the polyphenols, flavonoids, tocopherols and glutathione (GSH) levels as well as peroxidase (POX), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-s-transferase (GST) enzyme activities. On the contrary, the significant induction of antioxidants in N. muscorum was restricted to ascorbate, catalase (CAT) and ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR) enzyme activities. Although A. laxa accumulated more R-metalaxyl, it experienced less stress due to subsequent induction of antioxidants. Therefore, A. laxa may be a promising R-metalaxyl phycoremediator. Our results provided basic data for understanding the ecotoxicology of R-metalaxyl contamination in aquatic habitats and the toxicity indices among cyanobacteria.

In the marine environment, microplastic contamination and acidification may occur simultaneously, this study evaluated the effects of ocean acidification and microplastics on oxidative stress responses and digestive enzymes in mussels. The thick shell mussels Mytilus coruscus were exposed to four concentrations of polystyrene microspheres (diameter 2 μm, 0, 10, 10⁴ and 10⁶ particles/L) under two pH levels (7.7 and 8.1) for 14 days followed by a 7-day recovery acclimation. Throughout the experiment, we found that microplastics and ocean acidification exerted little oxidative stress to the digestive gland. Only catalase (CAT) and glutathione (GSH) showed a significant increase along with increased microplastics during the experiment, but recovered to the control levels once these stressors were removed. No significant effects of pH and microplastics on glutathione peroxidase (GPx) and superoxide dismutase (SOD) were observed. The responses of digestive enzymes to both stressors were more pronounced than antioxidant enzymes. During the experiment, pepsin (PES), trypsin (TRS), alpha-amylase (AMS) and lipase (LPS) were significantly inhibited under microplastics exposure and this inhibition was aggravated by acidification conditions. Only PES and AMS tended to recover during the recovery period. Lysozyme (LZM) increased significantly under microplastic exposure conditions, but acidification did not exacerbate this effect. Therefore, combined stress of microplastics and ocean acidification slightly impacts oxidative responses but significantly inhibits digestive enzymes in mussels.