Industrialization releases significant amounts of various air pollutants such as F, Cd, Pb, particulate matter, etc., which can in turn have a deleterious effect on a variety of biochemical and physiological processes as well as the structural organization within the cells. Responses from plants species to air pollutants is varied with certain species being very sensitive to such pollutants, ending up with well visible and measurable symptoms. Morphological damage is generally visible through lesions on the aerial parts, while biochemical and physiological changes which are invisible can be measured and quantified. This study has been designed to investigate the biochemical and physiological biomarkers of apricot (Prunus armeniaca L.) exposed to air pollution. It has been observed that, in comparison to unpolluted sites, lipid peroxidation level has increased in the leaves of apricot trees, grown in polluted areas, whereas photosynthetic capacity (Net photosynthesis, stomatal conductance, transpiration rate, total chlorophyll, and carotenoids) along with osmotic regulator (proline and soluble sugars) levels have declined. In P. armeniaca leaves, these symptoms can be used as indicators of air pollution stress for its early diagnosis, making them a reliable marker for a particular physiological disorder.

Perfluorooctane sulfonate (PFOS) is among the most commonly per- and poly-fluoroalkyl substances (PFAS) found in environmental samples. Nevertheless, the effect of this legacy persistent organic contaminant has never been investigated on corals to date. Corals are the keystone organisms of coral reef ecosystems and sensitive to rising ocean temperatures, but it is not understood how the combination of elevated temperature and PFOS exposure will affect them. Therefore, the aims of the present study were (1) to evaluate the time-dependent bioconcentration and depuration of PFOS in the scleractinian coral Stylophora pistillata using a range of PFOS exposure concentrations, and (2) to assess the individual and combined effects of PFOS exposure and elevated seawater temperature on key physiological parameters of the corals. Our results show that the coral S. pistillata rapidly bioconcentrates PFOS from the seawater and eliminates it 14 days after ceasing the exposure. We also observed an antagonistic effect between elevated temperature and PFOS exposure. Indeed, a significantly reduced PFOS bioconcentration was observed at high temperature, likely due to a loss of symbionts and a higher removal of mucus compared to ambient temperature. Finally, concentrations of PFOS consistent with ranges observed in surface waters were non-lethal to corals, in the absence of other stressors. However, PFOS increased lipid peroxidation in coral tissue, which is an indicator of oxidative stress and enhanced the thermal stress-induced impairment of coral physiology. This study provides valuable insights into the combined effects of PFOS exposure and ocean warming for coral's physiology. PFOS is usually the most prevalent but not the only PFAS defected in reef waters, and thus it will be also important to monitor PFAS mixture concentrations in the oceans and to study their combined effects on aquatic wildlife.

Exposure to tobacco smoke during pregnancy has been associated with a series of adverse reproductive outcomes; however, the underlying molecular mechanisms are not well-established. We conducted an untargeted metabolome-wide association study to identify the metabolic perturbations and molecular mechanisms underlying the association between cotinine, a widely used biomarker of tobacco exposure, and adverse birth outcomes. We collected early and late pregnancy urine samples for cotinine measurement and serum samples for high-resolution metabolomics (HRM) profiling from 105 pregnant women from the Atlanta African American Maternal-Child cohort (2014–2016). Maternal metabolome perturbations mediating prenatal tobacco smoke exposure and adverse birth outcomes were assessed by an untargeted HRM workflow using generalized linear models, followed by pathway enrichment analysis and chemical annotation, with a meet-in-the-middle approach. The median maternal urinary cotinine concentrations were 5.93 μg/g creatinine and 3.69 μg/g creatinine in early and late pregnancy, respectively. In total, 16,481 and 13,043 metabolic features were identified in serum samples at each visit from positive and negative electrospray ionization modes, respectively. Twelve metabolic pathways were found to be associated with both cotinine concentrations and adverse birth outcomes during early and late pregnancy, including tryptophan, histidine, urea cycle, arginine, and proline metabolism. We confirmed 47 metabolites associated with cotinine levels, preterm birth, and shorter gestational age, including glutamate, serine, choline, and taurine, which are closely involved in endogenous inflammation, vascular reactivity, and lipid peroxidation processes. The metabolic perturbations associated with cotinine levels were related to inflammation, oxidative stress, placental vascularization, and insulin action, which could contribute to shorter gestations. The findings will support the further understanding of potential internal responses in association with tobacco smoke exposures, especially among African American women who are disproportionately exposed to high tobacco smoke and experience higher rates of adverse birth outcomes.

This study focused on the impacts of aged aquaculture microplastics (MPs) on oysters (Crassostrea gigas). Adult oysters were exposed for two months to a cocktail of MPs representative of the contamination of the Pertuis Charentais area (Bay of Biscay, France) and issuing from oyster framing material. The MPs mixture included 28% of polyethylene, 40% of polypropylene and 32% of PVC (polyvinyl chloride). During the exposure, tissues were sampled for various analyzes (MP quantification, toxicity biomarkers). Although no effect on the growth of adult oysters was noted, the mortality rate of bivalves exposed to MPs (0.1 and 10 mg. L⁻¹ MP) increased significantly (respectively 13.3 and 23.3% of mortalities cumulative). On the one hand, the responses of biomarkers revealed impacts on oxidative stress, lipid peroxidation and environmental stress. At 56 days of exposure, significant increases were noted for Glutathione S-Transferase (GST, 10 mg. L⁻¹ MP), Malondialdehyde (MDA, 10 mg. L⁻¹ MP) and Laccase (LAC, 0.1 and 10 mg. L⁻¹ MP). No variations were observed for Superoxyde Dismutase (SOD). Besides, ingestion of MPs in oyster tissues and the presence in biodeposits was highlighted. In addition, in vitro fertilisations were performed to characterize MPs effects on the offspring. Swimming behavior, development and growth of D-larvae were analysed at 24-, 48- and 72-h after fertilisation. D-larvae, from exposed parents, demonstrated reduced locomotor activity. Developmental abnormalities and arrest as well as growth retardation were also noted. This study highlighted direct and intergenerational effects of MPs from aged plastic materials on Pacific oysters.

Global warming and local disturbances such as pollution cause several impacts on coral reefs. Among them is the breakdown of the symbiosis between host corals and photosynthetic symbionts, which is often a consequence of oxidative stress. Therefore, we investigated if the combined effects of thermal stress and copper (Cu) exposure change the trophic behavior and oxidative status of the reef-building coral Mussismilia harttii. Coral fragments were exposed in a mesocosm system to three temperatures (25.0, 26.6 and 27.3 °C) and three Cu concentrations (2.9, 5.4 and 8.6 μg L⁻¹). Samples were collected after 4 and 12 days of exposure. We then (i) performed fatty acid analysis by gas chromatography-mass spectrometry to quantify changes in stearidonic acid and docosapentaenoic acid (autotrophy markers) and cis-gondoic acid (heterotrophy marker), and (ii) assessed the oxidative status of both host and symbiont through analyses of lipid peroxidation (LPO) and total antioxidant capacity (TAC). Our findings show that trophic behavior was predominantly autotrophic and remained unchanged under individual and combined stressors for both 4- and 12-day experiments; for the latter, however, there was an increase in the heterotrophy marker. Results also show that 4 days was not enough to trigger changes in LPO or TAC for both coral and symbiont. However, the 12-day experiment showed a reduction in symbiont LPO associated with thermal stress alone, and the combination of stressors increased their TAC. For the coral, the isolated effects of increase in Cu and temperature led to an increase in LPO. The effects of combined stressors on trophic behavior and oxidative status were not much different than those from the isolated effects of each stressor. These findings highlight that host and symbionts respond differently to stress and are relevant as they show the physiological response of individual holobiont compartments to both global and local stressors.

Prior human studies have explored effects of phthalate exposures on thyroid function, but the underlying biological mechanisms remain poorly unclear. We aimed to explore the associations between phthalate exposures and thyroid function among a potentially susceptible population such as patients with thyroid nodules, and further to assess the mediating role of oxidative stress. We measured eight phthalate metabolites, three oxidative stress biomarkers [8-hydroxy-2-deoxyguanosine (8-OHdG), 8-iso-prostaglandin F₂α (8-isoPGF₂α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)] in urine and three thyroid function biomarkers [thyroid-stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4)] in serum among 214 patients with thyroid nodules. Multivariate regression models were applied to assess the associations among urinary phthalate metabolites, oxidative stress and thyroid function biomarkers. The potential mediating role of oxidative stress was explored by mediation analysis. We observed that multiple urinary phthalate metabolites were associated with altered FT4 and increased oxidative stress biomarkers (all FDR-adjusted P ≤ 0.05). Meanwhile, we found that 8-isoPGF₂α was negatively associated with FT3/FT4 among patients with benign thyroid nodules (FDR-adjusted P = 0.08). The mediation analysis indicated that 8-isoPGF₂α mediated the associations of urinary MEHHP and %MEHP with FT3/FT4, with 55.6% and 32.6% proportion of the mediating effects, respectively. Our data suggest that lipid peroxidation may be an intermediate mechanism involved in the effects of certain phthalate exposures on altered thyroid function among patients with benign thyroid nodules.

Cadmium as a common environmental stressor may exert highly toxic effects on herbivorous insects. The question was whether possible elevation of an oxidative stress and imbalance of energetic reserves in insects may depend on developmental stage, sex and insect population’s multigenerational history of exposure to cadmium. So, the aim of this study was to compare of the development traits, total antioxidant capacity, lipid peroxidation, RSSR to RSH ratio and the concentration of carbohydrates, glycogen, lipids and proteins in whole individuals (larvae or pupae) of Spodoptera exigua originating from two strains: control and selected over 120 generations with sublethal metal concentration (44 Cd mg per dry weight of diet). Generally, the increase of the protein, carbohydrates, glycogen concentration and lipid peroxidation decrease with age of the larvae were found. Revealed cases of a higher mobilisation of carbohydrates and proteins, and changes in total antioxidant capacity or lipid peroxidation, in individuals being under metal exposure, occurred in strain-depended mode. Short-term Cd exposure effect was connected with possible higher engagement of proteins and glycogen in detoxification processes, but also higher concentration of lipid peroxidation. In turn, for long-term Cd exposure effect lower lipids concentration and higher thiols usage seemed to be more specific.

Iron-bearing nanoparticles (IBNPs) were abundant in particulate matter (PM). Due to their high reactivity, IBNPs were considered hazardous to human health, however, their toxic mode-of-action(s) are highly unclear. Ferroptosis is a novel programmed cell death (PCD) that highly associated with intracellular iron. However, the pro-ferroptotic effect of IBNPs has not been characterized. To this end, we ought to investigate whether and how IBNPs (synthetic γ-Fe₂O₃ and Fe₃O₄ NPs were selected as the model compounds) are involved in ferroptosis. We found that human umbilical vein endothelial cells (HUVECs) phagocytized large qualities of γ-Fe₂O₃ and Fe₃O₄ NPs, resulting in increased intracellular iron level. We further observed the disrupted cystine/glutamate reverse transporter (System Xc⁻) and glutathione peroxidase 4 (GPX4) signaling in γ-Fe₂O₃ and Fe₃O₄ NPs-challenged HUVECs. γ-Fe₂O₃ and Fe₃O₄ NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner. Together, the ferroptotic activity of IBNPs should be acknowledged for the risk assessment of PM associated health effects.

Carbon disulfide (CS₂) has been reported to induce disorder of glucose metabolism. However, the associations of CS₂ exposure with plasma glucose levels and risk of diabetes have not been explored in general population, and the underlying mechanisms remain unclear. We aim to examine the relationships between CS₂ exposure and fasting plasma glucose (FPG) levels, as well as diabetes, and assess the potential role of oxidative stress among the abovementioned relationships in Chinese general adults. The concentrations of urinary biomarkers of CS₂ exposure (2-thiothiazolidin-4-carboxylic acid, TTCA), and biomarkers for lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) and DNA oxidative damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) were measured among 3338 urban adults from the Wuhan-Zhuhai cohort. Additionally, FPG levels were tested promptly. Generalized linear models and logistic regression models were used to quantify the associations among urinary TTCA, oxidative damage markers, FPG levels and diabetes risk. Mediation analysis was employed to estimate the role of oxidative damage markers in the association between urinary TTCA and FPG levels. We discovered a significant relationship between urinary TTCA and FPG levels with regression coefficient of 0.080 (95% CI: 0.002,0.157). Besides, the risk of diabetes was positively related to urinary TTCA (OR:1.282, 95% CI: 1.055,1.558), particularly among those who did not exercise regularly. Each 1% increase of urinary TTCA concentration was associated with a 0.096% and 0.037% increase in urinary 8-iso-PGF₂α and 8-OHdG, respectively. Moreover, we found an upward trend of FPG level as urinary 8-iso-PGF₂α gradually increased (Pₜᵣₑₙd<0.05), and urinary 8-iso-PGF₂α mediated 21.12% of the urinary TTCA-associated FPG increment. Our findings indicated that urinary CS₂ metabolite was associated with increased FPG levels and diabetes risk in general population. Lipid peroxidation partly mediated the association of urinary CS₂ metabolite with FPG levels.