International audience | Antibiotics have been increasingly used over the past decades for human medicine, food-animal agriculture, aquaculture, and plant production. A significant part of the active molecules of antibiotics can be released into the environment, in turn affecting ecosystem functioning and biogeochemical processes. At lower organizational scales, these substances affect bacterial symbionts of insects, with negative consequences on growth and development of juveniles, and population dynamics. Yet, the multiple alterations of cellular physiology and metabolic processes have remained insufficiently explored in insects. We evaluated the effects of five antibiotics with different mode of action, i.e. ampicillin, cefradine, chloramphenicol, cycloheximide, and tetracycline, on the survival and ultrastructural organization of the flight muscles of newly emerged blow flies Chrysomya albiceps. Then, we examined the effects of different concentrations of antibiotics on mitochondrial protein content, efficiency of oxidative phosphorylation, and activity of transaminases (Glutamate oxaloacetate transaminase and glutamate pyruvate transaminase) and described the cellular metabolic perturbations of flies treated with antibiotics. All antibiotics affected the survival of the insects and decreased the total mitochondrial protein content in a dose-dependent manner. Ultrastructural organization of flight muscles in treated flies differs dramatically compared to the control groups and severe pathological damages/structures disorganization of mitochondria appeared. The activities of mitochondrial transaminases significantly increased with increased antibiotic concentrations. The oxidation rate of pyruvate + proline from isolated mitochondria of the flight muscles of 1-day-old flies was significantly reduced at high doses of antibiotics. In parallel, the level of several metabolites, including TCA cycle intermediates, was reduced in antibiotics-treated flies. Overall, antibiotics provoked a system-wide alteration of the structure and physiology of flight muscles of the blow fly Ch. albiceps, and may have fitness consequences at the organism level. Environmental antibiotic pollution is likely to have unwanted cascading ecological effects of insect population dynamics and community structure.

International audience | Antibiotics have been increasingly used over the past decades for human medicine, food-animal agriculture, aquaculture, and plant production. A significant part of the active molecules of antibiotics can be released into the environment, in turn affecting ecosystem functioning and biogeochemical processes. At lower organizational scales, these substances affect bacterial symbionts of insects, with negative consequences on growth and development of juveniles, and population dynamics. Yet, the multiple alterations of cellular physiology and metabolic processes have remained insufficiently explored in insects. We evaluated the effects of five antibiotics with different mode of action, i.e. ampicillin, cefradine, chloramphenicol, cycloheximide, and tetracycline, on the survival and ultrastructural organization of the flight muscles of newly emerged blow flies Chrysomya albiceps. Then, we examined the effects of different concentrations of antibiotics on mitochondrial protein content, efficiency of oxidative phosphorylation, and activity of transaminases (Glutamate oxaloacetate transaminase and glutamate pyruvate transaminase) and described the cellular metabolic perturbations of flies treated with antibiotics. All antibiotics affected the survival of the insects and decreased the total mitochondrial protein content in a dose-dependent manner. Ultrastructural organization of flight muscles in treated flies differs dramatically compared to the control groups and severe pathological damages/structures disorganization of mitochondria appeared. The activities of mitochondrial transaminases significantly increased with increased antibiotic concentrations. The oxidation rate of pyruvate + proline from isolated mitochondria of the flight muscles of 1-day-old flies was significantly reduced at high doses of antibiotics. In parallel, the level of several metabolites, including TCA cycle intermediates, was reduced in antibiotics-treated flies. Overall, antibiotics provoked a system-wide alteration of the structure and physiology of flight muscles of the blow fly Ch. albiceps, and may have fitness consequences at the organism level. Environmental antibiotic pollution is likely to have unwanted cascading ecological effects of insect population dynamics and community structure.

Recalcitrant plastics in the environment are gradually fragmented into weathered debris distinguished from their original state by the integrative action of influencing factors, such as UV light, heating and physical abrasion. As new artificial carbon-source substrates in aquatic ecosystems, plastic products can be colonized by biofilms and even utilized by microorganisms. To investigate the influences of weathering of plastics on the colonized biofilms, freshwater samples from the Yangtze River (Nanjing, China) were collected for biofilm incubation. Based on the characterization of plastics and biofilms, the effects of plastic surface properties on biofilm characteristics were revealed by the analysis of partial least squares regression (PLSR). Roughness was the principal influencing factor, while rigidity had the opposite effect to it. 16S rRNA gene high-throughput sequencing results indicated the high relative abundance of Cyanobacteria and rising proportion of harmful components (e.g., Flavobacterium) on photoaged polyethylene plastics. The microbial functional profiles (KEGG) predicted by Tax4Fun showed that the functions (e.g., membrane transport, energy metabolism, etc.) of biofilm on photoaged plastics were dissimilar with those on original ones. These findings suggested that the distinct microbial community and the adverse functional changes in biofilms on photoaged plastics potentially enhanced their environmental risks. On the other hand, 28-day cultured biofilms on original low-density polyethylene (LDPE) films were dominated by Exiguobacterium. The previously ignored potentials of this microorganism in rapidly accommodating to a hydrophobic substrate and its plastic degrading ability were both worthy of attention. Therefore, it is necessary to consider the weathering process of plastics in exploring the “plastisphere”, and to give further insights into the double-edged nature of the “plastisphere".

The consequence of the lockdowns implemented to address the COVID-19 pandemic on human health damage due to air pollution and other environmental issues must be better understood. This paper analyses the effect of reducing energy demand on the evolution of environmental impacts during the occurrence of 2020-lockdown periods in Italy, with a specific focus on life expectancy. An energy metabolism analysis is conducted based on the life cycle assessment (LCA) of all monthly energy consumptions, by sector, category and province area in Italy between January 2015 to December 2020. Results show a general decrease (by ∼5% on average) of the LCA midpoint impact categories (global warming, stratospheric ozone depletion, fine particulate matter formation, etc.) over the entire year 2020 when compared to past years. These avoided impacts, mainly due to reductions in fossil energy consumptions, are meaningful during the first lockdown phase between March and May 2020 (by ∼21% on average). Regarding the LCA endpoint damage on human health, ∼66 Disability Adjusted Life Years (DALYs) per 100,000 inhabitants are estimated to be saved. The analysis shows that the magnitude of the officially recorded casualties is substantially larger than the estimated gains in human lives due to the environmental impact reductions. Future research could therefore investigate the complex cause-effect relationships between the deaths occurred in 2020 imputed to COVID-19 disease and co-factors other than the SARS-CoV-2 virus.

Microorganisms are essential for modifying arsenic morphology, mobility, and toxicity. Still, knowledge of the microorganisms responsible for arsenic metabolism in specific arsenic-contaminated fields, such as metallurgical plants is limited. We sampled on-field soils from three depths at 70 day intervals to explore the distribution and transformation of arsenic in the soil. Arsenic-metabolizing microorganisms were identified from the mapped gene sequences. Arsenic metabolism pathways were constructed with metagenomics and AsChip analysis (a high-throughput qPCR chip for arsenic metabolism genes). It has been shown in the result that 350 genera of arsenic-metabolizing microorganisms carrying 17 arsenic metabolism genes in field soils were identified, as relevant to arsenic reduction, arsenic methylation, arsenic respiration, and arsenic oxidation, respectively. Arsenic reduction genes were the only genes shared by the 10 high-ranking arsenic-metabolizing microorganisms. Arsenic reduction genes (arsABCDRT and acr3) accounted for 73.47%–78.11% of all arsenic metabolism genes. Such genes dominated arsenic metabolism, mediating the reduction of 14.11%–19.86% of As(V) to As(III) in 0–100 cm soils. Arsenic reduction disrupts microbial energy metabolism, DNA replication and repair and membrane transport. Arsenic reduction led to a significant decrease in the abundance of 17 arsenic metabolism genes (p < 0.0001). The critical role of arsenic-reducing microorganisms in the migration and transformation of arsenic in metallurgical field soils, was emphasized with such results. These results were of pronounced significance for understanding the transformation behavior of arsenic and the precise regulation of arsenic in field soil.

Dinotefuran is a third-generation neonicotinoid pesticide and is increasingly used in agricultural production, which has adverse effects on nontarget organisms. However, the research on the impact of dinotefuran on nontarget organisms is still limited. Here the toxic effects of dinotefuran on an important economic species and a model lepidopteran insect, Bombyx mori, were investigated. Exposure to different doses of dinotefuran caused physiological disorders or death. Cytochrome P450, glutathione S-transferase, carboxylesterase, and UDP glycosyl-transferase activities were induced in the fat body at early stages after dinotefuran exposure. By contrast, only glutathione S-transferase activity was increased in the midgut. To overcome the lack of sensitivity of the biological assays at the individual organism level, RNA sequencing was performed to measure differential expressions of mRNA from silkworm larvae after dinotefuran exposure. Differential gene expression profiling revealed that various detoxification enzyme genes were significantly increased after dinotefuran exposure, which was consistent with the upregulation of the detoxifying enzyme. The global transcriptional pattern showed that the physiological responses induced by dinotefuran toxicity involved multiple cellular processes, including energy metabolism, oxidative stress, detoxification, and other fundamental physiological processes. Many metabolism processes, such as carbon metabolism, fatty acid biosynthesis, pyruvate metabolism, and the citrate cycle, were partially repressed in the midgut or fat body. Furthermore, dinotefuran significantly activated the MAPK/CREB, CncC/Keap1, PI3K/Akt, and Toll/IMD pathways. The links between physiological, biochemical toxicity and comparative transcriptomic analysis facilitated the systematic understanding of the integrated biological toxicity of dinotefuran. This study provides a holistic view of the toxicity and detoxification metabolism of dinotefuran in silkworm and other organisms.

Epidemiological studies have demonstrated a strong association of ambient fine particulate matter (PM₂.₅) exposure with the increasing mortality by ischemic heart disease (IHD), but the involved mechanisms remain poorly understood. Herein, we found that the chronic exposure of real ambient PM₂.₅ led to the upregulation of hypoxia-inducible factor-1 alpha (HIF-1α) protein in the myocardium of mice, accompanied by obvious myocardial injury and hypertrophy. Further data from the hypoxia-ischemia cellular model indicated that PM₂.₅-induced HIF-1α accumulation was responsible for the promotion of myocardial hypoxia injury. Moreover, the declined ATP level due to the HIF-1α-mediated energy metabolism remodeling from β-oxidation to glycolysis had a critical role in the PM₂.₅-increased myocardial hypoxia injury. The in-depth analysis delineated that PM₂.₅ exposure decreased the binding of prolyl hydroxylase domain 2 (PHD2) and HIF-1α and subsequent ubiquitin protease levels, thereby leading to the accumulation of HIF-1α. Meanwhile, factor-inhibiting HIF1 (FIH1) expression was down-regulated by PM₂.₅, resulting in the enhanced translocation of HIF-1α to the nucleus. Overall, our study provides valuable insight into the regulatory role of oxygen sensor-mediated HIF-1α stabilization and translocation in PM-exacerbated myocardial hypoxia injury, we suggest this adds significantly to understanding the mechanisms of haze particles-caused burden of cardiovascular disease.

Understanding the metabolic defense and compensation to maintain homeostasis is crucial for assessing the potential health risk of organic pollutants in crops. Currently, limited understanding is available regarding the targeted metabolic pathways and response mechanism under contaminant stress. This study showed that ciprofloxacin (CIP) at the environmental concentrations (1, 5, 25, 50 mg/L) did not significantly inhibit growth or cause severe oxidative damage to rice (Oryza sativa L.). Instead, the increment in CIP concentration induced a series of sequential metabolic disorders, which were characterized predominantly by primary and secondary metabolic disturbances, including phenylpropanoid biosynthesis, the carbohydrate, lipid and amino acid metabolism. After CIP in vivo exceeded a certain threshold level (>0.29 mg/g dry weight), β-glucosidases (BGLUs) mediated the transition from the activation of the genes related to phenylpropanoid biosynthesis to the inhibition of the genes related to carbohydrate metabolism in rice. In particular, starch and sucrose metabolism showed the most profound perturbation stressed by environmental concentrations of CIP (5 mg/L) and other tested organic pollutants (10 μg/L of tricyclazole, thiamethoxam, polybrominated diphenyl ethers, and polychlorinated biphenyls). Besides, the key genes encoding endoglucanase and BGLU were significantly downregulated (|log₂FC| > 3.0) under 100 μg/L of other tested organic pollutants, supporting the transition from the activation of secondary defense metabolism to the disruption of primary energy metabolism. Thus, in addition to bioaccumulation, changes in BGLU activity and starch and sucrose metabolism can reflect the potential adverse effects of pollutants on rice. This study explained the stepwise metabolic and transcriptional responses of rice to organic pollutants, which provided a new reference for the comprehensive evaluation of their environmental risks.

Microplastics (MPs) are widely found in coastal areas and oceans worldwide. The MPs are environmentally concerning due to their bioavailability and potential impacts on a wide range of marine biota, so assessing their impact on the biota has become an urgent research priority. In the present study, we exposed Crassostrea gigas oysters to irregular MPs of two polymer types (polyethylene (PE) and polyethylene terephthalate (PET)) at concentrations of 10 and 1000 μg L⁻¹ for 21 days. Accumulation of MPs, changes in metabolic enzyme activity, and histological damage were evaluated, and metabolomics analysis was conducted. Results demonstrated that PE and PET MPs were detected in the gills and digestive gland following exposure to both tested concentrations, confirming ingestion of MPs by the organisms. Moreover, both PE and PET MPs inhibited lipid metabolism, while energy metabolism enzyme activities were activated in the oysters. Histopathological damage of exposed oysters was also observed in this study. Integrated biomarker response (IBR) results showed that MPs toxicity increased with increasing MPs concentration, and the toxic effects of PET MPs on oysters was greater than PE MPs. In addition, metabolomics analysis suggested that MPs exposure induced alterations in metabolic profiles in oysters, with changes in energy metabolism and inflammatory responses. This study reports new insights into the consequences of MPs exposure in marine bivalves at environmentally relevant concentrations, providing valuable information for ecological risk assessment of MPs in a realistic conditions.

Several environmental pollutants, including pesticides, herbicides and persistent organic pollutants play an important role in the development of chronic diseases. However, most studies have examined environmental pollutants toxicity in target organisms or using a specific toxicological test, losing the real effect throughout the ecosystem. In this sense an integrative environmental risk of pollutants assessment, using different model organisms is necessary to predict the real impact in the ecosystem and implications for target and non-target organisms.The objective of this study was to use alachlor, a chloroacetanilide herbicide responsible for chronic toxicity, to understand its impact in target and non-target organisms and at different levels of biological organization by using several model organisms, including membranes of dipalmitoylphosphatidylcholine (DPPC), rat liver mitochondria, bacterial (Bacillus stearothermophilus), plant (Lemna gibba) and mammalian cell lines (HeLa and neuro2a).Our results demonstrated that alachlor strongly interacted with membranes of DPPC and interfered with mitochondrial bioenergetics by reducing the respiratory control ratio and the transmembrane potential. Moreover, alachlor also decreased the growth of B. stearothermophilus and its respiratory activity, as well as decreased the viability of both mammalian cell lines. The values of TC₅₀ increased in the following order: Lemna gibba < neuro2a < HeLa cells < Bacillus stearothermophilus. Together, the results suggest that biological membranes constitute a putative target for the toxic action of this lipophilic herbicide and point out the risks of its dissemination on environment, compromising ecosystem equilibrium and human health.