Morphological tools can assist in the evaluation of effects of insecticides on non-target insects. Pyriproxyfen, a juvenile hormone analog, is known to interfere with growth and metamorphosis of insects. However, there are studies showing indirect effects on natural enemies, including green lacewings. Few prior studies describe morphological effects of pyriproxyfen on target insect organs, especially on natural enemies. Through morphological tools, this study aimed to characterize the midgut and fat body, both important organs of digestion and great metabolic activity respectively, of the predator Ceraeochrysa claveri after chronic exposure to pyriproxyfen. Larvae of C. claveri were fed Diatraea saccharalis egg clusters treated with pyriproxyfen in solution of 50 or 100 mg a.i. L⁻¹ throughout the larval stage. The biological data revealed significant increases in development time, especially in the third instar, and in cumulative mortality from the prepupal into the pupal stage. Morphological analysis of adult midgut (≤24 h old) showed damage including formation of epithelial folds, intercellular spaces, emission of cytoplasmic protrusions. Both fat body regions presented decrease of lipid droplets, vacuolization of trophocytes and mitochondrial injury featuring a multisystemic action. In both organs, pyriproxyfen exposure induced significant oxidative stress by mitochondrial superoxide production. Cytoprotective responses were induced in midgut and fat body cells by augmenting the number of cytoplasmic granules containing calcium and expression of HSP 90. Both organs proved to be efficient in presenting histopathological alterations, showing the sensitivity and applicability of this morphological tool for evaluating other insecticides in non-target organisms.

Air pollution exposure is a public health emergency, which attributes globally to an estimated seven million deaths on a yearly basis We are all exposed to air pollutants, varying from ambient air pollution hanging over cities to dust inside the home. It is a mixture of airborne particulate matter and gases that can be subdivided into three categories based on particle diameter. The smallest category called PM₀.₁ is the most abundant. A fraction of the particles included in this category might enter the blood stream spreading to other parts of the body. As air pollutants can enter the body via the lungs and gut, growing evidence links its exposure to gastrointestinal and respiratory impairments and diseases, like asthma, rhinitis, respiratory tract infections, Crohn's disease, ulcerative colitis, and abdominal pain. It has become evident that there exists a crosstalk between the respiratory and gastrointestinal tracts, commonly referred to as the gut-lung axis. Via microbial secretions, metabolites, immune mediators and lipid profiles, these two separate organ systems can influence each other. Well-known immunomodulators and gut health stimulators are probiotics, prebiotics, together called synbiotics. They might combat air pollution-induced systemic inflammation and oxidative stress by optimizing the microbiota composition and microbial metabolites, thereby stimulating anti-inflammatory pathways and strengthening mucosal and epithelial barriers. Although clinical studies investigating the role of probiotics, prebiotics, and synbiotics in an air pollution setting are lacking, these interventions show promising health promoting effects by affecting the gastrointestinal- and respiratory tract. This review summarizes the current data on how air pollution can affect the gut-lung axis and might impact gut and lung health. It will further elaborate on the potential role of probiotics, prebiotics and synbiotics on the gut-lung axis, and gut and lung health.

The exposure of Caenorhabditis elegans to polystyrene (PS) beads of a wide range of sizes impedes feeding, by reducing food consumption, and has been linked to inhibitory effects on the reproductive capacity of this nematode, as determined in standardized toxicity tests. Lipid storage provides energy for longevity, growth, and reproduction and may influence the organismal response to stress, including the food deprivation resulting from microplastics exposure. However, the effects of microplastics on energy storage have not been investigated in detail. In this study, C. elegans was exposed to ingestible sizes of PS beads in a standardized toxicity test (96 h) and in a multigeneration test (∼21 days), after which lipid storage was quantitatively analyzed in individual adults using coherent anti-Stokes Raman scattering (CARS) microscopy. The results showed that lipid storage distribution in C. elegans was altered when worms were exposed to microplastics in form of PS beads. For example, when exposed to 0.1-μm PS beads, the lipid droplet count was 93% higher, the droplets were up to 56% larger, and the area of the nematode body covered by lipids was up to 79% higher than in unexposed nematodes. The measured values tended to increase as PS bead sizes decreased. Cultivating the nematodes for 96 h under restricted food conditions in the absence of beads reproduced the altered lipid storage and suggested that it was triggered by food deprivation, including that induced by the dilutional effects of PS bead exposure. Our study demonstrates the utility of CARS microscopy to comprehensively image the smaller microplastics (<10 μm) ingested by nematodes and possibly other biota in investigations of the effects at the level of the individual organism.

Cadmium (Cd) is a potentially hazardous element with substantial biological toxicity, adversely affecting plant growth and physiological metabolism. Therefore, it is necessary to explore practical and environment-friendly approaches to reduce toxicity. Jasmonic acid (JA) is an endogenous growth regulator which helps plants defend against biological and abiotic stresses. To determine how JA help relieve Cd toxicity in rice, both laboratory and field experiments were implemented. In the seedling stage, the role of JA in mediating rice Cd tolerance was investigated via a fluorescent probe in vivo localization, Fourier Transform Infrared Spectroscopy (FTIR), and colorimetry. At the mature growth stage of rice, field experiments were implemented to research the effects of JA on the Cd uptake and translocation in rice. In the seedling stage of rice, we found that JA application increased the cell wall compartmentalization of Cd by promoting the Cd combination on chelated-soluble pectin of rice roots and inhibited Cd movement into protoplasts, thereby reducing the Cd content in the roots by 30.5% and in the shoots by 53.3%, respectively. Application of JA reduced H₂O₂ content and helped relieve Cd-induced peroxidation damage of membrane lipid by increasing the level of catalase (CAT), peroxidase (POD), ascorbate peroxidase (APX), and glutathione (GSH), but had no significant effect on the superoxide dismutase (SOD) activity. Additionally, field experiments showed that foliar spraying of JA inhibited rice Cd transport from the stalk and root to the grain and reduced Cd concentration in grain by 29.7% in the high-Cd fields and 28.0% in the low-Cd fields. These results improve our understanding of how JA contributes to resistance against Cd toxicity in rice plants and reduces the accumulation of Cd in rice kernels.

RNA N⁶-methyladenosine (m⁶A) modification regulates the cell stress response and homeostasis, but whether titanium dioxide nanoparticle (nTiO₂)-induced acute pulmonary injury is associated with the m⁶A epitranscriptome and the underlying mechanisms remain unclear. Here, the potential association between m⁶A modification and the bioeffects of several engineered nanoparticles (nTiO₂, nAg, nZnO, nFe₂O₃, and nCuO) were verified thorough in vitro experiments. nFe₂O₃, nZnO, and nTiO₂ exposure significantly increased the global m⁶A level in A549 cells. Our study further revealed that nTiO₂ can induce m⁶A-mediated acute pulmonary injury. Mechanistically, nTiO₂ exposure promoted methyltransferase-like 3 (METTL3)-mediated m⁶A signal activation and thus mediated the inflammatory response and IL-8 release through the degeneration of anti-Mullerian hormone (AMH) and Mucin5B (MUC5B) mRNAs in a YTH m⁶A RNA-binding protein 2 (YTHDF2)-dependent manner. Moreover, nTiO₂ exposure stabilized METTL3 protein by the lipid reactive oxygen species (ROS)-activated ERK1/2 pathway. The scavenging of ROS with ferrostatin-1 (Fer-1) alleviates the ERK1/2 activation, m⁶A upregulation, and the inflammatory response caused by nTiO₂ both in vitro and in vivo. In conclusion, our study demonstrates that m⁶A is a potential intervention target for alleviating the adverse effects of nTiO₂-induced acute pulmonary injury in vitro and in vivo, which has far-reaching implications for protecting human health and improving the sustainability of nanotechnology.

Decabromodiphenyl ethane (DBDPE), as one of the most widely used new brominated flame retardants (NBFRs), can pose a potential threat to human health and the environment. An integrated transcriptome and proteome was performed for investigating the toxicological molecular mechanisms of Pleurotus ostreatus (P. ostreatus) during the biodegradation of DBDPE at the concentrations of 5 and 20 mg/L. A total of 1193/1018 and 92/126 differentially expressed genes/proteins (DEGs/DEPs) were found, respectively, with DBDPE exposure at 5 and 20 mg/L. These DEGs and DEPs were mainly involved in the cellular process as well as metabolic process. DEPs for oxidation-reduction process and hydrolase activity were up-regulated, and those for membrane, lipid metabolic process and transmembrane transport were down-regulated. The DEGs and DEPs related to some key enzymes were down-regulated, such as NADH dehydrogenase/oxidoreductase, succinate dehydrogenase, cytochrome C1 protein, cytochrome-c oxidase/reductase and ATP synthase, which indicated that DBDPE affected the oxidative phosphorylation as well as tricarboxylic acid (TCA) cycle. Cytochrome P450 enzymes (CYPs) might be involved in DBDPE degradation through hydroxylation and oxidation. Some stress proteins were induced to resist DBDPE toxicity, including major facilitator superfamily (MFS) transporter, superoxide dismutase (SOD), molecular chaperones, heat shock proteins (HSP20, HSP26, HSP42), 60S ribosomal protein and histone H4. The findings help revealing the toxicological molecular mechanisms of DBDPE on P. ostreatus, aiming to improve the removal of DBDPE.

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.

Oxytetracycline (OTC) and Cu are prevalent in aquatic ecosystems and their pollution are issues of serious concern. The present working hypothesis is that the toxicity of Cu and OTC mixture on physiological activity of fish was different from single OTC and Cu alone. The present study indicated that, compared to single OTC or Cu alone, Cu+OTC mixture reduced growth performance and feed utilization of grass carp, escalated the contents of Cu, OTC and TG, increased lipogenesis, induced oxidative stress, damaged the mitochondrial structure and functions and inhibited the lipolysis in the liver tissues and hepatocytes of grass carp. Cu+OTC co-treatment significantly increased the mRNA abundances and protein expression of Nrf2. Moreover, we found that Cu+OTC mixture-induced oxidative stress promoted Nrf2 recruitment to the SREBP-1 promoter and increased SREBP-1-mediated lipogenesis; Nrf2 sited at the crossroads of oxidative stress and lipid metabolism, and mediated the regulation of oxidative stress and lipid metabolism. Our findings clearly indicated that OTC and Cu mixture differed in environmental risks from single antibiotic or metal element itself, and thus posed different toxicological responses to aquatic animals. Moreover, our findings suggested that Nrf2 functioned as an important antioxidant regulator linking oxidative stress to lipogenic metabolism, and thus elucidated a novel regulatory mechanism for lipid metabolism.

While polychlorinated biphenyl (PCB)-related risks have been reported at the cellular, organ, and individual levels in some marine mammals, studies quantifying the PCB-associated population-level effects are limited. Here, we combined chemical analysis and individual-based model simulation to investigate the impact of PCBs on the Indo-Pacific humpback dolphin (sub)population from the Pearl River Estuary (PRE). An annual PCB accumulation rate of 0.29 ± 0.07 mg/kg lipid per year was estimated based on the measured age-specific male data as males continue to accumulate PCBs throughout their lifetime, without depurating contaminant loads. Using the Taiwan Strait dolphin population with low PCBs as a baseline, we compare our model simulations in PRE population to estimate relative population impacts of PCBs and other stressors. When using the current vital rates of the PRE dolphins which have been affected by PCBs and other stressors (e.g., underwater noise, prey limitation, etc.), our simulations revealed a substantial decline (8.1%) in the annual population growth rate (λ) of PRE metapopulation compared to baseline over the next 100 years. At the estimated PCB accumulation rate, the PCB-mediated effects on calf survival and immunity would cause a slight decline (0.9%) in λ relative to baseline. Our findings suggest a relatively limited impact of PCBs on the long-term survival of PRE dolphins among all stressors. However, it should be noted that even under model simulations where dietary PCBs were eliminated, humpback dolphins would still need a long time to reduce their PCB burdens to a relatively “safe” level through biological cycling. Considering that the baseline vital rates might also have been affected by PCBs and other stressors, our results are considered relative rather than absolute. This study provides a starting point for quantifying population-level consequences of contaminant exposure on humpback dolphins, although more efforts are needed to perfect this type of analysis.