The increased frequency and intensity of short-term extreme warming phenomena have been associated to harsh biological and ecosystem outcomes (i.e., mass mortalities in marine organisms). Marine heatwaves (MHWs), occurring when seasonal temperature threshold is exceeded for at least 5 consecutive days, may reduce the tolerance of coastal species toward additional pressures, but interactions between such multiple stressors are virtually unexplored. The present study aimed to characterize in Mytilus galloprovincialis the influence of a simulated MHW scenario on the toxicological effects of the pharmaceutical carbamazepine (CBZ), ubiquitously detected in the marine environment and chosen as model compound for this relevant class of emerging contaminants. The bioaccumulation of CBZ and responsiveness of various biological parameters, including immune system, antioxidant status, lipid metabolism and cellular integrity, were analyzed in exposed mussels both during and after the end of the heatwave. MHW appeared to strongly modulate accumulation of CBZ, paralleled by weakened immunocompetence and onset of oxidative disturbance that finally evolved to cellular damages and lipid metabolism disorders. Elaboration of the overall results through a quantitative Weight of Evidence model, revealed the highest hazard in organisms exposed to both the stressors 10 days after the end of the heatwave, suggesting that MHWs could leave a footprint on the capability of mussels to counteract CBZ toxicity, thus affecting their vulnerability and predisposition to adverse effects toward multiple stressors.

Unplanned urbanization and heavy automobile use by the rapidly growing population contribute to a variety of environmental issues. Roadside plants can mitigate air pollution by modifying their enzymatic activity, physiological and anatomical traits. Plant enzymes, physiological and anatomical traits play an important role in adaptation and mitigation mechanisms against vehicular emissions. There is a significant gap in understanding of how plant enzymes and anatomical traits respond or how they participate in modulating the effect of vehicular emissions/air pollution. Modulation of leaf anatomical traits is also useful in regulating plant physiological behavior. Hence, the present study was conducted to evaluate the effects of vehicular pollution on the enzymatic activity, physiological, and anatomical traits of plant species that grow in forests (S1) and alongside roads (S2-1 km away from the S1 site) during different seasons. The present study examines four commonly found roadside tree species i.e. Grevillea robusta, Cassia fistula, Quercus leucotrichophora and Cornus oblonga. The study found that the activities of catalase and phenylalanine ammonium enzymes were higher in G. robusta species of roadside than control site (S1). Non-enzymatic antioxidants such as flavonoid and phenol were also found in higher concentrations in roadside tree species during the summer season. However, the measured values of physiological traits were higher in Q. leucotrichophora tree species of S1 during the summer season. When compared to the other species along the roadside, Q. leucotrichophora had the highest number of stomata and epidermal cells during the summer season. Hence, we found that tree species grown along the roadside adapted towards vehicular emissions by modulating their enzymatic, physiological, and anatomical traits to mitigate the effect of air pollution.

The decreasing ocean pH seems to adversely affect marine organisms, including crustaceans, which leads to potential threats to seafood safety. The present investigation evaluated the effect of seawater acidification on the edible marine mud crab Scylla serrata instars. The experimental setup was designed using a multi-cell cage based system assembled with 20 pre holed PVC pipes containing 20 individual crabs to avoid cannibalism. The crab instars were exposed to CO₂ driven acidified seawater at pH 7.8 (IPCC forecast pH at the end of the 21ˢᵗ century), 7.6, 7.4, 7.2, and 7.0 for 60 days. The crabs reared in seawater without acidification at pH 8.2 served as control. The present study revealed a notable decrease in survival, feed intake, growth, molting, tissue biochemical constituents, minerals, chitin, and alkaline phosphatase in S. serrata instar reared in acidified seawater, denotes the adverse effect of seawater acidification on crabs. The significant elevations in antioxidants, lipid peroxidation, and metabolic enzymes in all acidified seawater compared to ambient pH indicates the physiological stress of the crabs' instars. The changes in the metabolic enzymes reveal the metabolism of protein and glucose for additional energy required by the crabs to tolerate the acidic stress. Hence, the present study provides insight into the seawater acidification can adversely affect the crab S. serrata.

Rice is a staple crop, and food chain contamination of arsenic in rice grain possesses a serious health risk to billions of population. Arsenic stress negatively affects the rice growth, yield and quality of the grains. Nitric oxide (NO) is a major signaling molecule that may trigger various cellular responses in plants. The protective role of NO during arsenite (AsIII) stress and its relationship with plant physiological and metabolic responses is not explored in detail. Exogenous NO, supplemented through the roots in the form of sodium nitroprusside, has been shown to provide protection vis-à-vis AsIII toxicity. The NO-mediated variation in physiological traits such as stomatal density, size, chlorophyll content and photosynthetic rate maintained the growth of the rice plant during AsIII stress. Besides, NO exposure also enhanced the lignin content in the root, decreased total arsenic content and maintained the activities of antioxidant isoenzymes to reduce the ROS level essential for protecting from AsIII mediated oxidative damage in rice plants. Further, NO supplementation enhanced the GSH/GSSG ratio and PC/As molar ratio by modulating PC content to reduce arsenic toxicity. Further, NO-mediated modulation of the level of GA, IAA, SA, JA, amino acids and phenolic metabolites during AsIII stress appears to play a central role to cope up with AsIII toxicity. The study highlighted the role of NO in AsIII stress tolerance involving modulation of metalloid detoxification and physiological pathways in rice plants.

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by inflammation and impaired tissue regeneration, and is reported as the fourth leading cause of death worldwide by the Centers for Disease Control and Prevention (CDC). Environmental pollution and specifically motor vehicle emissions are known to play a role in the pathogenesis of COPD, but little is still known about the molecular mechanisms that are altered following diesel exhaust particles (DEP) exposure. Here we used lung organoids derived from co-culture of alveolar epithelial progenitors and fibroblasts to investigate the effect of DEP on the epithelial-mesenchymal signaling niche in the distal lung, which is essential for tissue repair. We found that DEP treatment impaired the number as well as the average diameter of both airway and alveolar type of lung organoids. Bulk RNA-sequencing of re-sorted epithelial cells and fibroblasts following organoid co-culture shows that the Nrf2 pathway, which regulates antioxidants' activity, was upregulated in both cell populations in response to DEP; and WNT/β-catenin signaling, which is essential to promote epithelial repair, was downregulated in DEP-exposed epithelial cells. We show that pharmacological treatment with anti-oxidant agents such as N-acetyl cysteine (NAC) or Mitoquinone mesylate (MitoQ) reversed the effect of DEP on organoids growth. Additionally, a WNT/β-catenin activator (CHIR99021) successfully restored WNT signaling and promoted organoid growth upon DEP exposure. We propose that targeting oxidative stress and specific signaling pathways affected by DEP in the distal lung may represent a strategy to restore tissue repair in COPD.

Ciprofloxacin (Cipro) is commonly detected in water worldwide, however, the ecotoxicological effects to aquatic biota is still not fully understood. In this study, using multiple biomarkers, it was investigated sublethal effects of short-term exposure to Cipro concentrations (1, 10 and 100 μg.L⁻¹) in the Neotropical catfish Rhamdia quelen compared to non-exposure treatment (Control). After 96 h of exposure, the fishes were anesthetized for blood collection to hematological and genotoxicity biomarkers analysis. After euthanasia, the brain and muscle were sampled for biochemical biomarkers analyses. Gills, liver and posterior kidney for genotoxicity, biochemical and histopathological biomarkers analysis and anterior intestine for histopathological biomarkers analysis. Genotoxicity was observed in all tissues, regardless of the Cipro concentrations. Hematological alterations, such as reduction of the number of erythrocytes and leucocytes, as well as in hematocrit concentration and histopathological damages, such as reduction of microridges in gill epithelium and necrosis in liver and posterior kidney, occurred mainly at 100 μg.L⁻¹. In addition, at 100 μg.L⁻¹, Cipro increased antioxidant system activity (Catalase in liver and posterior kidney). These results demonstrated that under short-term exposure, Cipro causes toxic effects in R. quelen that demands attention and surveillance of environmental aquatic concentrations of this antibiotic.

Systemic studies on the bioremediation of co-contaminated PAHs and heavy metals are lacking, and this paper provides an in-depth review on the topic. The released sources and transport of co-contaminated PAHs and heavy metals, including their co-occurrence through formation of cation-π interactions and their adsorption in soil are examined. Moreover, it is investigated that co-contamination of PAHs and heavy metals can drive a synergistic positive influence on bioremediation through enhanced secretion of extracellular polymeric substances (EPSs), production of biosynthetic genes, organic acid and enzymatic proliferation. However, PAHs molecular structure, PAHs-heavy metals bioavailability and their interactive cytotoxic effects on microorganisms can exert a challenging influence on the bioremediation under co-contaminated conditions. The fluctuations in bioavailability for microorganisms are associated with soil properties, chemical coordinative interactions, and biological activities under the co-contaminated PAHs-heavy metals conditions. The interactive cytotoxicity caused by the emergence of co-contaminants includes microbial cell disruption, denaturation of DNA and protein structure, and deregulation of antioxidant biological molecules. Finally, this paper presents the emerging strategies to overcome the bioavailability problems and recommends the use of biostimulation and bioaugmentation along with the microbial immobilization for enhanced bioremediation of PAHs-heavy metals co-contaminated sites. Better knowledge of the bioremediation potential is imperative to improve the use of these approaches for the sustainable and cost-effective remediation of PAHs and heavy metals co-contamination in the near future.

Paraquat, a widely used herbicide, causes environmental pollution, and liver injury in humans and animals. As a natural compound in fruits, ellagic acid (EA) shows anti-inflammatory and antioxidant effects. This study examines the beneficial effects of dietary EA against the paraquat-induced hepatic injury and further explores the underlying molecular mechanisms using a piglet model. Post-weaning piglets are fed basal diet supplemented with 50 mg/kg, 100 mg/kg, or 200 mg/kg EA for 3 weeks. At week 2, hepatic injury is induced by 4 mg/kg paraquat followed by 7 days recovery. EA supplementation significantly mitigates paraquat-induced hepatic fibrosis, steatosis, and high apoptotic rate. In agreement, EA supplementation reduces serum pro-inflammatory levels, ameliorates inflammatory cells infiltration into hepatic tissue, which are associated with suppressed NF-κB signaling during paraquat exposure. In addition, EA supplementation significantly improves activities of antioxidative enzymes which were correlated with activated Nrf2/Keap 1 signaling during paraquat exposure. Furthermore, EA supplementation restores cecal microbial community during paraquat exposure. The protective effect of EA is strongly linked with increased relative abundance of Lactobacillus reuteri and Lactobacillus amylovorus. Taken together, EA supplementation effectively reduced the occurrence of hepatic oxidative damage and inflammation induced by paraquat through modulating cecal microbial communities, which provides a novel nutritional therapeutic strategy for hepatic injury.

Household insecticide is largely used for insect and ectoparasite control, in city centers as well as in the countryside. The pyrethroids are the most used class of insecticide, these compounds in low doses have low toxicity for mammalians, in comparison to other compounds, with insecticide effects. The contact of these compounds in sublethal doses begins in early life and many cases, in intrauterine life. Considerable diseases still with undefined etiology, such as neurodegenerative conditions, and Huntington's Disease (HD) is one of them. HD is related to overexpression of Polyglutamine (PolyQ40), its aggregation, and non-solubilization, which leads to neural, behavioral, and cognitive damage. In our study, we evaluate the effect of two sublethal doses of a prallethrin-based insecticide (P-BI), in three different Caenorhabditis elegans life stages transgenerational, neonatal, and lifespan. We evaluated the Body bends and pharyngeal pumping rate, and social feeding as behavioral biomarkers. As well as acetylcholinesterase activity (AChE), PolyQ40 aggregation, antioxidant enzymes, and heat shock protein (HSP) expression. We observe that the toxic effect of P-BI is more pronounced on transgenerational and lifespan exposure. Both sublethal doses of P-BI decreased the AChE activity and retard the HSP expression as well as increased the PolyQ40 aggregates indicating a clear biomarker for possible effect in the progression of the HD, by the environmental contamination.

The increasing use of rare earth elements (REEs) in electric and electronic equipment has been associated with the presence of these elements in aquatic systems. The present study aimed to evaluate the toxicity of two REEs, Lanthanum (La) and Gadolinium (Gd), towards the mussel species Mytilus galloprovincialis. For this, the toxicity was assessed after a short-term exposure (14 days) to an environmentally relevant concentration of each element (10 μg/L), followed by a recovery period (14 days) in the absence of any contaminant. The measured biomarkers included energy-related parameters, activity of antioxidant and biotransformation enzymes, indicators of oxidative damage, levels of oxidized glutathione and neurotoxicity. After exposure mussels accumulated more La (0.54 μg/g) than Gd (0.15 μg/g). After recovery higher concentration decrease was observed for Gd (≈40% loss) compared to La exposed mussels (≈30% loss) which may be associated with lower detoxification capacity of mussels previously exposed to La. Mussels increased their metabolism (i.e., higher electron transport system activity) only after the exposure to Gd. Exposure to La and Gd resulted into lower energy expenditure, while when both elements were removed glycogen and protein concentrations decreased to values observed in non-contaminated mussels. Antioxidant and biotransformation capacity was mainly increased in the presence of Gd. This defense response avoided the occurrence of cellular damage but still loss of redox balance was found regardless the contaminant, which was re-established after the recovery period. Neurotoxicity was only observed in the presence of Gd with no effects after the recovery period. Results showed that a short-term exposure to La and especially to Gd can exert deleterious effects that may compromise specific biochemical pathways in aquatic species, such as M. galloprovincialis, but under low concentrations organisms can be able to re-establish their biochemical status to control levels after a recovery period.