Possibilities of the use of progressive methods in artificial regeneration of areas affected by air pollutants are namely modification of soil environment, active protection of planting stock against root desiccation, use of containerized planting stock for artificial regeneration of clearings, which resulted from air pollution

Sex determination is a complex process that can be influenced by environment in various taxa. Disturbed environments can affect population sex ratios and thus threaten their viability. Emerging evidences support a role of epigenetic mechanisms, notably DNA methylation, in environmental sex determination (ESD). In this work, using zebrafish as model and a transgenerational experiment comprising 4 successive generations, we report a strength link between the promotor methylation level of three genes in female gonads and population sex ratio. One generation of zebrafish was exposed throughout its lifetime to cadmium (Cd), a non-essential metal, at an environmentally relevant concentration. The subsequent generations were not exposed. At the first and the third generation a subset of individuals was exposed to an elevated temperature, a well-known masculinizing factor in zebrafish. While heat was associated to an increase in the methylation level of cyp19a1a gene and population masculinization, foxl2a/dmrt1 methylation levels appeared to be influenced by Cd and fish density leading to offspring feminization. Ancestral Cd exposure indeed led to a progressive feminization of the population over generations and affected the sex plastic response of zebrafish in response to heat. The effect of Cd on the methylation level of foxl2a was observed until the third generation, supporting potential transgenerational inheritance. Our results support (i) a key role of cyp19a1a methylation in SD in zebrafish in response to environmental cues and (ii) the fact that the environment experienced by parents, namely mothers in the present case, can affect their offspring sex ratio via environment-induced DNA methylation changes in gonads.

Atrazine is an herbicide commonly used in several countries. Due to its long half-life, associated with its use in large scales, atrazine residues remain as environmental pollutants in water bodies. Phytoremediation is often pointed out as an interesting approach to remove atrazine from the aquatic environment, but its practical application is limited by the high toxicity of this herbicide. Here, we characterize the damages triggered by atrazine in Pistia stratiotes, evaluating the role of nitric oxide (NO), a cell-signaling molecule, in increasing the tolerance to the pollutant and the phytoremediation potential of this species. Pistia stratiotes plants were exposed to four treatments: Control; Sodium nitroprusside (SNP) (0.05 mg L⁻¹); Atrazine (ATZ) (150 μg L⁻¹) and ATZ + SNP. The plants remained under those conditions for 24 h for biochemical and physiological analysis and 3 days for the evaluation of relative growth rate. The presence of atrazine in plant cells triggered a series of biochemical and physiological damages, such as the increase in the generation of reactive oxygen species, damages to cell membranes, photosynthesis impairment, and negative carbon balance. Despite this, the plants maintained greater growth rates than other aquatic macrophytes exposed to atrazine and showed high bioconcentration and translocation factors. The addition of SNP, a NO donor, decreased the herbicide toxicity, with an increase of over 60% in the IC₅₀ value (Inhibitor Concentration). Indeed, the NO signaling action was able to increase the tolerance of plants to atrazine, which resulted in increments in pollutant uptake and translocation, with the maintenance of overall cell (e.g. membranes) and organs (root system) structure, and the functioning of central physiological processes (e.g. photosynthesis). These factors allowed for more quickly and efficient removal of the pollutant from the environment, reducing costs, and increasing the viability of the phytoremediation process.

Pendimethalin (PDM) is a dinitroaniline crop pesticide that is extensively utilized worldwide. However, the reproductive toxicity and cellular mechanisms of PDM have not been identified. Therefore, we elucidated the adverse effects of PDM on the reproductive system using mouse testicular Leydig and Sertoli cells (TM3 and TM4 cells, respectively). Our results demonstrated that PDM suppressed the viability and proliferation of TM3 and TM4 cells. Additionally, PDM induced cytosolic calcium upregulation and permeabilization of mitochondrial membrane potential in both TM3 and TM4 cells. We also verified that PDM activates the endoplasmic reticulum (ER) stress pathway and autophagy. Furthermore, we confirmed that activation of ER stress and autophagy were blocked by 2-aminoethoxydiphenyl borate (2-APB) treatment. Finally, we confirmed PDM-induced cell cycle arrest and apoptosis in TM3 and TM4 cells. Thus, we first demonstrated that PDM impedes the survival of testis cells, and further, their function.

The objective of this study was to evaluate the biological and nutritional characteristics of Spodoptera frugiperda (Lepidoptera: Noctuidae), an arthropod pest widely distributed in agricultural regions, after exposure to nano-CeO₂ via an artificial diet and to investigate the presence of cerium in the body of this insect through X-ray fluorescence mapping. Nano-CeO₂, micro-CeO₂, and Ce(NO₃)₃ were incorporated into the diet (0.1, 1, 10, and 100 mg of Ce L⁻¹). Cerium was detected in caterpillars fed with diets containing nano-CeO₂ (1, 10 and 100 mg of Ce L⁻¹), micro-CeO₂ and Ce(NO₃)₃, and in feces of caterpillars from the first generation fed diets with nano-CeO₂ at 100 mg of Ce L⁻¹ as well. The results indicate that nano-CeO₂ caused negative effects on S. frugiperda. After it was consumed by the caterpillars, the nano-CeO₂ reduced up to 4.8% of the pupal weight and 60% of egg viability. Unlike what occurred with micro-CeO₂ and Ce(NO₃)₃, nano-CeO₂ negatively affected nutritional parameters of this insect, as consumption rate two times higher, increase of up to 80.8% of relative metabolic rate, reduction of up to 42.3% efficiency of conversion of ingested and 47.2% of digested food, and increase of up to 1.7% of metabolic cost and 8.7% of apparent digestibility. Cerium caused 6.8–16.9% pupal weight reduction in second generation specimens, even without the caterpillars having contact with the cerium via artificial diet. The results show the importance of new ecotoxicological studies with nano-CeO₂ for S. frugiperda in semi-field and field conditions to confirm the toxicity.

Evidence about the adverse effects of methamphetamine (METH) on invertebrates is scarce. Hence, C. elegans, a representative invertebrate model, was exposed to METH at environmental levels to estimate chronic and transgenerational toxicity. The results of chronic exposure were integrated into an underlying toxicity framework of METH in invertebrates (e.g., benthos) at environmentally relevant concentrations. The induction of cellular oxidative damage-induced apoptosis and fluctuation of ecologically important traits (i.e., feeding and locomotion) might be attributed by the activation of the longevity regulating pathway regulated by DAF-16/FOXO, and detoxification by CYP family enzymes. The adverse effects to the organism level included impaired viability and decreased fecundity. The results from transgenerational exposure elucidated the cumulative METH-induced damage in invertebrates. Finally, a new risk assessment method named toxicity indicator sensitivity distribution (TISD) analysis was proposed by combining multiple toxicity indicator test data (ECₓ) to derive the hazardous concentration for 10% indicators (C₁₀) of one species. The risk quotient (RQ) values calculated by measured environmental concentrations and C₁₀ in southern China, southeastern Australia, and the western US crossed the alarm line (RQ = 5), suggesting a need for long-term monitoring.

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.

Whether virulent human pathogenic coronaviruses (SARS-CoV, MERS-CoV, SARS-CoV-2) are effectively transmitted by aerosols remains contentious. Transmission modes of the novel coronavirus have become a hot topic of research with the importance of airborne transmission controversial due to the many factors that can influence virus transmission. Airborne transmission is an accepted potential route for the spread of some viral infections (measles, chickenpox); however, aerosol features and infectious inoculum vary from one respiratory virus to another. Infectious virus-laden aerosols can be produced by natural human respiratory activities, and their features are vital determinants for virus carriage and transmission. Physicochemical characteristics of infectious respiratory aerosols can influence the efficiency of virus transmission by droplets. This critical review identifies studies reporting instances of infected patients producing airborne human pathogenic coronaviruses, and evidence for the role of physical/chemical characteristics of human-generated droplets in altering embedded viruses’ viability. We also review studies evaluating these viruses in the air, field studies and available evidence about seasonality patterns. Ultimately the literature suggests that a proportion of virulent human coronaviruses can plausibly be transmitted via the air, even though this might vary in different conditions. Evidence exists for respirable-sized airborne droplet nuclei containing viral RNA, although this does not necessarily imply that the virus is transmittable, capable of replicating in a recipient host, or that inoculum is sufficient to initiate infection. However, evidence suggests that coronaviruses can survive in simulated droplet nuclei for a significant time (>24 h). Nevertheless, laboratory nebulized virus-laden aerosols might not accurately model the complexity of human carrier aerosols in studying airborne viral transport. In summary, there is disagreement on whether wild coronaviruses can be transmitted via an airborne path and display seasonal patterns. Further studies are therefore required to provide supporting evidence for the role of airborne transmission and assumed mechanisms underlying seasonality.

Excess fluoride in drinking water is an environmental issue of increasing worldwide concern, because of its adverse effect on human health. Skeletal fluorosis caused by chronic exposure to excessive fluoride is a metabolic bone disease characterized by accelerated bone turnover accompanied by aberrant activation of osteoblasts. It is not clear whether Wnt/β-catenin signaling, an important signaling pathway regulating the function of osteoblasts, mediates the pathogenesis of skeletal fluorosis. A cross-sectional case-control study was conducted in Tongyu County, Jilin Province, China showed that fluoride stimulated the levels of OCN and OPG, resulting in accelerated bone turnover in patients with skeletal fluorosis. To investigate the influence of fluoride on Wnt/β-catenin signaling pathway, 64 male BALB/c mice were allotted randomly to four groups and treated with deionized water containing 0, 55, 110 and 221 mg/L NaF for 3 months, respectively. The results demonstrated that fluoride significantly increased mouse cancellous bone formation and the protein expression of Wnt3a, phospho-GSK3β (ser 9) and Runx2. Moreover, partial correlation analysis indicated that there was no significant correlation between fluoride exposure and Runx2 protein levels, after adjusting for β-catenin, suggesting that β-catenin might play a crucial role in fluoride-induced aberrant osteogenesis. In vivo, viability of SaoS2 cells was significantly facilitated by 4 mg/L NaF, and fluoride could induce the abnormal activation of Wnt/β-catenin signaling, the expression of its target gene Runx2 and significantly increased Tcf/Lef reporter activity. Importantly, inhibition of β-catenin suppressed fluoride-induced Runx2 protein expression and the osteogenic phenotypes. Taken together, the present study provided in vivo and in vitro evidence reveals a potential mechanism for fluoride-induced aberrant osteoblast activation and indicates that β-catenin is the pivot molecule mediating viability and differentiation of osteoblasts and might be a therapeutic target for skeletal fluorosis.