Melatonin (M) is a pleiotropic molecule that improves plant growth and increases heavy metal tolerance. The role of M for improving plant growth and tolerance under cadmium (Cd) stress, and mitigation of Cd-induced toxicity has not yet been sufficiently examined. Therefore, here we conducted a glasshouse experiment to explore the influence of various M dosages on Cd detoxification and stress-tolerance responses of Brassica napus under high Cd content (30 mg kg⁻¹). The effects of M on the modulation of Cd tolerance in B. napus plants have been investigated using various growth attributes, Cd accumulation and tolerance indices, and secondary metabolic parameters. We found that Cd stress inhibited root growth (by 11.9%) as well as triggered reactive oxygen species accumulation (by 31.2%) and MDA levels (by 18.7%); however, exogenous M substantially alleviated the adverse effect of oxidative stress by decreasing levels of H₂O₂ (by 38.7%), MDA (by 13.8%) and EL (by 1.8%) in the Cd-stressed plants, as compared to the M-untreated plants (control). Interestingly, exogenous M reduced Cd accumulation in roots (∼48.2–58.3-fold), stem (∼2.9–5.0-fold) and leaves (∼4.7–6.6-fold) compared to control plants, which might be due to an M-induced defense and/or detoxification response involving a battery of antioxidants. Overall, addition of the exogenous M to the Cd-stressed plants profoundly enhanced Cd tolerance in B. napus relative to control plants. These results suggested the biostimulatory role (at the physiological and molecular level) of M in improving growth, Cd tolerance, and Cd detoxification in B. napus, which indicate the potentiality of M for green remediation of Cd contaminated soils. This green trial would provide a reference for producing renewable bioenergy crops under Cd stress in contaminated soils. However, these recommendations should be verified under field conditions and the potential mechanisms for the interaction between Cd and M should be explicitly explored.

Nowadays, marine ecosystems are under severe threat from the simultaneous presence of multiple stressors, including microplastics (MPs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (B[a]P). In addition to their presence in various marine compartments, there are increasing concerns on the potential capacity of MPs to sorb, concentrate and transfer these pollutants in the environment. Although their ecotoxicological impacts are currently evident, few works have studied the combined effects of these contaminants. Therefore, the major purpose of this work was to assess the toxicity of environmental relevant concentrations of MPs (<30 μm) and B[a]P, alone and in mixture, in the seaworm Hediste diversicolor by exploring their accumulation and hazardous biological effects for 3 and 7 days. Environmental MPs were able to increase B[a]P in a time-dependent manner. The obtained results showed that individual treatments, as well as co-exposure to contaminants, caused cytotoxicity and genotoxicity in the cœlomic fluid cells, while oxidative stress effects were observed at tissue and gene levels associated with alteration in neurotransmission. Overall, our findings provide additional clues about MPs as organic pollutant vectors in the marine environment, and contribute to a clearer understanding of their toxicological risk to aquatic invertebrates.

The experiment was conducted to investigate the effects of Cadmium (Cd) on growth performance, blood biochemical parameters, oxidative stress, hepatocyte apoptosis and autophagy of weaned piglets. A total of 12 healthy weaned piglets were randomly assigned to the control and the Cd group, which were fed with a basal diet and the basal diet supplemented with 15 ± 0.242 mg/kg CdCl₂ for 30 d, respectively. Our results demonstrated that Cd significantly decreased final body weight, average daily feed intake (ADFI), average daily gain (ADG) and increased feed-to-gain (F/G) ratio (P < 0.05). For blood biochemical parameters, Cd treatment significantly decreased the red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), total protein, albumin, copper content and iron content (P < 0.05). In addition, liver injury was observed in the Cd-exposed group. Our results also demonstrated that Cd exposure contributed to the production of ROS, activated the AMPK/PPAR-γ/NF-κB pathway (increasing the expressions of P-AMPK/AMPK, NF-κB, I-κB-β, COX-2, and iNOS, decreasing the expressions of PPAR-γ and I-κB-α), finally induced autophagy (increasing the expressions of Beclin-1, the ratio of LC3-II/LC3-I and p62), and apoptosis (increasing the expressions of Bax, Bak, Caspase-9, and Caspase-3, decreasing the expression of Bcl-2). Overall, these findings revealed the vital role of AMPK/PPAR-γ/NF-κB pathway in Cd-induced liver apoptosis and autophagy, which provided deeper insights into a better understanding of Cd-induced hepatotoxicity.

Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

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.

Hydrothermal carbonization is considered a powerful technology to convert sewage sludge (SS) into a valuable carbonaceous solid known as hydrochar (HC). Up to now criteria for landfill application of SS and HC are based only on physicochemical properties and levels of pollutant residues. Nevertheless, to ensure their safe environmental applications it is mandatory to develop biosensors which can provide relevant information on their toxic potential for natural ecosystems. Therefore, this study aimed to assess the suitability of a contact assay using zebrafish embryo/larvae combined with sub-lethal end-points to evaluate the hazard associated with SS and related HC exposure. A suite of biomarkers was also applied on larvae, related to detoxification and oxidative stress as the activity of Ethoxyresorufin-O-deethylase, glutathione-S-transferase, and catalase, the content of reactive oxygen species and the behavioral assay using the DanioVision™ chamber. Legacy priority pollutants were also measured either in SS and HC tested samples and in contact waters. The exposure to SS caused higher lethality compared to HC. No significant changes in the activity of oxidative stress markers was observed upon exposure to both matrices. The behavioral test showed a hypoactivity condition in larvae exposed to both SS and HC with the effects of SS stronger than HC. Chemical analysis revealed the presence of trace elements and halogenated compounds in either SS, HC. Heavy metals were also released in contact waters, while volatile hydrocarbons (C6–C10) and halogenated compounds resulted below LOD (<0.05 μ L⁻¹). Our study highlights the suitability of zebrafish embryotoxicity test, coupled with behavioral traits, as screening tool for assessing potential risks, associated with the landfill application of both SS and HC, for aquatic wildlife.

Mutations are an important origin of antibiotic resistance in bacteria. While there is increasing evidence showing promoted resistance mutations by environmental stresses, no retrospective research has yet been conducted on this phenomenon and its mechanisms. Herein, we summarized the phenomena of stress-elevated resistance mutations in bacteria, generalized the regulatory mechanisms and discussed the environmental and human health implications. It is shown that both chemical pollutants, such as antibiotics and other pharmaceuticals, biocides, metals, nanoparticles and disinfection byproducts, and non-chemical stressors, such as ultraviolet radiation, electrical stimulation and starvation, are capable of elevating resistance mutations in bacteria. Notably, resistance mutations are more likely to occur under sublethal or subinhibitory levels of these stresses, suggesting a considerable environmental concern. Further, mechanisms for stress-induced mutations are summarized in several points, namely oxidative stress, SOS response, DNA replication and repair systems, RpoS regulon and biofilm formation, all of which are readily provoked by common environmental stresses. Given bacteria in the environment are confronted with a variety of unfavorable conditions, we propose that the stress-elevated resistance mutations are a universal phenomenon in the environment and represent a nonnegligible risk factor for ecosystems and human health. The present review identifies a need for taking into account the pollutants’ ability to elevate resistance mutations when assessing their environmental and human health risks and highlights the necessity of including resistance mutations as a target to prevent antibiotic resistance evolution.

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.

Exposure to endocrine disruptors such as bisphenols, can lead to and be the explanation for idiopathic infertility. In our study, we assessed the effect of exposure to bisphenol S (BPS) via breast milk on the testicular tissue health of adult male mice. Milking dams were exposed to BPS through drinking water (0.216 ng g bw/day and 21.6 ng g bw/day) from post-natal day 0–15. Although there was no significant difference in testicular histopathology between the control and experimental groups, we observed an increase in the number of tight and gap junctions in the blood-testis barrier (BTB) of adult mice after nursing BPS exposure. Moreover, there was an increase in oxidative stress markers in adult testicular tissue of mice exposed during nursing. Our nursing model indicates that breast milk is a route of exposure to an endocrine disruptor that can be responsible for idiopathic male infertility through the damage of the BTB and weakening of oxidative stress resistance in adulthood.

The main intent of the current research was to appraise if combined application of hydrogen sulfide (H₂S, 0.2 mM) and silicon (Si 2.0 mM) could improve tolerance of tomato plants to arsenic (As as sodium hydrogen arsenate heptahydrate, 0.2 mM) stress. Plant growth, chlorophylls (Chl), PSII maximum efficiency (Fv/Fm), H₂S concentration and L-cysteine desulfhydrase activity were found to be suppressed, but leaf and root As, leaf proline content, phytochelatins, malondialdehyde (MDA) and H₂O₂ as well as the activity of lipoxygenase (LOX) increased under As stress. H₂S and Si supplied together or alone enhanced the concentrations of key antioxidant biomolecules such as ascorbic acid, and reduced glutathione and the activities of key antioxidant system enzymes including catalase (CAT), superoxide dismutase (SOD), dehydroascorbate reductase (DHAR), glutathione reductase (GR), and glutathione S-transferase (GST). In comparison with individual application of H₂S or Si, the joint supplementation of both had better effect in improving growth and key biochemical processes, and reducing tissue As content, suggesting a putative collaborative role of both molecules in improving tolerance to As-toxicity in tomato plants.