Cadmium (Cd) and lead (Pb) are known to enhance immune cell damages and to decrease cellular immunity, promoting higher susceptibility to infectious diseases. Selenium (Se) is an essential element involved in immunity and reactive oxygen species scavenging. This study aimed at evaluating how Cd and Pb and low nutritional (Se) quality modulate immune response to a bacterial lipopolysaccharide (LPS) challenge in wood mice (Apodemus sylvaticus). Mice were trapped near a former smelter in northern France in sites of High or Low contamination. Individuals were challenged immediately after capture or after five days of captivity, fed a standard or a Se-deficient diet. Immune response was measured with leukocyte count and plasma concentration of TNF-α, a pro-inflammatory cytokine. Faecal and plasma corticosterone (CORT), a stress-hormone involved in anti-inflammatory processes, was measured to assess potential endocrine mechanisms. Higher hepatic Se and lower faecal CORT were measured in free-ranging wood mice from High site. LPS-challenged individuals from High site showed steeper decrease of circulating leukocytes of all types, higher TNF-α concentrations, and a significant increase of CORT, compared to individuals from Low site. Challenged captive animals fed standard food exhibited similar patterns (decrease of leukocytes, increase of CORT, and detectable levels of TNF-α), with individuals from lowly contaminated site having higher immune responses than their counterparts from highly polluted site. Animals fed Se-deficient food exhibited lymphocytes decrease, no CORT variation, and average levels of TNF-α. These results suggest (i) a higher inflammatory response to immune challenge in free-ranging animals highly exposed to Cd and Pb, (ii) a faster recovery of inflammatory response in animals lowly exposed to pollution when fed standard food than more exposed individuals, and (iii) a functional role of Se in the inflammatory response. The role of Se and mechanisms underlying the relationship between glucocorticoid and cytokine remain to be elucidated.

A pre-diabetes syndrome induced by endocrine disruptors (ED) was recently demonstrated in the model amphibian Silurana (Xenopus) tropicalis and was suggested to be a potential cause of amphibian population decline. However, such effects have not been found in wild type frogs exposed to ED and the capacity of amphibians to physiologically develop diabetes under natural conditions has not been confirmed. This study showed that a high fat diet (HFD) model displaying the important characteristics of mammal HFD models including glucose intolerance, insulin resistance and nonalcoholic fatty liver disease (NAFLD) can be developed with green frogs (Pelophylax spp.). Wild green frogs exposed to 10 μg L⁻¹ benzo [a]pyrene (BaP) for 18 h also displayed several characteristics of the pre-diabetes phenotype previously observed in Xenopus including glucose intolerance, gluconeogenesis activation and insulin resistance. The study results confirmed that metabolic disorders induced by ED in wild green frogs are typical of the pre-diabetes phenotype and could serve as a starting point for field studies to determine the role of ED in the decline of amphibian populations. From an environmental perspective, the response of wild green frogs to different ED (10 μg L⁻¹) suggests that a simple glucose-tolerance test could be used on wild anurans to identify bodies of water polluted with metabolic disruptors that could affect species fitness.

A large number of toxicity studies report abnormalities in early life-stage (ELS) fish that are described here as a sublethal toxicity syndrome (TxSnFELS) and generally include a reduced heart rate, edemas (yolk sac and cardiac), and a variety of morphological abnormalities. The TxSnFELS is very common and not diagnostic for any chemical or class of chemicals. This sublethal toxicity syndrome is mostly observed at high exposure concentrations and appears to be a baseline, non-specific toxicity response; however, it can also occur at low doses by specific action. Toxicity metrics for this syndrome generally occur at concentrations just below those causing mortality and have been reported for a large number of diverse chemicals. Predictions based on tissue concentrations or quantitative-structure activity relationship (QSAR) models support the designation of baseline toxicity for many of the tested chemicals, which is confirmed by observed values. Given the sheer number of disparate chemicals causing the TxSnFELS and correlation with QSAR derived partitioning; the only logical conclusion for these high-dose responses is baseline toxicity by nonspecific action and not a lock and key type receptor response. It is important to recognize that many chemicals can act both as baseline toxicants and specific acting toxicants likely via receptor interaction and it is not possible to predict those threshold doses from baseline toxicity. We should search out these specific low-dose responses for ecological risk assessment and not rely on high-concentration toxicity responses to guide environmental protection. The goal for toxicity assessment should not be to characterize toxic responses at baseline toxicity concentrations, but to evaluate chemicals for their most toxic potential. Additional aspects of this review evaluated the fish ELS teratogenic responses in relation to mammalian oral LD50s and explored potential key events responsible for baseline toxicity.

Concerns about the environmental and human health implications of TiO₂ nanoparticles (nTiO₂) are growing with their increased use in consumer and industrial products. Investigations of the underlying molecular mechanisms of nTiO₂ tolerance in organisms will assist in countering nTiO₂ toxicity. In this study, the countermeasures exhibited by the slime mold Physarum polycephalum macroplasmodium against nTiO₂ toxicity were investigated from a physiological, transcriptional, and metabolic perspective. The results suggested that the countermeasures against nTiO₂ exposure include gene-associated metabolic rearrangements in cellular pathways involved in amino acid, carbohydrate, and nucleic acid metabolism. Gene-associated nonmetabolic rearrangements involve processes such as DNA repair, DNA replication, and the cell cycle, and occur mainly when macroplasmodia are exposed to inhibitory doses of nTiO₂. Interestingly, the growth of macroplasmodia and mammal cells was significantly restored by supplementation with a combination of responsive metabolites identified by metabolome analysis. Taken together, we report a novel model organism for the study of nTiO₂ tolerance and provide insights into countermeasures taken by macroplasmodia in response to nTiO₂ toxicity. Furthermore, we also present an approach to mitigate the effects of nTiO₂ toxicity in cells by metabolic intervention.

Increasing levels of road noise are creating new anthropogenic soundscapes that may affect wildlife globally. Bats, which form about a third of all mammal species, are sensitive bioindicators, and may be particularly vulnerable because of their dependency on echolocation. Here we present the first controlled field experiment with free-living bats. Using a Before-After-Control-Impact phantom road experimental design, we examine the impacts of traffic noise on their activity and feeding behaviour. Disentangling the impacts of traffic noise from other co-varying exposures such as habitat quality, the experiment demonstrates a significant negative effect on the activity of each of the five, ecologically different, species (genus for Myotis spp.) examined. This suggests that the results are widely applicable. The negative effects are largely attributable to noise in the sonic spectrum, which elicited aversive responses in all bat species tested,whereas responses to ultrasoundwere restricted to a single species. Our findings demonstrate that traffic noise can affect bat activity at least 20m away from the noise source. For Pipistrellus pipistrellus and Pipistrellus pygmaeus, feeding behaviour, as well as overall activity, was negatively affected. Ecological Impact Assessments are therfore needed wherever there are significant increases in traffic flow, and not just when new roads are built. Further research is required to identify effective mitigation strategies, to delineate the zone of influence of road noise, and to assess whether there is any habituation over time.

Tributyltin (TBT) is an organotin environmental pollutant widely used as an agricultural and wood biocide and in antifouling paints. Countries began restricting TBT use in the 2000s, but their use continues in some agroindustrial processes. We studied the acute effect of TBT on cardiac function by analyzing myocardial contractility and Ca²⁺ handling. Cardiac contractility was evaluated in isolated papillary muscle and whole heart upon TBT exposure. Isolated ventricular myocytes were used to measure calcium (Ca²⁺) transients, sarcoplasmic reticulum (SR) Ca²⁺ content and SR Ca²⁺ leak (as Ca²⁺ sparks). Reactive oxygen species (ROS), as superoxide anion (O2•⁻) was detected at intracellular and mitochondrial myocardium. TBT depressed cardiac contractility and relaxation in papillary muscle and intact whole heart. TBT increased cytosolic, mitochondrial ROS production and decreased mitochondrial membrane potential. In isolated cardiomyocytes TBT decreased both Ca²⁺ transients and SR Ca²⁺ content and increased diastolic SR Ca²⁺ leak. Decay of twitch and caffeine-induced Ca²⁺ transients were slowed by the presence of TBT. Dantrolene prevented and Tiron limited the reduction in SR Ca²⁺ content and transients. The environmental contaminant TBT causes cardiotoxicity within minutes, and may be considered hazardous to the mammalian heart. TBT acutely induced a negative inotropic effect in isolated papillary muscle and whole heart, increased arrhythmogenic SR Ca²⁺ leak leading to reduced SR Ca²⁺ content and reduced Ca²⁺ transients. TBT-induced myocardial ROS production, may destabilize the SR Ca²⁺ release channel RyR2 and reduce SR Ca²⁺ pump activity as key factors in the TBT-induced negative inotropic and lusitropic effects.

Recently, the essentiality and fatalness of cardiovascular diseases is attracting much attention. Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants, which could induce the toxic effect and have been implicated in the occurrence and development of cardiovascular diseases. However, it is unclear how autophagy and apoptosis induced by BDE-209 in endothelial cells are regulated. The aim of the present study was to investigate the effects of BDE-209 on human umbilical vein endothelial cells (HUVECs) and elucidate the mechanisms involved. HUVECs were treated with a wide range concentration of BDE-209 for 24 h. The appearance of autophagy was tested by the testing index such as outcomes of monodansylcadaverine (MDC) staining and lysotracker staining, observation of autophagosomes and conversion between autophagy marker light chain 3 (LC3)-I and LC3-II. Besides, the apoptotic cell rate was detected with flow cytometry. In addition, BDE-209 induced endoplasmic reticulum (ER) stress was detected by transmission electron microscopy (TEM). Our data suggest that the exposure of BDE-209 could induce autophagy, which was confirmed by MDC staining, transmission electron microscopy observation, lysotracker staining and LC3-I/LC3-II conversion. Besides, the ER stress-related inositol-requiring enzyme 1α (IRE1α)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway could be activated by reactive oxygen species (ROS) to regulate autophagy. Moreover, the apoptosis of endothelial cells was alleviated when autophagy was blocked by 3-Methyladenine (3-MA). The results demonstrated that BDE-209 could induce the production of ROS and ER stress, activate autophagy through IRE1α/AKT/mTOR signaling pathway and ultimately induce apoptosis of vascular endothelial cells. These findings indicate that exposure to PBDE is possible to be a potential risk factor for cardiovascular diseases.

Bats are particularly suited as bioindicators of trace element pollution due to their longevity and their position in the trophic chain. In this study, the concentrations of ten non-essential trace elements (Al, As, Ba, Cd, Hg, Pb, Sb, Sr, Th, Tl) were determined in the tissues (whole body, skin-fur, skinned body, liver, kidney and bone) of lactant Tadarida teniotis from a nursery colony in Rome. A large number of bats from this nursery died before fledging and had bone deformities and fractures. The concentrations of non-essential trace elements in bone and whole body were also analysed in adult specimens of Miniopterus schreibersii from a colony located in a natural park in Northern Italy. In lactant T. teniotis, the Pb concentration decreased in the following order: bone>liver>skinned body>whole body>skin-fur>kidney, and exceeded the toxic threshold associated with negative effects reported for different mammalian species. The levels of the other non-essential trace elements were within a range indicative of low environmental contamination in both species. Significant interspecies differences (P < 0.05) were observed for concentrations of Pb and Ba, higher in the bones of T. teniotis, and of Cd, Hg and Sr, higher in the bones of M. schreibersii. In lactant T. teniotis, the different sources of Pb exposure, through inhalation and/or food, may represent a potential threat to the colony of this synanthropic European bat.

Chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) caused great concerns recently as novel fluorinated alternatives. However, information on their bioconcentration, bioaccumulation and biomagnification in marine ecosystems is limited. In this study, 152 biological samples including invertebrates, fishes, seabirds and mammals collected from Bohai Sea of China were analyzed to investigate the residual level, spatial distribution, bioaccumulation and biomagnification of Cl-PFESAs. 6:2 Cl-PFESA was found in concentrations ranging from <MDL (method detection limit) to 3.84 ng/g ww and it is the dominant congener when compared with concentrations of 8:2 Cl-PFESA. Compared with other bays and regions, levels of 6:2 Cl-PFESA are relatively high in bivalves and fishes from Liaodong Bay. These levels were also found to tend to increase as compared with those in 2010–2014. Logarithm bioaccumulation factors (BAFs) for 6:2 Cl-PFESA ranged from 2.23 to 4.21, implying the bioaccumulation of this compound. The trophic magnification factor (BMF) for 6:2 Cl-PFESA was determined to be 3.37 in the marine food web, indicating biomagnification potential along the marine food chain.