The effect of chronic exposure of freshwater cladoceran Daphnia magna to low, environmentally relevant concentrations i.e 4 μgL⁻¹of ibuprofen (a nonsteroidal anti-inflammatory drug) in a laboratory experiment was studied. We observed the key life history traits of first and fifth generation individuals: age and size at first reproduction, number of first clutch eggs and individual growth rate. Moreover, chosen molecular/subcellular markers of experimental animals stress response such as triglyceride content, heat shock proteins (HSP) expression and DNA:RNA ratio were collected. Overall, chronic exposure to ibuprofen had no significant effect on the molecular markers nor on the life history parameters of the Daphnia. It did, however, caused lethal morphological deformities in embryos and juvenile daphnids. Depending on the clonal affiliation, exposure to a low dosage of ibuprofen over five generations resulted in the deformation of ∼3%–∼10% of the first clutch of offspring. Also, up to 90% of females carried at least one deformed embryo. This is the first time that research has revealed such an effect of ibuprofen on D. magna.

It is a common method to analyse physiological mechanisms of organisms – commonly referred to as biomarkers – to indicate the presence of environmental pollutants. However, as biomarkers respond to a wide range of stressors we want to direct the attention on natural stressors, i.e. on parasites. After two years maintenance under controlled conditions, roach (Rutilus rutilus) revealed no influence on levels of metallothionein by the parasite Ligula intestinalis. The same was found for Gammarus fossarum infected with Polymorphus minutus. However, the heat shock protein (HSP70) response was affected in both host-parasite systems. While the infection of roach resulted in reduced levels of HSP70 compared to uninfected roach, the infection in G. fossarum led to higher levels of HSP70. We also analysed the effect of a 14 days Cd exposure (4 μg/L) on the uninfected and infected gammarids. The exposure resulted in induced levels for both, metallothionein and HSP70 whereas the combination of stressors, parasite and exposure, revealed a decrease for levels of HSP70 in comparison to the metal exposure only. Accordingly, parasites as natural parts of aquatic ecosystems have to be considered in ecotoxicological research.

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.

Particulate matter 2.5 (PM₂.₅) is an inflammatory-inducing factor that is considered to be related to many adverse respiratory problems, especially in the elderly. This study aimed to examine whether pre-exercise training could prevent pulmonary injury induced by urban PM₂.₅ in aging rats and investigate its relationship with inflammatory pathways. Male Wistar rats (aged 16 months) were randomly divided into four groups: sedentary, exercise, sedentary + PM₂.₅ exposure, and exercise + PM₂.₅ exposure. All rats in exercise-related groups were treadmill-trained for 8 weeks (65%–75% VO₂ₘₐₓ for 30 min every other day). Sedentary groups’ rats lived freely in cages without exercise intervention. Rats in the PM-related groups were exposed to ambient PM₂.₅ (4 h day⁻¹) for 2 weeks after an 8-week exercise intervention or sedentary treatment. Finally, all rats’ pulmonary function, lung morphology, degree of inflammation, and relevant protein and mRNA transcript expression levels were examined. The results indicated that PM₂.₅ exposure induced lung injury in the sedentary + PM₂.₅ exposure group, as evidenced by the deterioration of pulmonary function, histopathological characteristics, and inflammatory changes. Aerobic exercise alleviated PM₂.₅-induced airway obstruction, deterioration of pulmonary function, bronchial mucosal exfoliation, and inflammatory responses in aging rats. These effects in exercise groups were associated with the increased expression of intracellular 70 kDa heat shock protein (iHSP70) and the suppression of nuclear transcription factor-κB (NF-κB) activation, as confirmed by increased expression of inhibitor of NF-κB (IκBα) and a reduction in phospho-IKBα (p-IκBα), which is regulated by inhibiting kappa B kinase beta (IKKβ). Taken together, aerobic pre-exercise had protective effects on lung injury and reduced vulnerability to inflammation induced by PM₂.₅ exposure, possibly through the toll-like receptor 4 (TLR4)/NF-κB signaling pathways mediated by the extracellular-to-intracellular HSP70 ratio. Pre-exercise training may be an effective way to protect against PM₂.₅-induced lung toxicity in aging individuals.

To assess the time-dependent stress evidence in dynamic allocation of physiological metabolism of Nilaparvata lugens nymphs in response to elevated CO₂, we measured the time-dependent allocation of nutrient compositions and physiological metabolism in the bodies of N. lugens at 1h, 4h and 12h under elevated CO₂. Elevated CO₂ significantly increased the contents of nutrient compositions (protein, glucose and total amino acids) and catalase (CAT) enzyme activity in the body of N. lugens at 12h relative to 1h and 4h (P < 0.05). Significantly higher genes expression levels of acetylcholinesterase (AChE), heat shock protein (HSP70) and vitellogenin gene (vg) were observed in the body of N. lugens compared with those in ambient CO₂ at 4h (P < 0.05). These results showed that there was an instantaneous reaction of N. lugens nymphs to elevated CO₂, which indicated N. lugens may enhance stress defense response to future increasing CO₂ levels.

Triclosan (TCS) is a synthetic microbial compound widely used in the formulation of various personal care products. Its frequent detection in marine ecosystems, along with its physical and chemical properties, suggest that TCS can be highly persistent, being easily bioaccumulated by biota and, therefore, eliciting various toxicological responses. Yet, TCS's mechanisms of bioaccumulation and toxicity still deserve further research, particularly focusing on the interactive effects with climate change-related stressors (e.g. warming and acidification), as both TCS chemical behaviour and marine species metabolism/physiology can be strongly influenced by the surrounding abiotic conditions. Hence, the aim of this study was to assess TCS bioaccumulation and ecotoxicological effects (i.e. animal fitness indexes, antioxidant activity, protein chaperoning and degradation, neurotoxicity and endocrine disruption) in three tissues (i.e. brain, liver and muscle) of juvenile Diplodus sargus exposed to the interactive effects of TCS dietary exposure (15.9 μg kg−1 dw), seawater warming (ΔTºC = +5 °C) and acidification (ΔpCO2 ∼ +1000 μatm, equivalent to ΔpH = −0.4 units). Muscle was the primary organ of TCS bioaccumulation, and climate change stressors, particularly warming, significantly reduced TCS bioaccumulation in all fish tissues. Furthermore, the negative ecotoxicological responses elicited by TCS were significantly altered by the co-exposure to acidification and/or warming, through either the enhancement (e.g. vitellogenin content) or counteraction/inhibition (e.g. heat shock proteins HSP70/HSC70 content) of molecular biomarker responses, with the combination of TCS plus acidification resulting in more severe alterations. Thus, the distinct patterns of TCS tissue bioaccumulation and ecotoxicological responses induced by the different scenarios emphasized the need to further understand the interactive effects between pollutants and abiotic conditions, as such knowledge enables a better estimation and mitigation of the toxicological impacts of climate change in marine ecosystems.

Heavy metal tolerance of microorganisms is the basis of heavy metal removal by growing cells. In this study, a cross-protection effect generated by salt stress significantly enhanced the cadmium tolerance of multi-stress-tolerant Pichia kudriavzevii. Comparative transcriptome analysis using RNA-Seq linked with physiological and biochemical observation was used to elucidate the underlying mechanisms of the improved cadmium tolerance. The expression of cadmium transport related genes (GSTY2, GLR1, GLO2, YCF1 and YOR1), GSH content and GST activity were elevated by salt stress, suggesting enhanced cadmium conjugation and detoxification in yeast cells. The inhibited cadmium uptake by ZRT1 and enhanced cadmium efflux by YOR1 contributed to the decrease in the intracellular cadmium concentration. The improved expression of antioxidant enzyme genes (SOD1, SOD2, SOD6, CAT1 and PRXIID), along with the enhanced activities of antioxidant enzymes (SOD, CAT and POD) resulted in a decrease in cadmium-induced ROS production, protein carbonylation, lipid peroxidation and cell death. The abundant expression of heat shock protein genes (HSP12, HSP10 and SSC1) and genes related to trehalose synthesis (TPS1 and TSL1) induced by salt stress protected yeast cells against complex stress conditions, contributing to the improved cadmium tolerance. These findings will be useful to develop cadmium-tolerant yeasts for cadmium removal by growing cells.

In current study, we investigated the changes of proteome profiles of Pycnoporus sanguineus after a single exposure of Cr(VI), TBBPA and a combined exposure of TBBPA and Cr(VI), with the goal of illuminating the cellular mechanisms involved in the interactions of co-existed TBBPA and Cr(VI) with the cells of P. sanguineus at the protein level. The results revealed that some ATP-binding cassette (ABC) transporters were obviously induced by these pollutants to accelerate the transportation, transformation and detoxification of TBBPA and Cr(VI). Cr(VI) could inhibit the bioremoval of its organic co-pollutants TBBPA through suppressing the expression of several key proteins related to the metabolism of TBBPA by P. sanguineus, including two cytochrome P450s, pentachlorophenol 4-monooxygenase and glutathione S-transferases. Furthermore, Cr(VI) possibly reduced the cell vitality and growth of P. sanguineus by enhancing the expression of imidazole glycerol phosphate synthase as well as by decreasing the abundances of proteins associated with the intracellular metabolic processes, such as the tricarboxylic acid cycle, purine metabolism and glutathione biosynthesis, thereby adversely affecting the biotransformation of TBBPA. Cr(VI) also inhibited the expression of peptidyl prolyl cis/trans isomerases, thus causing the damage of cell membrane integrity. In addition, some important proteins participated in the resistance to Cr(VI) toxicity were observed to up-regulate, including heat shock proteins, 26S proteasome, peroxiredoxins and three critical proteins implicated in S-adenosyl methionine synthesis, which contributed to reducing the hazard of Cr(VI) to P. sanguineus. The results of this study provide novel insights into the physiological responses and molecular mechanism of white rot fungi P. sanguineus to the stress of concomitant TBBPA and Cr(VI).

Development of stress markers for the invader freshwater zebra mussel (Dreissena polymorpha) is of great interest for both conservation and biomonitoring purposes. Gene expression profiles of several putative or already established gene expression stress markers (Metallothionein, Superoxide dismutase, Catalase, Glutathione S transferase, Glutathione peroxidase, Cytochrome c oxidase, the multixenobiotic resistance P-gp1, and heat shock proteins HSP70 and HSP90) were analyzed by quantitative Real-Time PCR in adults and pediveliger larvae after exposure to metals (Hg, Cu, Cd). A defined pattern of coordinated responses to metal exposure and, presumably, to oxidative stress was observed in gills and digestive gland from adults. A similar, albeit partial response was observed in larvae, indicating an early development of stress-related gene responses in zebra mussel. The tools developed in this study may be useful both for future control strategies and for the use of zebra mussel as sentinel species in water courses with stable populations.

Deciphering the potential mechanism of chemical-induced toxicity enables us to alleviate the cellular and organismal dysfunction. The environmental presence of nonylphenol (endocrine disruptor) has a major health concern due to its widespread usage in our day-to-day life. The current study establishes a novel functional link among nonylphenol-induced oxidative stress, Heat shock protein 27 (Hsp27, member of stress protein family), and Ecdysone receptor (EcR, a nuclear receptor), which eventually coordinates the nonylphenol-induced sub-cellular and organismal level toxicity in a genetically tractable model Drosophila melanogaster. Drosophila larvae exposed to nonylphenol (0.05, 0.5 and 5.0 μg/mL) showed a significant decrease in Hsp27 and EcR mRNA levels in the midgut. In concurrence, reactive oxygen species (ROS) levels were increased with a corresponding decline in glutathione (GSH) level and Thioredoxin reductase (TrxR) activity. Increased lipid peroxidation (LPO), protein carbonyl (PC) contents, and cell death were also observed in a correlation with the nonylphenol concentrations. Sub-cellular toxicity poses a negative organismal response, which was evident by delayed larval development and reduced Drosophila emergence. Subsequently, a positive genetic correlation (p < 0.001) between EcR and Hsp27 revealed that nonylphenol-dependent EcR reduction is a possible link for the downregulation of Hsp27. Further, Hsp27 overexpression in midgut cells showed a reduction in nonylphenol-induced intracellular ROS, LPO, PC content, and cell death through the TrxR mediated regenerative pathway and reduced GSH level improving the organismal response to the nonylphenol exposure. Altogether, the study elucidates the potential EcR-Hsp27 molecular interactions in mitigating the nonylphenol-induced cellular and organismal toxicity.