Cadmium (Cd) is a toxic heavy metal that can be discharged into water environment through industrial activities, threatening the health of aquatic organisms and humans. MicroRNA (miRNA) plays an important role in the process of autophagy. The purpose of this experiment was to study the mechanism of Cd-induced autophagy in common carp hepatopancreas. We established a Cd poisoning model of common carp and explored ultrastructure, two oxidation indicators, three antioxidant indicators, miR-25-3p, two heat shock proteins (Hsps), and nine autophagy-related genes. The results confirmed that deleterious effect of Cd caused the injury of hepatopancreas and the appearance of hepatopancreas autophagic cells in common carp. At the same time, Cd exposure increased the contents of hydrogen peroxide (H₂O₂) and malonaldehyde (MDA), and decreased the activities of catalase (CAT), superoxide dismutase (SOD), and total antioxidative capacity (T-AOC), meaning that Cd caused oxidative stress via the imbalance between peroxide level and antioxidant capacity. Moreover, exposure to Cd increased mRNA expression of microtubule associated protein-1 light chain 3 beta (LC3-II), Dynein, Beclin 1, autophagy-related gene 5 (Atg5), and autophagy-related gene 12 (Atg12); and decreased mRNA expression of mechanistic target of rapamycin kinase (mTOR), indicating that excess Cd caused autophagy, and AMPK/mTOR/ULK1 signaling pathway took part in autophagy induced by Cd in common carp hepatopancreas. Furthermore, Cd down-regulated miR-25-3p and up-regulated its three target genes (AMPK, ULK1 as well as PTEN), suggesting that miR-25-3p mediated autophagy induced by Cd. In addition, we found that Hsps were activated via the up-regulation of Hsp70 and Hsp90. Moreover, oxidative stress mediated autophagy via Hsps in Cd-treated common carp hepatopancreas and Cd-induced autophagy was time dependent. In summary, miR-25-3p, oxidative stress, and Hsps participated in autophagy caused by Cd in common carp hepatopancreas. This study provided a new idea for the mechanism of Cd-induced autophagy in hepatopancreas.

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.

Nanoplastics can be used in various fields, such as personal care products. Nevertheless, the effect of nanoplastic exposure on metabolism and its association with stress response remain largely unclear. Using Caenorhabditis elegans as an animal model, we determined the effect of nanopolystyrene exposure on lipid metabolism and its association with the response to nanopolystyrene. Exposure (from L1-larave to adult day-3) to 100 nm nanopolystyrene (≥1 μg/L) induced severe lipid accumulation and increase in expressions of mdt-15 and sbp-1 encoding two lipid metabolic sensors. Meanwhile, we found that SBP-1 acted downstream of intestinal MDT-15 during the control of response to nanopolystyrene. Intestinal transcriptional factor SBP-1 activated two downstream targets, fatty acyl CoA desaturase FAT-6 and heat-shock protein HSP-4 (a marker of endoplasmic reticulum unfolded protein response (ER UPR)) to regulate nanopolystyrene toxicity. Both MDT-15 and SBP-1 were involved in the activation of ER-UPR in nanopolystyrene exposed nematodes. Moreover, SBP-1 regulated the innate immune response by activating FAT-6 in nanopolystyrene exposed nematodes. In the intestine, function of MDT-15 and SBP-1 in regulating nanopolystyrene toxicity was under the control of upstream signaling cascade (PMK-1-SKN-1) in p38 MAPK signaling pathway. Therefore, our data raised an important molecular basis for potential protective function of lipid metabolic response in nanopolystyrene exposed nematodes.

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).

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.

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.

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.

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.

Microplastic (MP) pollution is everywhere. In terrestrial environments, microfibres (MFs) generated from textile laundering are believed to form a significant component of MPs entering soils, mainly through sewage sludge and compost applications. The aim of this study was to assess the effect of MFs on a keystone soil organism. We exposed the earthworm Lumbricus terrestris to soil with polyester MFs incorporated at rates of 0, 0.1 and 1.0 %w/w MF for a period of 35 days (in the dark at 15 °C; n = 4 for each treatment). Dried plant litter was applied at the soil surface as a food source for the earthworms. We assessed earthworm vitality through mortality, weight change, depurate production and MF avoidance testing. In addition, we measured stress biomarker responses via the expression of metallothionein-2 (mt-2), heat shock protein (hsp70) and superoxide dismutase (sod-1). Our results showed that exposure and ingestion of MFs (as evidenced by subsequent retrieval of MFs within earthworm depurates) were not lethal to earthworms, nor did earthworms actively avoid MFs. However, earthworms in the MF1.0% treatment showed a 1.5-fold lower cast production, a 24.3-fold increase in expression of mt-2 (p < 0.001) and a 9.9-fold decline in hsp70 expression (p < 0.001). Further analysis of soil and MF samples indicated that metal content was not a contributor to the biomarker results. Given that burrowing and feeding behaviour, as well as molecular genetic biomarkers, were modulated in earthworms exposed to MFs, our study highlights potential implications for soil ecosystem processes due to MF contamination.