The present study evaluated the interactive effects of global change and heavy metals on the growth and development of three soybean [Glycine max (L.) Merrill] cultivars and the consequences on yield and food safety. Soybean cultivars (Alim 3.14 from Argentina, and ES Mentor and Sigalia, from Germany) were grown until maturity in heavy metals polluted soils from the Rhine Valley, Germany, at two CO₂ concentrations (400 and 550 ppm) and heat stress (HS) episodes (9 days with 10 °C higher than maximum regular temperature) during the critical growth period in controlled environmental chambers. Different morpho-physiological parameters, heavy metal concentration in aerial organs, seed quality parameters, and toxicological index were recorded. The results showed that no morphological differences were observed related to CO₂. Moreover, Alim 3.14 showed the highest yield under control conditions, but it was more sensitive to climatic conditions than the German cultivars, especially to heat stress which strongly reduces the biomass of the fruits. Heavy metals concentration in soil exceeds the legislation limits for agricultural soils for Cd and Pb, with 1.6 and 487 mg kg⁻¹ respectively. In all cultivars, soybeans accumulated Cd in its aerial organs, and it could be translocated to fruits. Cd concentration in seeds ranged between 0.6 and 2.4 mg kg⁻¹, which exceed legislation limits and with toxicological risk to potential Chinese consumers. Pb levels were lower than Cd in seeds (0.03–0.17 mg kg⁻¹), and the accumulation were concentrated in the vegetative organs, with 93% of the Pb incorporated. Moreover, pods accumulated 11 times more Pb than seeds, which suggests that they act as a barrier to the passage of Pb to their offspring. These results evidence that soybean can easily translocate Cd, but not Pb, to reproductive organs. No regular patterns were observed in relation to climatic influence on heavy metal uptake.

Silver nanomaterials (AgNMs) are broadly used and among the most studied nanomaterials. The underlying molecular mechanisms (e.g. protein and metabolite response) that precede phenotypical effects have been assessed to a much lesser extent. In this paper, we assess differentially expressed proteins (DEPs) and metabolites (DEMs) by high-throughput (HTP) techniques (HPLC-MS/MS with tandem mass tags, reversed-phase (RP) and hydrophilic interaction liquid chromatography (HILIC) with mass spectrometric detection). In a time series (0, 7, 14 days), the standard soil model Enchytraeus crypticus was exposed to AgNM300K and AgNO₃ at the reproduction EC20 and EC50. The impact on proteins/metabolites was clearly larger after 14 days. NM300K caused more upregulated DEPs/DEMs, more so at the EC20, whereas AgNO₃ caused a dose response increase of DEPs/DEMs. Similar pathways were activated, although often via opposite regulation (up vs down) of DEPs, hence, dissimilar mechanisms underlie the apical observed impact. Affected pathways included e.g. energy and lipid metabolism and oxidative stress. Uniquely affected by AgNO₃ was catalase, malate dehydrogenase and ATP-citrate synthase, and heat shock proteins (HSP70) and ferritin were affected by AgNM300K. The gene expression-based data in Adverse Outcome Pathway was confirmed and additional key events added, e.g. regulation of catalase and heat shock proteins were confirmed to be included. Finally, we observed (as we have seen before) that lower concentration of the NM caused higher biological impact. Data was deposited to ProteomeXchange, identifier PXD024444.

Heat stress (HS) during gestation has been associated with negative outcomes, such as preterm birth or postnatal metabolic syndromes. The intestinal microbiota is a unique ecosystem playing an essential role in mediating the metabolism and health of mammals. Here we hypothesize late gestational HS alters maternal microbial transmission and structures offspring’s intestinal microbiota and serum metabolic profiles. Our results show maternal HS alters bacterial β-diversity and composition in sows and their piglets. In the maternal intestine, genera Ruminococcaceae UCG-005, [Eubacterium] coprostanoligenes group and Halomonas are higher by HS (q < 0.05), whereas the populations of Streptococcus, Bacteroidales RF16 group_norank and Roseburia are decreased (q < 0.05). In the maternal vagina, HS mainly elevates the proportions of phylum Bacteroidetes and Fusobacteria (q < 0.05), whereas reduces the population of Clostridiales Family XI (q < 0.05). In the neonatal intestine, maternal HS promotes the population of Proteobacteria but reduces the relative abundance of Firmicutes (q < 0.05). Moreover, the core Operational taxonomic units (OTU) analysis indicates the proportions of Clostridium sensu stricto 1, Romboutsia and Turicibacter are decreased by maternal HS in the intestinal and vaginal co-transmission, whereas that of phylum Proteobacteria and Epsilonbacteraeota, such as Escherichia-Shigella, Klebsiella, Acinetobacter, and Comamonas are increased in both the intestinal and vaginal co-transmission and the vagina. Additionally, Aeromonas is the only genus that is transmitted from environmental sources. Lastly, we evaluate the importance of neonatal differential OTU for the differential serum metabolites. The results indicate Acinetobacter significantly contributes to the differences in the adrenocorticotropic hormone (ACTH) and glucose levels due to HS (P < 0.05). Further, Stenotrophomonas is the most important variable for Cholesterol, low-density lipoprotein (LDL), diamine oxidase (DAO), blood urea nitrogen (BUN) and 5-hydroxytryptamine (5-HT) (P < 0.10). Overall, our data provides evidence for the maternal HS in establishing the neonatal microbiota via affecting maternal transmission, which in turn affects the maintenance of metabolic health.

Decabromodiphenyl ethane (DBDPE), as one of the most widely used new brominated flame retardants (NBFRs), can pose a potential threat to human health and the environment. An integrated transcriptome and proteome was performed for investigating the toxicological molecular mechanisms of Pleurotus ostreatus (P. ostreatus) during the biodegradation of DBDPE at the concentrations of 5 and 20 mg/L. A total of 1193/1018 and 92/126 differentially expressed genes/proteins (DEGs/DEPs) were found, respectively, with DBDPE exposure at 5 and 20 mg/L. These DEGs and DEPs were mainly involved in the cellular process as well as metabolic process. DEPs for oxidation-reduction process and hydrolase activity were up-regulated, and those for membrane, lipid metabolic process and transmembrane transport were down-regulated. The DEGs and DEPs related to some key enzymes were down-regulated, such as NADH dehydrogenase/oxidoreductase, succinate dehydrogenase, cytochrome C1 protein, cytochrome-c oxidase/reductase and ATP synthase, which indicated that DBDPE affected the oxidative phosphorylation as well as tricarboxylic acid (TCA) cycle. Cytochrome P450 enzymes (CYPs) might be involved in DBDPE degradation through hydroxylation and oxidation. Some stress proteins were induced to resist DBDPE toxicity, including major facilitator superfamily (MFS) transporter, superoxide dismutase (SOD), molecular chaperones, heat shock proteins (HSP20, HSP26, HSP42), 60S ribosomal protein and histone H4. The findings help revealing the toxicological molecular mechanisms of DBDPE on P. ostreatus, aiming to improve the removal of DBDPE.

Cadmium (Cd) exposure poses a serious environmental problem due to the metal’s bioaccumulation and difficult to eliminate from body. Understanding the mechanisms of Cd detoxification and resistance can provide insights into methods to protect against the damaging effects of the heavy metal. In the present study, we found that heat shock (HS) pretreatment increased Cd resistance of the nematode Caenorhabditis elegans by reducing the bagging phenotype and protecting the integrity of the intestinal barrier. HS pretreatment increased the expression of heat shock protein-16.2 (HSP-16.2) prior to Cd exposure, and HS-induced Cd resistance was absent in worms with hsp-16.2 loss-of-function mutation. Worm strain with daf-2(e1370) mutation presented enhanced HS-induced Cd resistance, which was eliminated in worm strains of daf-16(mu86) and hsf-1(sy441). HS pretreatment increased DAF-16 nuclear localization and HSF-1 granule formation prior to Cd exposure. DAF-16 and HSF-1 was essential in reducing bagging formation and protecting the integrity of intestinal barrier after HS pretreatment. In conclusion, the present study demonstrated that HS-induced Cd resistance in C. elegans is regulated by the DAF-16/FOXO and HSF-1 pathways through regulation of HSP-16.2 expression.

Climatic stressors and chemicals should not be treated as isolated problems since they often occur simultaneously, and their combined effects must be evaluated including their possible interactive effects. In the present study we subjected springtails (Folsomia candida) to combined exposure to phenanthrene and dynamic heat cycles in a full factorial experiment. In a microcosm experiment, we studied the population growth of springtails subjected to a range of sub-lethal concentrations of phenanthrene. During the 28-day experiment we further subjected microcosms to varying numbers of repeated dynamic heat cycles (0–5 cycles) simulating repeated heat waves. We found a synergistic interaction between the effects of phenanthrene and the number of heat waves on both body mass of adults and juvenile production of F. candida showing that the negative effects of phenanthrene were intensified when animals were heat stressed, and/or vice versa. This interaction was not related to internal concentrations of phenanthrene in adult springtails, nor was it due to altered degradation of phenanthrene in soil. We argue that both phenanthrene (by its partitioning into membrane bilayers) and heat have detrimental effects on the physical conditions of cellular membranes in a dose-dependent manner, which, under extreme circumstances, can increase membrane fluidity to a level which is sub-optimal for normal membrane functioning. We discuss the possibility that the synergistic interactions subsequently reduce life-history parameters such as growth and reproduction.

Short- and long-term changes in the methanol-extractable UV-absorbing compounds and biomass of the pioneer moss Polytrichum juniperinum in response to natural and enhanced UV radiation were studied. Under natural conditions, the compounds were found to fluctuate seasonally. In summer these compounds correlated negatively with irradiation. The concentration was low in July after a period of simultaneous heat, drought and high irradiation. Transient positive correlation between daily concentration and UV was seen in June. The concentration increased towards autumn and was relatively high under snow. Two enhanced UV experiments were performed. Seasonality in the compounds was again observed, with negative correlations with irradiation. During the first weeks, a transient inhibition of compound production was observed after the daily UV-B treatment. After six years of modulated UV-treatment in situ, photosynthesising biomass decreased under UV-B and increased under UV-A. A larger variation in the UV-absorbing compounds was observed under UV-B treatment. Juniper polytrichum moss is affected by drought, overwintering conditions and UV.

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.

With the rapid development of science and technology, 5G technology will be widely used, and biosafety concerns about the effects of 5G radiofrequency radiation on health have been raised. Drosophila melanogaster was selected as the model organism for our study, in which a 3.5 GHz radiofrequency radiation (RF-EMR) environment was simulated at intensities of 0.1 W/m², 1 W/m², and 10 W/m². The activity of parent male and offspring (F1) male flies was measured using a Drosophila activity monitoring system under short-term and long-term 3.5 GHz RF-EMR exposure. Core genes associated with heat stress, the circadian clock and neurotransmitters were detected by QRT-PCR technology, and the contents of GABA and glutamate were detected by UPLC-MS. The results show that short-term RF-EMR exposure increased the activity level and reduced the sleep duration while long-term RF-EMR exposure reduced the activity level and increased the sleep duration of F1 male flies. Under long-term RF-EMR, the expression of heat stress response-related hsp22, hsp26 and hsp70 genes was increased, the expression of circadian clock-related per, cyc, clk, cry, and tim genes was altered, the content of GABA and glutamate was reduced, and the expression levels of synthesis, transport and receptor genes were altered. In conclusion, long-term RF-EMR exposure enhances the heat stress response of offspring flies and then affects the expression of circadian clock and neurotransmitter genes, which leads to decreased activity, prolonged sleep duration, and improved sleep quality.

Cadmium (Cd) pollution in the environment could cause toxic damage to animals and humans. MAPK pathways could regulate their downstream inflammatory factors, and plays a crucial role in necrosis. Since the swine kidney tissue is an important accumulation site of Cd and target organ of its toxic damage, but the damage form of Cd to swine kidney and the role of MAPK pathways in it are still not clear, we selected six week old weaned piglets as the research object, and fed a diet supplemented CdCl₂ (20 mg/kg) to establish the model of liver injury induced by Cd. The expressions and phosphorylation of MAPK pathways (ERK, JNK, p38), expression levels of inflammatory factors (TNF-α, NF-κB, iNOS, COX-2 and PTGE) and necrosis related genes (MLKL, RIPK1, RIPK3 and FADD) and heat shock proteins (HSPs) were detected by RT-PCR and Western blot. H.E. staining was used to determine the damage of kidney caused by Cd exposure. The results showed that Cd exposure could activate p38 and JNK pathway phosphorylation, rather than ERK 1/2, up regulated the expressions of inflammatory factors, finally induced programmed necrosis (increasing the expressions of MLKL, RIPK1, RIPK3 and FADD) in swine kidney. Our study elucidated the mechanism of Cd-damage to swine kidney and the relationship among MAPK pathways, inflammatory factors and programmed necrosis in swine.