With the widespread occurrence and accumulation of plastic waste in the world, plastic pollution has become a serious threat to ecosystem and ecological security, especially to estuarine and coastal areas. Understanding the impacts of changing nanoplastics concentrations on aquatic organisms living in these areas is essential for revealing the ecological effects caused by plastic pollution. In the present study, we revealed the effects of exposure to gradient concentrations (0.005, 0.05, 0.5 and 50 mg/L) of 75 nm polystyrene nanoplastics (PS-NPs) for 48 h on metabolic processes in muscle tissue of a bivalve, the razor clam Sinonovacula constricta, via metabolomic and transcriptomic analysis. Our results showed that PS-NPs caused dose-dependent adverse effects on energy reserves, membrane lipid metabolism, purine metabolism and lysosomal hydrolases. Exposure to PS-NPs reduced energy reserves, especially lipids. Membrane lipid metabolism was sensitive to PS-NPs with contents of phosphocholines (PC), phosphatidylethanolamines (PE) and phosphatidylserines (PS) increasing and degradation being inhibited in all concentrations. High concentrations of PS-NPs altered the purine metabolism via increasing contents of guanosine triphosphate (GTP) and adenine, which may be needed for DNA repair, and consuming inosine and hypoxanthine. During exposure to low concentrations of PS-NPs, lysosomal hydrolases in S. constricta, especially cathepsins, were inhibited while this influence was improved transitorily in 5 mg/L of PS-NPs. These adverse effects together impacted energy metabolism in S. constricta and disturbed energy homeostasis, which was manifested by the low levels of acetyl-CoA in high concentrations of PS-NPs. Overall, our results revealed the effects of acute exposure to gradient concentrations of PS-NPs on S. constricta, especially its metabolic process, and provide perspectives for understanding the toxicity of dynamic plastic pollution to coastal organisms and ecosystem.

To compare aquatic organisms’ responses to the toxicity of copper oxide (CuO) nanoparticles (NPs) with those of CuO microparticles (MPs) and copper (Cu) ions, a global metabolomics approach was employed to investigate the changes of both polar and nonpolar metabolites in microalga Chlorella vulgaris after 5-day exposure to CuO NPs and MPs (1 and 10 mg/L), as well as the corresponding dissolved Cu ions (0.08 and 0.8 mg/L). Unchanged growth, slight reactive oxygen species production, and significant membrane damage (at 10 mg/L CuO particles) in C. vulgaris were demonstrated. A total of 75 differentiated metabolites were identified. Most metabolic pathways perturbed after CuO NPs exposure were shared by those after CuO MPs and Cu ions exposure, including accumulation of chlorophyll intermediates (max. 2.4–5.2 fold), membrane lipids remodeling for membrane protection (decrease of phosphatidylethanolamines (min. 0.6 fold) and phosphatidylcholines (min. 0.2–0.7 fold), as well as increase of phosphatidic acids (max. 1.5–2.9 fold), phosphatidylglycerols (max. 2.2–2.3 fold), monogalactosyldiacylglycerols (max. 1.2–1.4 fold), digalactosylmonoacylglycerols (max. 1.9–3.8 fold), diacylglycerols (max. 1.4 fold), lysophospholipids (max. 1.8–3.0 fold), and fatty acids (max. 3.0–6.2 fold)), perturbation of glutathione metabolism induced by oxidative stress, and accumulation of osmoregulants (max. 1.3–2.6 fold) to counteract osmotic stress. The only difference between metabolic responses to particles and those to ions was the accumulation of fatty acids oxidation products: particles caused higher fold changes (particles/ions ratio 1.9–3.0) at 1 mg/L and lower fold changes (particles/ions ratio 0.4–0.7) at 10 mg/L compared with ions. Compared with microparticles, there was no nanoparticle-specific pathway perturbed. These results confirm the predominant role of dissolved Cu ions on the toxicity of CuO NPs and MPs, and also reveal particle-specific toxicity from a metabolomics perspective.

Serious environmental pollution of heavy metals has attracted people's attention in recent years and halophiles seem to be potential bioremediation in the controlling of heavy metals contamination. In this study, the adaptive mechanism of halophilic Brachybacterium muris (B. muris) in response to salt stress and its mitigation of copper (Cu) toxicity in hydroponic plants were investigated. The cell morphology was observed using transmission electron microscopy. The cell membrane composition and fluidity were examined by the combination of gas chromatography, gas chromatography-mass spectrometry, ultra-high performance liquid chromatography-mass spectrometry, and fluorescence spectrophotometry. Moreover, the metabolic pathways of B. muris in response to salt stress were analyzed using the prokaryotic transcriptomics approach. A hydroponic co-culture model was further conducted to explore the effects of B. muris on wheat seedlings subjected to Cu toxicity. It was found that B. muris can respond to high osmotic pressure by improving the cell membrane fluidity, altering the cell morphology and cell membrane compositions. The proportion of unsaturated fatty acids, phosphatidylethanolamine, and phosphatidylinositol in B. muris cell membranes increased significantly, while zymosterol, fecosterol, and ergosterol contents decreased under a high salinity situation. Further transcriptomic analysis showed that genes encoding L-glutamate synthase, glutamate ABC transporter ATP-binding protein, and sodium cotransporter were up-regulated, indicating that both the synthesis and transport of glutamate were significantly enhanced under high osmotic pressure. Additionally, B. muris alleviated the inhibitory effect of Cu²⁺ on wheat seedlings' growth, causing a 30.14% decrease in H₂O₂ content and a significant increase of 83.86% and 45.96% in POD activity and GSH content in wheat roots, respectively. The findings of this study suggested that the salt-tolerant B. muris may serve as a promising strategy for improving the bioremediation of metal-contaminated saline water and soils.

Although triphenyl phosphate (TPHP) has been reported to disrupt lipid metabolism, the effect of TPHP on lipid saturation remains unexplored. In this study, a lipidomic analysis demonstrated decreases in the levels of poly-unsaturated phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS) in RAW264.7 murine macrophage cells exposed to 10 μM TPHP. The expression of the gene encoding lysophosphatidylcholine acyltransferase 3 (Lpcat3) was significantly downregulated by 0.76 ± 0.03 and 0.70 ± 0.08-fold in 10 and 20 μM TPHP exposure groups, relative to the control group. This finding explains the observed decrease in lipid saturation. Correspondingly, exposure to 10 and 20 μM TPHP induced endoplasmic reticulum (ER) stress and inflammatory responses, which have been linked to metabolic dysfunction such as insulin resistance and hypertriglyceridemia. Therefore, TPHP may pose a risk to human health by promoting metabolic diseases.

Studies have shown that environmental carcinogens exerted an important function in the high incidence of esophageal cancer (EC). Nitrosamines have been identified as important environmental carcinogens for EC. This study aimed to investigate the metabolic disturbances and new key toxicological markers in the malignant transformation process of normal esophageal epithelial cells (Het-1A) induced by MNNG (N-methyl-N′-nitro-N-nitrosoguanidine). Untargeted metabolomic and lipidomic profiling analysis by using ultra-high-performance liquid chromatography coupled with mass spectrometry (UHPLC-MS) were applied to explore the metabolic network alterations of Het-1A cells. The metabolomic results showed that significant alterations were observed in metabolic signatures between different generations (P5, P15, P25, P35) and the control cell group (P0). A total of 48 differential endogenous metabolites were screened and identified, mainly containing fatty acids, amino acids, and nucleotides. The differential metabolites were predominantly linked to the pathway of biosynthesis of unsaturated fatty acids metabolism. The cell lipidomic profiling revealed that the most differential lipids contained fatty acids (FAs), phosphatidylcholines (PC), phosphatidylethanolamines (PE), and phosphatidylserines (PS). The enrichment of the lipidomic pathway also confirmed that the lipid metabolism of biosynthesis of unsaturated fatty acids was the significant variation during the cell malignant transformation. Furthermore, we detected the expression of the upstream regulatory enzymes related to the unsaturated fatty acids to explore the regulation mechanism. The expression of stearoyl-CoA desaturase (SCD), ELOVL fatty acid elongase 1 (ELOVL1) promoted, and fatty acid desaturase 1 (FADS1) inhibited the key fatty acids of unsaturated fatty acids metabolism compared to the control cell group. Overall, our results revealed that lipid fatty acid metabolism was involved in the malignant transformation of Het-1A cells induced by MNNG and deepened the awareness of the carcinogenic mechanism of environmental exposure pollutants.

Decachlorobiphenyl (DCB) is one of the 209 polychlorinated biphenyls congeners characterized by its high toxicity and chemical stability. It is produced by industrial activities. A possible strategy to eliminate DCB is by bacterial degradation. The main objective of this study was to define the optimal conditions for biodegradation and bioaccumulation of DCB by Pseudomonas extremaustralis ADA-5 isolated from a worm intestine. Bacterial growth kinetics were determined in minimal medium with added biphenyl and DCB. By GC coupled to mass spectrometry, we found that the strain had the ability to degrade 9.75% of available DCB, using it as a carbon source and was able to accumulate 19.98% of this pollutant in biomass. Membrane lipids may be altered by DCB. Phosphatidylethanolamine (PE), phosphatidylglycerol (PG), and cardiolipin (CL) were identified by thin-layer chromatography as the membrane lipids of the cell. At 250 mg L⁻¹ of DCB in the culture medium, membranes showed a 30% decrease in the PE concentration, an 18% increase in the PG, and a 12% increase in CL. ADA-5 was able to catabolize DCB and may be used for bioremediation of highly chlorinated toxic compounds in soil.

Heat stress (HS) by high-temperature environment reduced the production performance of poultry and caused losses to the breeding industry. The present study was conducted to investigate the effects of HS on serum lipidomics in Chinese indigenous slow-growing broiler chickens (Huaixiang chickens). A total of 40 8-week-old female Huaixiang chickens were randomly allocated to two groups, including normal temperature (NT, fed basal diet) and HS (fed basal diet), and each group consisted of five replicates with four birds per replicate. NT and HS groups were exposed to 21.3 ± 1.2 °C and 32.5 ± 1.4 °C for 4 weeks, respectively. Serum lipidomics in broilers was determined by liquid chromatography-mass spectrometry (LC-MS)-based metabolomics. The results indicated that there were significant differences in metabolic spectra between the groups, and a total of 17 differential metabolites were screened. Compared with NT group, HS group reduced the serum ceramide (cer) (d18:1/22:0), cer (d18:1/24:1), cer (d20:2/22:2), lyso-phosphatidylcholine (LPC) (18:0), phosphatidylcholine (PC) (18:0/20:4), PC (15:0/23:4), PC (18:0/22:6), PC (18:2/18:2), phosphatidylethanolamine (PE) (18:1/18:1), polyethylene terephthalate (PEt) (37:3/8:0), phosphatidylglycerol (PG) (32:1/16:2), phosphatidyl methyl ethanolamine (PMe) (19:3/13:0), PMe (26:1/9:0), sphingomyelin (SM) (d16:0/18:1), triglycerides (TG) (18:0/18:1/18:2), and TG (19:4/21:6/21:6) levels [variable importance in the projection (VIP > 1 and P < 0.05)], while HS group increased serum PC (17:0/17:0) content (VIP > 1 and P < 0.05). Also, metabolic pathway analysis showed that the pathways of glycerolphospholipid, linoleic acid and α-linolenic acid metabolism, and glycosylphosphatidylinositol (GPI)-anchored biosynthesis were changed (P < 0.05). In conclusion, HS led to the disorders of serum lipid metabolism in broilers, and mainly downregulated serum content of phospholipids. These findings provide novel insights into the effects of HS on serum lipidomics in indigenous slow-growing chickens.