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Strawberry (Fragaria × ananassa) is among the most widely cultivated fruits with good taste and rich nutrients. Many strawberry species, including white strawberries, are planted all over the world. The metabolic profiles of strawberry and distinctions among different cultivars are not fully understood. In this study, non-targeted metabolomics based on UHPLC-Q-Exactive Orbitrap MS was used to analysis the metabolites in 10 strawberry species. A total of 142 compounds were identified and were divided into six categories. Tochiotome may differ most from the white strawberry (Baiyu) by screening 72 differential metabolites. Histidine, apigenin, cyanidin 3-glucoside and peonidin 3-glucoside had potential as biomarkers for distinguishing Baiyu and another 11 strawberry groups. Amino acid metabolisms, anthocyanin biosynthesis and flavonoid biosynthesis pathways were mainly involved in the determination of the nutrition distinctions. This research contributes to the determination of the nutrition and health benefits of different strawberry species. [ABSTRACT FROM AUTHOR]

Maternal exposure to antibiotics existing in the environment is a predisposing factor for developmental malformation with metabolic disorders in offspring. In this study, female zebrafish (3 months) were exposed to 0.05 mg/L and 0.5 mg/L florfenicol (FF) for 28 days. After pairing and spawning with healthy male fish, F1 embryos were collected and developed to 5 d post-fertilization (dpf) in clear water. And the adverse effects on the F1 generation were examined thoroughly. The fecundity of F0 female fish and the hatchability, mortality, and body length of F1 larvae significantly decreased in the treatment group. Meanwhile, multi-malformation types were found in the exposure group, including delayed yolk sac absorption, lack of swim bladder, and spinal curvature. Metabolomic and transcriptomic results revealed alterations in metabolism with dysregulation in tricarboxylase acid cycle, amino acid metabolism, and disordered lipid metabolism with elevated levels of glycerophospholipid and sphingolipid. Accompanying these metabolic derangements, decreased levels of ATP and disordered oxidative-redox state were observed. These results were consistent with the damaged mitochondrial membrane potential and respiratory chain function, suggesting that the developmental toxicity and perturbed metabolic signaling in the F1 generation were related to the mitochondrial injury after exposing F0 female zebrafish to FF. Our findings highlighted the potential toxicity of FF to offspring generations even though they were not directly exposed to environmental contaminants. • The adverse effect of maternal exposure to florfenicol on F1 larvae was studied. • Decreased hatchability and increased malformation rate were observed. • The level of metabolites, lipids, and related gene expression were changed. • Impaired mitochondrial and disordered cellular oxidative state were observed. [ABSTRACT FROM AUTHOR]

As persistent organic pollutants, polychlorinated biphenyls (PCBs) accumulate in the bodies of animals and humans, resulting in toxic effects on the reproductive, immune, nervous, and endocrine systems. The biological and toxicological characteristics of enantiomers of chiral PCBs may differ, but these enantioselective effects of PCBs have not been fully characterized. In this study, we performed metabolomics analysis, using ultra-high performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) to investigate the enantioselective toxic effects of PCB95 in zebrafish (Danio rerio) embryos after exposure to three dose levels of 0.1, 1, and 10 μg/L for 72 h. Multivariate analysis directly reflected the metabolic perturbations caused by PCB95. The effects of (-)-PCB95 and (+)-PCB95 were more prominent than those of the racemate in zebrafish embryos. A total of 26 endogenous metabolites were selected as potential marker metabolites with variable importance at projection values larger than 1 and significant differences (p<0.05). These metabolites included amino acids, organic acids, nucleosides, betaine, and choline. The changes in these biomarkers were dependent on the enantiomer-specific structures of PCB95. Fifteen metabolic pathways were significantly affected, and several nervous and immune system-related metabolites were significantly validated after exposure. These metabolic changes indicated that the toxic effects of PCB95 may be associated with the interaction of PCB95 with the nervous and immune systems, thus resulting in disruption of energy metabolism and liver function. [ABSTRACT FROM AUTHOR]

Fipronil and its metabolites (fipronil sulfone, fipronil sulfide and fipronil desulfinyl) adversely affect the environment and human health. Targeted metabolomics and lipidomics based on ultra-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) was used to analyse the alterations of glycerophospholipids and amino acids after exposure to fipronil and its metabolites at dosages of 0.5, 12.5 and 50 μM for 72 h and to evaluate their different toxic effects. Results showed that fipronil sulfone and fipronil desulfinyl are more toxic than their parent compound, with fipronil desulfinyl as the most toxic and fipronil sulfide as the least toxic. Fipronil and its metabolites affected the metabolism of PC18:1/16:0, PI18:0/20:4, arginine, leucine and tyrosine and the "phenylalanine, tyrosine and tryptophan biosynthesis" pathway, indicating their possible inducing role in cellular macromolecule damage, nerve signal transmission disturbance and energy metabolism disruption caused by oxidative stress. Importantly, fipronil sulfone and fipronil desulfinyl more strongly influenced lipid and amino acid metabolism, mainly reflected in the number of changed glycerophospholipids and differential metabolites associated with oxidative stress, including PS18:0/20:4, glutamate, phenylalanine and histidine for fipronil sulfone and PS18:0/20:4, glutamate, phenylalanine, serine and aspartic acid for fipronil desulfinyl. Therefore, the higher toxicity of fipronil desulfinyl and fipronil sulfone may be also related to oxidative stress. This study provides implications for risk assessment and toxic mechanism research on fipronil and its metabolites. [Display omitted] • Fipronil and its metabolites caused cellular damage to PC12 cells by interfering with lipid and amino acid metabolism. • Fipronil desulfinyl and fipronil sulfone have a greater impact on lipid and amino acid metabolism. • The reason behind the differences can be attributed to oxidative stress. [ABSTRACT FROM AUTHOR]

2,2′,3,5',6-Pentachlorobiphenyl (PCB95) is known as a persistent pollutant that was found in eggs in China. PCB 95 can be metabolized into OH-PCB95 and MeO-PCB95 in liver microsomes. However, the toxicity and its mechanism of PCB95 or its metabolites have been little studied on laying hens. Herein, chicken embryo liver cells of laying hens were selected and treated with different levels of PCB95 and its two metabolites, and the EC 50 of PCB95, OH-PCB95, MeO-PCB95 was 80.85, 4.81 and 107.04 μg/mL respectively, indicating that OH-PCB95 is much more cytotoxic than PCB95 or MeO-PCB95. Targeted metabolomics was further used to study the effects of the parent compound and its metabolites on cell metabolism. The results showed that four primary types of glycerophospholipids were down-regulated after exposure to PCB95 and its metabolites, especially PE and PS (60% more than the control for PCB95, 40% for OH-PCB95, and less than 40% for MeO-PCB95). KEGG pathway analysis based on amino acid metabolism showed that PCB95 may mainly interfere with the amino acids involved in immune regulation (phenylalanine and tyrosine), and OH-PCB95 may be associated with genetic disoders (cysteine, methionine and purine metabolism). However, the metabolic pathways induced by MeO-PCB95 are quite different from those induced by PCB95 and OH-PCB95, affecting mainly D-glutamine and D-glutamate metabolism, alanine and glutamate metabolism, and arginine and proline metabolism; these pathways mainly regulate the elimination of excess purines and are involved in the synthesis of the amino acids required by cells. These results showed that OH-PCB95 has the highest toxicity on chicken embryo liver cells and MeO-PCB95 could be a detoxification product of PCB95 and OH-PCB95. This study contributes to the understanding of the different effects of PCB95 and its metabolites on cellular metabolism, and the data are helpful in evaluating the hepatotoxic effects of these compounds. Image 1 • Most PCBs contamination was reported only in eggs, but not in Chicken Embryo Liver Cells of Laying Hens. • The cytotoxicity of PCB95 and its metabolites was compared. • The mechanism of PCBS on cells was analysed for the perspective of metabolome. • Further demonstration that methoxyl metabolites may be detoxifying substances of hydroxyl metabolites. [ABSTRACT FROM AUTHOR]

Di-(2-ethylhexyl) phthalate (DEHP) is one of the most important environmental pollutants and affects multiple pathways upon human exposure. DEHP could induce MCF-7 cell proliferation at a very low dose; however, the possible linkage between DEHP and the cell proliferation effect is still unclear. Here, we carried out a comprehensive metabolome and transcriptome analysis to depict the possible molecular mechanisms of the effect of DEHP exposure on MCF-7 proliferation. In this paper, MCF-7 cells treated with DEHP at a dose of 1 μM for 48 h were selected for metabolome and transcriptome analysis. Untargeted and targeted metabolomics identified 8 differential metabolites, including amino acids, purine, pyrimidine and nucleotides. The metabolite changes were associated with 9 metabolic pathways. Disorders in riboflavin, histidine, beta-alanine metabolism, and nitrogen metabolism caused by DEHP exposure are important concerns for MCF-7 proliferation. Moreover, a transcriptomics study of the MCF-7 cells found a total of 500 differentially expressed genes (DEGs). KEGG enrichment analyses showed that pathways in cancer had stronger responses. The results of integrated analysis of the interactions between the DEGs and metabolites revealed significant changes in the purine metabolism pathway, which will shed light on the mechanism of MCF-7 cell proliferation after DEHP exposure. Overall, this study depicts the possible contribution of DEHP exposure to MCF-7 cell proliferation and highlights the power of omics platforms to deepen the mechanistic understanding of toxicity caused by endocrine disrupting chemicals. • Eight differentially metabolites were identified based on metabolomics analysis, including amino acids, purine, pyrimidine. • Disorders in riboflavin and histidine metabolism caused by DEHP exposure are important concerns for MCF-7 proliferation. • The purine metabolism pathway had a significant influence on MCF-7 cell viability after DEHP exposure at 1 μM for 48 h. [ABSTRACT FROM AUTHOR]