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The widespread use of Triphenyl phosphate (TPhP) as a substitute flame retardant in various commercial products has raised global concerns for its health risks. Previously, we found that gestational and lactational TPhP exposure disturbed lipid metabolism and gut microbiota in offspring sex-dependently. In this study, we further explored the prenatal TPhP exposure on lipid metabolism in male offspring, and the role of gut-bile acids-liver axis in it. The results showed that gestational TPhP exposure would induce hyperlipidemia in male offspring, it dose-dependently increased the weight of body and liver, levels of serum lipid, and enlarged lipid droplets in white adipose tissue. The expression of lipid metabolism-related genes was significantly changed in the liver and adipose tissue. The gut microbiome of male offspring was also altered, with different profiles between the low and high dose treatment group. Target bile acids (BAs) metabolites analysis revealed a significant increased levels of primary BAs cholic acid (CA), but decreased levels of chenodeoxycholic acid (CDCA), and decreased levels of the secondary BAs deoxycholic acid (DCA), hyodeoxycholic acid (HDCA), ursodeoxycholic acid (UDCA), and lithocholic acid (LCA) in TPhP treatment group. Measurements of gene expression along the gut-BAs-liver axis showed that the TPhP treatment group had an increase in cholesterol-7alpha-hydroxylase (CYP7A1) and a decrease in apical sodium-dependent bile acid transporter (ASBT), with only the low-dose group exhibiting an increase in carbohydrate response element binding protein (ChREBP). Correlation and mediation analysis highlighted associations of Burkholderiaceae in low-dose treatment group and Erysipelotrichaceae in high dose group with lipid metabolism and BAs metabolites. No consistent correlations were observed in two treatment group. Additionally, Mantel tests did not reveal a consistent correlation between the microbiome network community and lipid metabolism or the gut-bile acids-liver axis. Overall, our findings indicate that gestational TPhP exposure induces hyperlipidemia in male offspring, and while the gut-BAs-liver axis plays a role, other mechanisms warrant further investigation.

Abstract Background Antibiotic exposure can occur in medical settings and from environmental sources. Long-term effects of brief antibiotic exposure in early life are largely unknown. Results Post a short-term treatment by ceftriaxone to C57BL/6 mice in early life, a 14-month observation was performed using 16S rRNA gene-sequencing technique, metabolomics analysis, and metagenomics analysis on the effects of ceftriaxone exposure. Firstly, the results showed that antibiotic pre-treatment significantly disturbed gut microbial α and β diversities (P

Arsenic (As) is a widespread global pollutant, and there is significant controversy surrounding its complex relationship with obesity, primarily focused on short-term exposure. Recognizing the prolonged nature of dietary arsenic exposure, this study involved feeding mice with arsenic-contained food for 14 months. The results showed that mice exposed to arsenic developed a non-alcoholic fatty liver condition, characterized by a light-yellow hue on the liver surface and various pathological alterations in the liver cells, including enlarged nuclei, cellular necrosis, inflammatory infiltration, dysfunctional mitochondria, and endoplasmic reticulum disorganization. There were also disruptions in biochemistry indices, with a significant increase in total cholesterol (TC) level and a decrease in high-density lipoprotein (HDL) level. However, some contradictory observations occurred, such as a significant decrease in body weight, triglyceride (TG) level, and the numbers of lipid droplets. Several genes related to lipid metabolism were tested, and a model was used to explain these discrepancies. Besides, examinations of the colon revealed compromised intestinal barrier function and signs of inflammation. Fecal 16S rRNA sequencing and pseudo-targeted metabolomics revealed disruptions in internal homeostasis, such as modules, nodes, connections, and lipid-related KEGG pathways. Fecal targeted metabolomics analyses of short-chain fatty acids (SCFAs) and bile acids (BAs) demonstrated a significant upregulation in three primary bile acids (CA, CDCA, TCDCA), four secondary bile acids (TUDCA, DCA, LCA, GUDCA), and total SCFAs level. Oxidative stress and inflammation were also evident. Additionally, based on correlation analysis and mediation analysis, it was assumed that changes in the microbiota (e.g., Dubosiella) can impact the liver metabolites (e.g., TGs) through alterations in fecal metabolites (e.g., LPCs). These findings provide a theoretical reference for the long-term effect of arsenic exposure on liver lipid metabolism.

A rapid high-performance liquid chromatography (HPLC) protocol for the determination of amino acids with 6-aminoquinolyl-N-hydroxysuccinimidyl carbamate (AQC) derivatization was successfully developed for assessing amino acid levels in six species of representative commercial bee pollen. Based on a poroshell column, a favorable chromatographic separation of seventeen amino acids was achieved in approximately 10 min with satisfactory resolution. The LOD and LOQ of this method were less than 0.034 μg/mL and 0.232 μg/mL, and the intra- and inter-day RSDs ranged between 0.86–5.28 % and 3.21–6.50 %, respectively. The matrix effect (ME) ranged from −8 to 3, implying that the matrix effect was not significant. Under the optimum conditions, the established method was adopted to determine amino acids in six types of bee pollens. The results showed that the total amino acid content ranged from 151.94 mg/g (Rosa rugosa) to 214.52 mg/g (Leonurus artemisia) in the six bee pollen species. Notably, proline (Pro), valine (Val), leucine (Leu), and phenylalanine (Phe) were abundant in the majority of samples. To identify the suspicious samples, principal component analysis (PCA) was performed, and each type of bee pollen was differentiated. Results showed that, in the market, the qualification rate of RR was 100 %, but that of NN was merely 62.5 %, revealing that a few of them were counterfeit. This method offers advantages such as high speed, low cost, and outstanding performance.

Arsenic, a ubiquitous environmental toxicant with various forms and complex food matrix interactions, can reportedly exert differential effects on the liver compared to drinking water exposure. To examine its specific liver-related harms, we targeted the liver in C57BL/6 J mice (n=48, 8-week-old) fed with arsenic-contaminated food (30 mg/kg) for 60 days, mimicking the rice arsenic composition observed in real-world scenarios (iAsV: 7.3%, iAsIII: 72.7%, MMA: 1.0%, DMA: 19.0%). We then comprehensively evaluated liver histopathology, metabolic changes, and the potential role of the gut-liver axis using human hepatocellular carcinoma cells (HepG2) and microbiota/metabolite analyses. Rice arsenic exposure significantly altered hepatic lipid (fatty acids, glycerol lipids, phospholipids, sphingolipids) and metabolite (glutathione, thioneine, spermidine, inosine, indole-derivatives, etc.) profiles, disrupting 33 metabolic pathways (bile secretion, unsaturated fatty acid biosynthesis, glutathione metabolism, ferroptosis, etc.). Pathological examination revealed liver cell necrosis/apoptosis, further confirmed by ferroptosis induction in HepG2 cells. Gut microbiome analysis showed enrichment of pathogenic bacteria linked to liver diseases and depletion of beneficial strains. Fecal primary and secondary bile acids, short-chain fatty acids, and branched-chain amino acids were also elevated. Importantly, mediation analysis revealed significant correlations between gut microbiota, fecal metabolites, and liver metabolic alterations, suggesting fecal metabolites may mediate the impact of gut microbiota and liver metabolic disorders. Gut microbiota and its metabolites may play significant roles in arsenic-induced gut-liver injuries. Overall, our findings demonstrate that rice arsenic exposure triggers oxidative stress, disrupts liver metabolism, and induces ferroptosis.

Abstract Zebrafish (Danio rerio) have attracted much attention over the past decade as a reliable model for gut microbiome research. Owing to their low cost, strong genetic and development coherence, efficient preparation of germ‐free (GF) larvae, availability in high‐throughput chemical screening, and fitness for intravital imaging in vivo, zebrafish have been extensively used to investigate microbiome‐host interactions and evaluate the toxicity of environmental pollutants. In this review, the advantages and disadvantages of zebrafish for studying the role of the gut microbiome compared with warm‐blooded animal models are first summarized. Then, the roles of zebrafish gut microbiome on host development, metabolic pathways, gut‐brain axis, and immune disorders and responses are addressed. Furthermore, their applications for the toxicological assessment of aquatic environmental pollutants and exploration of the molecular mechanism of pathogen infections are reviewed. We highlight the great potential of the zebrafish model for developing probiotics for xenobiotic detoxification, resistance against bacterial infection, and disease prevention and cure. Overall, the zebrafish model promises a brighter future for gut microbiome research.

Gut microbiome can participate in arsenic metabolism. However, its efficacy in the host under arsenic stress is still controversial. To clarify their roles in fecal arsenic excretion, tissue arsenic accumulation, host physiological states and metabolism, in this study, ninety-six C57BL/6 male mice were randomly divided to four groups, groups A and B were given sterile water, and groups C and D were given the third generation of broad-spectrum antibiotic (ceftriaxone) to erase the background gut microbiome. Subsequently, groups B and D were subchronicly exposed to arsenic containing feed prepared by adding arsenical mixture (rice arsenic composition) into control feed. In group D, the fecal total arsenic (CtAs) decreased by 25.5 %, iAsIII composition increased by 46.9 %, unclarified As (uAs) composition decreased by 92.4 %, and the liver CtAs increased by 26.7 %; the fecal CtAs was positively correlated with microbial richness and some metabolites (organic acids, amino acids, carbohydrates, SCFAs, hydrophilic bile acids and their derivatives); and fecal DMA was positively correlated with microbial richness and some metabolites (ferulic acid, benzenepropanoic acid and pentanoic acid); network analysis showed that the numbers of modules, nodes, links were decreased and vulnerability was increased; some SCFAs and hydrophilic bile acid decreased, and hydrophobic bile acids increased (Ps

Long-term consumption of arsenic-contaminated rice has become a public health issue that urgently needs to be addressed. In this study, mice were exposed to arsenic in rice (low dose, 0.91 mg/kg; medium dose, 9.1 mg/kg) for 30 days and 60 days, respectively, and the effects on pathological structures of spleen and skin, as well as the structure of the fecal microbiome were examined. The findings revealed dose/time cumulative effects on pathological changes, with even a low dose exposure for 30 days causing destruction of splenic follicular structure and thickening of dermal keratinized and epidermal layers. The Firmicutes/Bacteroidetes ratio in the community and the positive/negative ratio in network links were higher in arsenic groups, suggesting that arsenic resulted in a less healthy and unstable microbiome for the host. Thus lifetime consumption of arsenic in rice may have potential health effects on humans and must be carefully assessed to safeguard human health. Furthermore, in arsenic groups, arsenic-resistant bacteria or arsenic hazards remediation bacteria changed to be the dominant bacteria and acted as the core bacteria in the network modules. Some microbial arsenic transforming genes (arsC, arsR, arsA, ACR3, and aoxB) differed, indicating that the gut microbiome changed to withstand arsenic stress. Furthermore, Faecalibaculum, Lachnospiraceae_NK4A136_group, Angelakisella, Ruminiclostridium, and Desulfovibrionaceae are positively associated with arsenic dosage and may be useful in the early detection of arsenicals.

Arsenic can cause neurodegenerative diseases of the brain, but the definite mechanism is still unknown. In this study, to discuss the disturbances on brain metabolome and lipidome under subchronic arsenic exposure, we treated mice with the arsenic-containing feed (concentration of total arsenic = 30 mg/kg) prepared in accordance with the proportion of rice arsenicals for 16 weeks and performed metabolomics and lipidomics studies respectively using UHPLC-Triple-TOF-MS/MS and UHPLC-Q Exactive Focus MS/MS on mice brain. In addition, the distributions of arsenical metabolites along the feed-gut-blood-brain chain were analyzed by ICP-MS and HPLC-ICP-MS, and fecal microbial variations were investigated by 16 s sequencing. The data showed that although only a tiny amount of arsenic (DMA=0.101 mg/kg, uAs=0.071 mg/kg) enters the brain through the blood-brain barrier, there were significant changes in brain metabolism, including 118 metabolites and 17 lipids. These different metabolites were involved in 30 distinct pathways, including glycometabolism, and metabolisms of lipid, nucleic acid, and amino acid were previously reported to be correlated with neurodegenerative diseases. Additionally, these different metabolites were significantly correlated with 12 gut bacterial OTUs, among which Lachnospiraceae, Muribaculaceae, Ruminococcaceae, and Erysipelotrichaceae were also previously reported to be related to the distortion of metabolism, indicating that the disturbance of metabolism in the brain may be associated with the disturbance of gut microbes induced by arsenic. Thus, the current study demonstrated that the brain metabolome and lipidome were significantly disturbed under subchronic arsenic exposure, and the disturbances also significantly correlated with some gut microbiome and may be associated with neurodegenerative diseases. Although preliminary, the results shed some light on the pathophysiology of arsenic-caused neurodegenerative diseases.

Background Chinese cordyceps (Lepidoptera: Ophiocordyceps sinensis)is a larval-fungus complex. The concentration and distribution of arsenic (As) may vary during the stroma (ST) germination process and between the sclerotium (SC) and the ST. The soil-to-Chinese cordyceps system is an environmental arsenic exposure pathway for humans. We studied the As concentration in the soil, the SC, and the ST of Chinese cordyceps, and performed a risk assessment. Methods Soil and Chinese cordyceps samples were collected from the Tibetan Plateau in China. The samples were analyzed for the total As concentration and As species determination, which were conducted by inductively coupled plasma mass spectrometry (ICP-MS) and HPLC-ICP-MS, respectively. Results The concentration of total As in the soil was much higher than in SC and ST. The major As species in the soil was inorganic AsV. In SC and ST, organic As was predominant, and the majority of As was an unknown organic form. There are significant differences in the As distribution and composition in soil, SC, and ST. Our risk assessment indicated that chronic daily ingestion was higher than inhalation and dermal exposure in children and adults. The hazard index (HI) of the non-carcinogenic and cancer risks (CR) for human health were HI ≤ 1 and CR

Background: Arsenic, a global pollutant and a threshold-free primary carcinogen, can accumulate in rice. Previous studies have focused on arsenic poisoning in drinking water and the effects on gut microbes. The research on arseniasis through food, which involves the bio-transformation of arsenic, and the related changes in gut microbiome is insufficient. Method: Mice were exposed from animal feed prepared with four arsenic species (iAsIII, iAsV, MMA, and DMA) at a dose of 30 mg/kg according to the arsenic species proportion in rice for 30 days and 60 days. The levels of total arsenic (tAs) and arsenic species in mice feces and urine samples were determined using ICP-MS and HPLC-ICP-MS, respectively. 16S rRNA and ITS gene sequencing were conducted on microbial DNA extracted from the feces samples. Results: At 30 days and 60 days exposure, the tAs levels excreted from urine were 0.0092 and 0.0093 mg/day, and tAs levels in feces were 0.0441 and 0.0409 mg/day, respectively. We found significant differences in arsenic species distribution in urine and feces (p

Ophiocordyceps sinensis is a widely known medicinal entomogenous fungus, which parasitizes the soil-borne larva of Thitarodes (Hepialidae, Lepidoptera) distributed in the Qinghai−Tibetan Plateau and its adjacent areas. Previous research has involved artificial cultivation of Chinese cordyceps (the fungus-caterpillar complex), but it is difficult to achieve large-scale cultivation because the coupling relation between the crucial microbes and their hosts is not quite clear. To clarify the influence of the internal microbial community on the occurrence of Chinese cordyceps, in this study, the unfertilized eggs of Thitarodes of different sampling sites were chosen to analyze the bacterial and fungal communities via 16S rRNA and ITS sequencing for the first time. The results showed that for bacteria, 348 genera (dominant genera include Wolbachia, Spiroplasma, Carnobacterium, Sphingobium, and Acinetobacter) belonging to 26 phyla (dominant phyla include Proteobacteria, Firmicutes, Tenericutes, Actinobacteria, Acidobacteria, and Bacteroidetes), 58 classes, 84 orders, and 120 families were identified from 1294 operational taxonomic units (OTUs). The dominant bacterial genus (Spiroplasma) may be an important bacterial factor promoting the occurrence of Chinese cordyceps. For fungi, 289 genera, mainly including Aureobasidium, Candida, and Cryptococcus, were identified, and they belonged to 5 phyla (Ascomycota, Basidiomycota, Chytridiomycota, Glomeromycota, and Zygomycota), 26 classes, 82 orders, and 165 families. Eight bacterial OTUs and 12 fungal OTUs were shared among all of the detected samples and were considered as core species. Among them, Wolbachia, Spiroplasma, Carnobacterium, Aureobasidium, and Phoma may play important roles in helping the host larva to digest foods, adapt to extreme environments, or resist pathogens. On the other hand, the external (soil) microbial community was synchronously and comparatively analyzed. Comparative analysis revealed that external microbial factors might play a more significant role in the occurrence of Chinese cordyceps, owing to the significant differences revealed by α-diversity and β-diversity analyses among different groups. In summary, the results of this study may contribute to the large-scale cultivation of Chinese cordyceps.

The exposure and harm of arsenic have attracted wide attention. Rice is an arsenic-rich crop. The purpose of this study was to learn the distribution of arsenic species and the pathological changes in tissues of mice exposed to arsenic-supplemented food simulating rice. Test groups of mice were orally exposed with prepared arsenic feeds supplemented with four arsenic species (arsenite iAsIII, arsenate iAsV, monomethylarsonate MMA, and dimethylarsinate DMA) at three doses (total As concentration: 0.91, 9.1 and 30 µg/g), which simulated the arsenic species ratio in rice. After 112 days, the concentrations of the arsenic species in the spleen, thymus, heart, skin and hair were detected, and histopathology of the spleen, heart and skin was observed. Each arsenic species was detected and their total concentration increased in a dose-dependent manner with a few exceptions. One interesting phenomenon is that ratio of the organic arsenic to inorganic arsenic also increased in a dose-dependent manner. For the other, the order of tissues from high to low arsenic concentration was the same in the medium- and high-dose groups. The histopathological sections of the spleen, heart and skin showed dose-dependent debilitating alterations in tissue architecture. Hyperplasia, hyaline degeneration and sclerosis of fibrous connective tissue occurred in the spleen. Myocardial cell atrophy and interstitial edema occurred in the heart. Hyperpigmentation, hyperkeratosis and atypia of basal cells occurred in the skin. In summary, the long-term intake of high arsenic rice has a health risk. Further studies are needed to assess it. [ABSTRACT FROM AUTHOR]

Due to the fractionation of stable carbon isotopes in plant photosynthesis, bio-decomposition processes, environmental factors, plant physiology, geographical factors, climatic conditions and agricultural practices, different foods exhibit significant differences in stable carbon isotope ratios. Therefore, stable carbon isotope ratio analysis (SCIRA) presents an effective tool for detecting food adulteration and food traceability control. In addition, stable carbon isotopes can frequently be used as markers to identify veterinary drug residues, pesticide residues and toxic substances remaining in foods by isotope dilution mass spectrometry (IDMS). The emphasis of this review, which will help readers to modify stable carbon isotope technologies more easily and extend their application in adulteration and traceability for foods, is on the characteristics of various instruments and the data processing methods in SCIRA and IDMS technologies. The latest research is also reviewed and highlighted. This paper reviews potential applications of these technologies to improve current food detection and protect consumers' rights. [ABSTRACT FROM AUTHOR]