Prolonged physical fatigue impairs physiological homeostasis and quality of life, necessitating effective interventions. This study aimed to investigate the anti-fatigue effects and underlying mechanisms of a novel L-β-galactoglucan (APG) with two distinct molecular weights in mice under two different swimming load models using multiomics approaches. The results showed that APG could significantly extend exhaustive swimming time, reduce elevated serum lactate and blood urea nitrogen levels, increase muscle glycogen storage, and mitigate swimming-induced skeletal muscle and mitochondrial damage. Compared with its medium-molecular-weight counterpart, high-molecular-weight APG was more effective at improving these indicators. APG optimized the gut microbiota and increased the content of short-chain fatty acids. Specifically, it increased the ratio of Bacteroidetes/Bacillota and promoted the abundance of beneficial bacteria, including Dubosiella, Lachnospiraceae_UCG-006, Parabacteroides, Roseburia, Faecalibaculum and norank_o_Clostridia_vadinBB60_group, while increasing the concentrations of acetic, propanoic, and isobutyric acids. Notably, APG exerted load-specific regulatory effects: In the weight-bearing model, APG modulated mainly purine metabolism, whereas in the non-weight-bearing model, it predominantly regulated tryptophan metabolism. Both pathways converge to synergistically activate AMPK/SIRT1/PGC-1α signaling. Molecular docking further verified that APG exhibited strong binding affinity to key targets in these pathways. Collectively, these findings demonstrate that APG exerts anti-fatigue effects in a molecular weight-dependent and load-specific manner via the gut-muscle axis, providing a scientific basis for the development of APG as a targeted anti-fatigue functional ingredient.

Per- and polyfluoroalkyl substances (PFAS) have been associated with adverse maternal and developmental health outcomes. However, studies on PFAS profile in multiple matched mother-infant samples remain limited. In this study, we aimed to characterize exposure levels and maternal-to-fetal transfer patterns of both conventional and emerging PFAS in a birth cohort from Chengdu, China. Concentrations of 24 PFAS were quantitatively determined in 47 pairs of maternal and infant samples, including maternal serum, cord serum, amniotic fluid, maternal urine, infant urine, and breast milk, using high-performance liquid chromatography-tandem mass spectrometry. The concentration ratios of PFAS in cord serum, amniotic fluid, and breast milk to maternal serum were calculated to assess their distribution across maternal, fetal, and neonatal matrices. The results indicated that both pregnant women and their offsprings were extensively exposed to PFAS. Emerging PFAS, including 6:2 chlorinated perfluoroalkyl ether sulfonic acid (6:2 Cl-PFESA), 6:2 fluorotelomer sulfonic acid, and sodium p-perfluorous nonenoxybenzene sulfonate (OBS), were generally detected in maternal serum, cord serum, and amniotic fluid. Perfluoroundecanoic acid (PFUnDA) was the predominant PFAS in maternal and cord serum, whereas the emerging compound OBS was the dominant PFAS in amniotic fluid. Perfluorooctanoic acid (PFOA), PFUnDA, and 6:2 Cl-PFESA in cord serum and amniotic fluid showed significant positive correlations with maternal serum levels (p < 0.05). Notably, emerging PFAS, particularly OBS, exhibited significantly higher transplacental transfer efficiencies (as indicated by cord-maternal concentration ratios) compared to legacy PFAS, such as PFOA and PFUnDA, OBS also had the highest accumulation in amniotic fluid. These findings highlight a potentially greater fetal exposure risk to these emerging contaminants, providing critical data for understanding PFAS exposure characteristics and informing public health policies aimed at protecting maternal and child health in China.

Increasing evidence suggests that carotenoids play an important role in visual and cognitive development during early life. This study aimed to depict the carotenoid profile in maternal/cord plasma and breast milk in three northern cities of China while investigating the association between dietary carotenoid intake and breast milk carotenoid levels. We enrolled 990 lactating mothers from three urban northern Chinese cities to collect breast milk (including colostrum, transitional milk, early mature milk, middle mature milk, and late mature milk). Among them, 90 participants also provided maternal/cord blood. The dietary carotenoid intake was recorded in the corresponding stages according to the Food Frequency Questionnaire and 24-hour dietary recall. The levels of carotenoids (lutein, zeaxanthin, beta-cryptoxanthin, beta-carotene, and lycopene) in maternal/cord plasma and breast milk were analyzed using high-performance liquid chromatography. We found a significant correlation between carotenoid concentrations in maternal and cord plasma. Moreover, carotenoid concentrations in maternal plasma were significantly higher than those in cord plasma. The total carotenoid levels in breast milk decreased from colostrum to late mature milk. beta-Carotene predominated in colostrum, whereas lutein dominated in transitional and mature milk. We also found that breast milk carotenoid levels correlated with dietary carotenoid intake to a certain extent, particularly during the early stages of lactation. Therefore, we encourage women to appropriately increase their dietary intake of carotenoid-rich vegetables and fruits during pregnancy and lactation, particularly during work hours after lactation leave. Moreover, the variance of the carotenoid profile in maternal/cord plasma and breast milk across the three cities implied the necessity of further depicting the carotenoid status and influencing factors across different areas in China.

Bisphenol S (BPS) is the main substitute for bisphenol A (BPA). However, the neurodevelopmental toxicity of BPS and the underlying mechanisms remain unraveled. In present study, the neuro-differentiating human embryonic stem cells, hESC, was exposed to BPS (0-375 mu M) at different stages (the precursor stage, the precursor to maturation stage, and the whole differentiation stage) to assess the potential neurodevelopmental toxicity and its mechanisms. The results revealed that BPS exposure interrupted axonogenesis, manifesting a trend of initial stimulating followed by inhibition, and peaked at the intermediate dose (3.75 mu M) significantly, then reached the nadir at the high dose (375 mu M) significantly in the precursor to maturation stage and the whole differentiation stage. Transcriptomics analysis showed that the main interrupted pathway enriched in axonogenesis, myelination, and neurotransmitter secretion by the GO function analysis and immune-related pathway by the KEGG analysis, besides, conserved axon guidance (Slit-Robo, Netrin-DCC, Semaphorin-Plexin) and WNT signaling pathway was also enriched in KEGG pathway analysis, which previously proved to regulate axonogenesis by directly acting on growth cones and inhibit axon growth by neuroinflammatory responses. And we found that a higher neuroinflammatory response may be induced through whole-differentiation-stage exposure than the response of exposure through the precursor to maturation stage. Overall, our findings indicated the nonmonotonic neurodevelopmental toxicity of BPS exposure, and the inhibition of axonogenesis was possibly mediated by conserved axon guidance and WNT signaling pathway, while neuro-immune related pathway should be further investigated.

BACKGROUND:Sodium alginate (SA), a dietary fiber, is known to influence lipid metabolism and gut microbiota. However, its long-term effects of viscosity/dose and sex-specific differences remain underexplored. This study investigates the impact of SA with different viscosities and doses on lipid metabolism and gut microbiota in 120 male and female Sprague-Dawley rats over 90 days. RESULTS:Both low-viscosity high-dose (Lv-SA-H, 250-350 mPa s, 8.00 g kg-1) and high-viscosity (Hv-SA, 600-800 mPa s, 8.00 g kg-1) SA significantly reduced body fat. Three treatments - low-viscosity low-dose SA (Lv-SA-L, 250-350 mPa s, 4.00 g kg-1), Lv-SA-H and Hv-SA - decreased serum triglyceride levels and increased serum total bile acid levels in serum. SA also elevated the levels of acetic and butyric acids in feces, modulated the fecal bile acids profile by promoting the excretion of 23-nordeoxycholic acid (NorDCA) and increased the levels of 3β-ursodeoxycholic acid (β-UDCA). 16S rDNA gene amplicon sequencing revealed that Lv-SA-H supplementation increased the relative abundance of Akkermansia and Bacteroides, while Lv-SA-L, Lv-SA-H and Hv-SA all reduced the abundance of Flavonifractor. Furthermore, a positive correlation was observed between NorDCA levels and the relative abundance of Flavonifractor in female rats, while β-UDCA levels were positively correlated with the relative abundance of Bacteroides in male rats. CONCLUSION:Our study suggests that SA regulates lipid metabolism by modulating the gut microbiota, which in turn affects the profiles of short-chain fatty acids and bile acids. These effects vary by sex and viscosity, emphasizing the importance of precision in future nutritional interventions. © 2025 Society of Chemical Industry.

Yak milk is a promising lipid source substitute for infant formulas designed to mimic human milk. However, comparative studies on the lipid profiles between human and yak milk are scarce. To address this gap, in this study, we thoroughly analysed and compared the lipidome and fatty acid (FA) composition of human colostrum, human mature milk and yak mature milk. A total of 2686 lipid species from 30 lipid classes were identified in the three milk types. Notably, yak mature milk surpassed both human milk stages in the total content of lipid species, triglycerides (TG) and saturated FA. In particular, three potential lipid biomarkers, namely TG(6,0_8,0_14:0) + NH4, TG(16,0_6,0_8:0) + NH4 and TG(10,0_12,0_12,0) + NH4, were identified to differentiate yak mature milk from human colostrum and mature milk. Moreover, upon analysing the lipid metabolic pathways, it was found that the lipids involved in the pathways of acetylcholine synthesis, as well as starch and sucrose metabolism, may not manifest notable differences between yak mature milk and human colostrum, indicating the presence of similar neurodevelopment-regulating and metabolic characteristics in yak milk as in colostrum. Therefore, this comprehensive comparison offers novel insights into the potential of yak mature milk lipids to enhance the humanisation of infant formulas.

IntroductionBamboo charcoal powder (BCP) is increasingly used as a food colorant. This study aims to evaluate the effects of BCP consumption on improving high-fat diet-induced hyperlipidemia.MethodsFifty male SD rats were randomly assigned into five groups, with 10 rats in each group: the control group was fed a low-fat diet (LFD); the model control group was fed a high-fat diet (HFD); the low-BCP dose group was fed a HFD and given 2.81 g of BCP/kg of body weight (BCP-L) by gavage; the medium-BCP dose group was fed a HFD and given 5.62 g of BCP/kg of body weight (BCP-M) by gavage; the high-BCP dose group was fed a HFD and given 11.24 g of BCP/kg of body weight (BCP-H) by gavage.ResultsAfter 90 days, the consumption of BCP caused a decrease in body weight, plasma lipids (triglyceride, cholesterol, and low-density lipoprotein (LDL)), liver triglyceride, and cholesterol levels, and liver histopathological scores. BCP caused a significant increase in superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC) in liver tissues. BCP also led to an increase in 72-h fecal dry weight and crude fat in a rat metabolic cage. The analysis of fecal samples with liquid chromatography time-of-flight mass spectrometry (LC-Q-TOF-MS) showed that the biomarkers associated with BCP consumption were mainly related to fatty and amino acid metabolism. Notably, BCP treatment significantly promoted linoleic acid metabolism.DiscussionThese results suggest that BCP may have a preventive effect against diet-induced hyperlipidemia through the promotion of fecal fat excretion. BCP may potentially be used as an alternative functional food component for people with diet-induced hyperlipidemia.

Background: In the plastics production sector, bisphenol S (BPS) has gained popularity as a replacement for bisphenol A (BPA). However, the mode of action (MOA) of female reproductive toxicity caused by BPS remains unclear and the safety of BPS is controversial. Methods: Human normal ovarian epithelial cell line, IOSE80, were exposed to BPS at human-relevant levels for short-term exposure at 24 h or 48 h, or for long-term exposure at 28 days, either alone or together with five signaling pathway inhibitors: ICI 18,2780 (estrogen receptor [ER] antagonist), G15 (GPR30 specific inhibitor), U0126 (extracellular regulated protein kinase [ERK] 1/2 inhibitor), SP600125 (c-Jun N-terminal kinase [JNK] inhibitor) or SB203580 (p38 mitogen-activated protein kinase [p38MAPK] inhibitor). MOA through ERO-MAPK signaling pathway interruption was explored, and potential thresholds were estimated by the benchmark dose method. Results: For short-term exposure, BPS exposure at human-relevant levels elevated the ESR2 and MAPK8 mRNA levels, along with the percentage of the G0/G1 phase. For long-term exposure, BPS raised the MAPK1 and EGFR mRNA levels, the ERS, p-ERK, and p-JNK protein levels, and the percentage of the G0/G1 phase, which was partly suppressed by U0126. The benchmark dose lower confidence limit (BMDL) of the percentage of the S phase after 24 h exposure was the lowest among all the BMDLs of a good fit, with BMDL5 of 9.55 mu M. Conclusions: The MOA of female reproductive toxicity caused by BPS at human-relevant levels might involve: molecular initiating event (MIE)-BPS binding to ERO receptor, key event (KE)1-the interrupted expression of GnRH, KE2-the activation of JNK (for short-term exposure) and ERK pathway (for long-term exposure), KE3-cell cycle arrest (the increased percentage of the G0/G1 phase), and KE4-interruption of cell proliferation (only for short-term exposure). The BMDL of the percentage of the S phase after 24 h exposure was the lowest among all the BMDLs of a good fit, with BMDL5 of 9.55 mu M.

OBJECTIVE:To investigate the effects of long-term(7 days and 14 days) bisphenol S(BPS) exposure on the ERβ-MAPK signaling pathway, hormone secretion phenotype and cell cycle in human normal ovarian epithelial cells IOSE 80 at actual human exposure level.METHODS:Physiologically based pharmacokinetic model combined with BPS levels in the serum of women along the Yangtze River in China was used to determine the dosing concentrations of BPS, and vehicle control and 17 β-estradiol(E_2) control were used. Complete medium with corresponding concentrations(0, 6.79×10~(-6), 6.79×10~(-4), 6.79×10~(-2), 6.79 μmol/L BPS and 10 nmol/L E_2) was replaced every 2 days. mRNA expressions of estrogen receptor(ERβ and GPR30), key genes in MAPK signaling pathway(P38/JNK/ERK signaling pathway) and gonadotropin-releasing hormone-related genes(GnRH-I, GnRH-II and GnRH-R) were measured by qPCR. The ERβ-MAPK signaling pathway inhibitors were employed to detect the effect of long-term exposure to BPS on the cell cycle by flow cytometry. Dose-response relationship analysis was performed to calculate the benchmark does lower confidence limits.RESULTS:Compared to the vehicle control, after 7 days exposure to BPS, the ratio of G_2/M phase was significantly increased(P&lt;0.05), and the mRNA expressions of GnRH-I, GnRH-II and GnRH-R were significantly decreased(P&lt;0.05); after 14 days exposure to BPS, the mRNA expressions of ESR2, MAPK3, and MAPK9 were significantly increased(P&lt;0.05), and the mRNA expressions of GnRH-II and GnRH-R were significantly decreased(P&lt;0.05). The GnRH-II mRNA expression level of BPS treatment for 7 days; the G_0/G_1 phase ratio, MAPK3 and MAPK8 mRNA expression level of BPS exposure for 14 days; and the GnRH-I mRNA expression level after BPS treatment for 7 days and 14 days showed a good dose-response relationship but with poor fit.CONCLUSION:Long-term low-dose exposure to BPS may cause cell cycle arrest by activating the ERβ-MAPK signaling pathway, and may lead to changes in the hormone secretion of IOSE 80 cells.

AbstractCarotenoids are important bioactive substances in breast milk, the profile of which is seldom studied. This study aimed to explore the profile of carotenoids in breast milk and maternal/cord plasma of healthy mother–neonate pairs in Shanghai, China, and their correlation with dietary intake. Maternal blood, umbilical cord blood and breast milk samples from five lactation stages (colostrum, transitional milk and early-, mid- and late-term mature milk) were collected. Carotenoid levels were analysed by HPLC. Carotenoid levels in breast milk changed as lactation progressed (P< 0·001).β-Carotene was the primary carotenoid in colostrum. Lutein accounted for approximately 50 % of total carotenoids in transitional milk, mature milk and cord blood. Positive correlations were observed between five carotenoids in umbilical cord blood and maternal blood (Pall < 0·001).β-Carotene levels were also correlated between maternal plasma and three stages of breast milk (r= 0·605,P< 0·001;r= 0·456,P= 0·011,r= 0·446;P= 0·013, respectively). Dietary carotenoid intakes of lactating mothers also differed across lactation stages, although no correlation with breast milk concentrations was found. These findings suggest the importance of exploring the transport mechanism of carotenoids between mothers and infants and help guide the development of formulas for Chinese infants as well as the nutritional diets of lactating mothers.

Organophosphate esters (OPEs) have been widely produced and used, while little is known about their occurrence in the food chain and potential sources. In this study, raw cow milk, cow drinking water, and feed were collected from pastures across China, and OPEs were tested to explore the occurrence and transmission of OPEs in the food chain and to further assess daily OPE intakes for cows and humans via certain food consumption. The median level of & sum;OPEs (sum of 15 OPEs) in raw milk was 2140 pg/mL, and tris(1-chloro-2-propyl) phosphate (TCIPP) was the most abundant OPE. Levels of OPEs in water were lower than those in raw milk except for triethyl phosphate (TEP), while levels of most OPEs in feed were significantly higher than those in raw milk (adjusted by dry weight). The estimated dietary intake of OPEs via feed for cows was 2530 ng/kg bw/day, which was much higher than that via water (742 ng/kg bw/day), indicating that feed was a more critical exposure source. For liquid milk consumers, the high-exposure (95th) estimated daily intakes (EDIs) of & sum;15OPE were 20 and 7.11 ng/kg bw/day for 3-17 years and adults, respectively, and it is obvious that cows had much heavier OPE intake. Finally, the calculated hazard indexes (HIs) suggested that the intake of OPEs via cow milk consumption would not pose significant health risks to the Chinese population.

Bisphenol A (BPA), a common endocrine disruptor, has shown cardiovascular toxicity in several epidemiological studies, as well as in vivo and in vitro experimental studies. However, the related adverse outcome pathway (AOP) of BPA toxicity remains unraveled. This study aimed to develop an AOP for the cardiac toxicity of BPA through bioinformatics analysis. The interactions among BPA, genes, phenotypes, and cardiac toxicity were retrieved from several databases, including the Comparative Toxicogenomics Database, Computational Toxicology, DisGeNet, and MalaCards. The target genes and part of target phenotypes were obtained by Venn analysis and literature screening. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were performed for target genes by using the DAVID online analysis tool to obtain other target phenotypes. AOP hypotheses from BPA exposure to heart disease were established and evaluated comprehensively by a quantitative weight of evidence (QWOE) method. The target genes included ESR2, MAPK1, TGFB1, and ESR1, and the target phenotypes included heart contraction, cardiac muscle contraction, cellular Ca2+ homeostasis, cellular metabolic process, heart development, etc. Overall, the AOP of BPA cardiac toxicity was deduced to be as follows. Initially, BPA bound with ERα/β and then activated the MAPK, AKT, and IL-17 signaling pathways, leading to Ca2+ homeostasis disorder and increased inflammatory response. Subsequently, cardiac function was impaired, causing coronary heart disease, arrhythmia, cardiac dysplasia, and other heart diseases. According to the Bradford-Hill causal considerations, the score of AOP by QWOE was 69, demonstrating a moderate confidence and providing clues on cardiotoxicity-assessment procedure and further studies on BPA.

Bisphenol S (BPS) has been put into production as a wide range of Bisphenol A (BPA) alternatives, while little is known regarding its cardiac developmental toxicity. To explore the effect of BPS on cardiomyocyte differentiation and its mechanism, our study established the human embryonic stem cell-cardiomyocyte differentiation model (hESC-CM), which was divided into early period of differentiation (DP1:1-8d), anaphase period of differentiation (DP2:9-16d) and whole stage of differentiation (DP3:1-16d) exposed to human-related levels of BPS. We found that the survival rate of cardiomyocytes was more sensitive to BPS at the early stage of differentiation than at the anaphase stage of differentiation, and exposure to higher than 30 µg/mL BPS throughout the differentiation period decreased the expression of cTnT. BPS may affect cardiomyocyte differentiation by activating ERβ-NF-κB/ERK signaling pathway, and the signaling pathway of each stage might be different. During DP1, 3 µg/mL of BPS may increase the inflammatory effect of cardiomyocytes mainly through the ERβ-NF-κB signaling pathway, thereby inhibiting cell proliferation, and leading to impaired cardiac function in early differentiation. During DP2, BPS may activate the ERβ-ERK signaling pathway, increase cardiomyocyte apoptosis, alter the establishment of the outer matrix, and thus affect myocardial differentiation. However, exposure to BPS throughout the differentiation stage may disrupt the immune response and cell differentiation, which in turn interrupts heart function. The benchmark dose lower confidence limit (BMDL) of the relative expression of cTnT mRNA exposed by BPS during DP3 was the lowest among all the BMDLs of a good fit, with BMDL5 of 1.96 × 10-2 µg/mL, which is lower than the current reported exposure levels of BPS in maternal serum (0.03-0.07 ng/mL) and maternal umbilical cord serum (0.03-0.12 ng/mL).

Aflatoxins(AFs)are fungal secondary metabolites that can contaminate various agricultural crops and their derived products,posing a significant global food safety challenge.The International Agency for Research on Cancer(IARC)has classified AFB1,AFB2,AFG1 and AFG2 as Group 1 carcinogens,primarily causing hepatocellular carcinoma(HCC)in humans,but also affecting growth and development in children and damaging the human immune system,resulting in varying degrees of health burden to populations.The World Health Organization published the global burden of foodborne AF in 2015,and several countries and regions have conducted population-based studies on the burden of foodbome AF.This article reviews the progress of foodborne AF disease burden research from 2010 to 2023,providing a foundation for more comprehensive disease burden studies in the future.

Bisphenol A (BPA) is a typical food chemical contaminant with various detrimental effects, especially on reproductive system. Male prostate damage is also one of its major adverse health effects, of which mode of action (MOA) remains unclear. This study aims to explore the MOA for prostate toxicity of BPA using human normal prostate epithelial cell RWPE-1 for 28-day human-relevant-level exposure. A physiological based pharmacokinetic model was used to determine the concentration of BPA based on the actual oral exposure in China. The possible key events were identified by high-throughput transcriptome sequencing and validated by qPCR, Western blot and cell cycle assay, and the benchmark concentration analysis were conducted. The enriched KEGG pathways include the endocytosis, cell cycle, cellular senescence, MAPK and TNF signaling pathways. With increasing BPA concentrations, the increased mRNA and/or protein expressions of MAPKAPK2, c-JUN and c-fos in the MAPK signaling pathway, the increased mRNA expressions of CCND1 and CDKN1A, the decreased mRNA expression of CDC25C, the increased proportion of G0/G1 phase and S phase, as well as the decreased proportion of G2/M phase, were observed. The lowest value of benchmark concentration lower confidence limit (BMCL) was retrieved from G2/M phase ratio, with 110.580 and 175.862 nM for BMCL5 and BMCL10, respectively, much higher than the male gonad maximum concentration of 0.019 nM of BPA at the current exposure level of adult Chinese males. In conclusion, the MOA of BPA induced male prostatic toxicity at human-relevant levels may include: key event (KE)1-MAPK signaling pathway activation, KE2-disorder of cell cycle regulatory gene expression (increased expression of CCND1 and CDKN1A, decreased expression of CDC25C), and KE3-disturbance of cell cycle (increased proportion of G0/G1 and S phases, decreased proportion of G2/M phases). However, more studies are needed to validate and complete the MOA.

Bisphenol A (BPA) is a known endocrine disruptor mimicking natural estrogens with the potential to affect human health, especially during prenatal and postnatal exposure at or below current acceptable daily intake levels. Different adverse effects of BPA are still under investigation, and multiple mechanisms of action remain unexplored. This may be one of the reasons for the continuously changing tolerable daily intake (TDI) of BPA with the emergence of new adverse health effects over time. In addition, translational modelling through in vitro-in vivo extrapolation (IVIVE) can act as prerequisite bridge for translating in-vitro finding into human risk assessment. The objective of this study was to conduct in-vitro experiments and utilize an IVIVE-pregnancy physiologically based pharmacokinetic (P-PBPK) modeling to investigate developmental neurotoxicity and embryotoxicity in humans. The data obtained from human embryonic stem cells-based assays (study conducted between October 2020-2021) were used for the IVIVE-P-PBPK models to obtain the human equivalent doses (HEDs) which were further extrapolated to reference doses (RfDs). The results showed that simulated mean RfDs (μg/kg/day) derived from the HSD3B1 and NFATC2 gene of embryotoxicity and neurodevelopmental toxicity tests, respectively, were 4.94 and 5.18. The simulated RfDs were close to the temporary-tolerable daily intake (t-TDI) recommended by European Food Safety Authority (EFSA) in 2015 (t-TDI: 4 μg/kg·bw) and higher than the TDI of 2023 (0.2 ng/kg·bw). In conclusion, in-vitro toxicogenomics dose-response data combined with PBPK modeling can become a promising alternative new approach methodology (NAM) to support decision-making in chemical risk assessment. Based on the simulated RfDs derived from this NAM, the t-TDI set by EFSA in 2015 may be considered a safe exposure limit for mothers and fetuses at the current BPA intake levels in Chinese mothers. This study provided an animal-free new strategy for NAMs based risk assessment by combining toxicogenomics and computational toxicology.

In China， food for special medical purpose （FSMP） is defined as “formula food specially processed and prepared in order to meet the special nutrient or diet needs for people with food restriction， digestion and absorption disorder， metabolic disorder or specific disease state”. The development of FSMP in China started relatively late. Since the revised “Food Safety Law of the People’s Republic of China” in 2015 officially brought FSMP into the track of legal management， the supervision of FSMP has gradually improved， and the number of products approved for registration has gradually increased. This article briefly introduces the relevant regulations， standards and regulatory requirements of FSMP in China， as well as the basic situation of the products approved for registration， and puts forward some suggestions for the reference of relevant personnel and interested readers.

后生元是指对宿主健康有益的无生命微生物和/或其成分的制剂,由菌体代谢产物和菌体组成成分两类构成.随着研究技术和方法的不断进步,对后生元健康益处的研究也愈来愈多.本文对后生元的健康益处及作用机制进行综述,重点介绍后生元的免疫调节、抗菌、促进消化道健康、调节代谢等作用及机制,以期为后生元健康益处深入研究及产品开发提供参考.