Given that many organic pollutants have been reported to facilitate the plasmid-mediated conjugative transfer of antibiotic resistance genes (ARGs), it was naturally deduced that nonylphenol (NP) can also have this kind of effect. Whereas, this study demonstrates an entirely different result that environmentally relevant concentrations of NP attenuate plasmid-mediated ARGs conjugative transfer (maximum inhibition rate 64 %), further study show that NP exposure had no significant effect on bacterial growth, cell vitality, oxidative stress response, and expression of conjugation-relevant genes, which were reported to closely relate to the conjugative transfer in numerous studies. Conclusively, it was found that the dispersant function of NP impeded the occurrence of cell mating, thus was responsible for the decline of conjugative transfer. This study shows a new perspective on understanding the effect of organic pollutants like NP on the ARGs horizontal dissemination in environment.

BACKGROUND: Alkylphenols can originate from numerous products containing alkylphenol ethoxylates, including cleaning products, household items, and cosmetics. Some phenols, such as nonylphenol, are known to be endocrine disruptors, and exposure to them is thought to have contributed to the recent increase in allergic diseases such as asthma. However, the impacts of prenatal phenol exposure on asthma development in children are still unclear.
METHODS: We analyzed the association between maternal urinary phenol concentrations during early pregnancy and the development of asthma in children at the age of 4, using data from the Japan Environment and Children\'s Study (JECS), a large-scale nationwide birth cohort study.
RESULTS: We recruited 3,513 pairs of mothers and children participating in the Sub-Cohort Study of JECS. We measured 24 phenols, including nitrophenol, parabens, bisphenol, octylphenol, and nonylphenol, in urine samples taken during the first trimester of pregnancy. The urinary levels of these phenols differed markedly, and some showed a broad spectrum of distribution. Methylparaben was detected at high levels in almost every participant (267.7 ng/ml, standard deviation 433.78). Logistic regression analysis revealed that the odds ratio of asthma onset for high exposure to butylparaben was 1.54 (95% confidence interval: 1.11-2.15). Additionally, logistic regression analysis by gender revealed an asthma development odds ratio of 2.09 (95% confidence interval: 1.20-3.65) for males and 0.65 (95% confidence interval: 0.25-1.70) for females born to mothers in whom 4-nonylphenol was detected, suggesting a gender difference.
CONCLUSIONS: Our current analysis using large cohort data suggests that high exposure to butylparaben and low exposure to 4-nonylphenol during pregnancy are risk factors for asthma development in children. These findings establish a valuable foundation for formulating recommendations about prenatal phenol exposure.

Developmental exposure to nonylphenol (NP) results in irreversible impairments of the central nervous system (CNS). The neural precursor cell (NPC) pool located in the subgranular zone (SGZ), a substructure of the hippocampal dentate gyrus, is critical for the development of hippocampal circuits and some hippocampal functions such as learning and memory. However, the effects of developmental exposure to NP on this pool remain unclear. Thus, our aim was to clarify the impacts of developmental exposure to NP on this pool and to explore the potential mechanisms. Animal models of developmental exposure to NP were created by treating Wistar rats with NP during pregnancy and lactation. Our data showed that developmental exposure to NP decreased Sox2-and Ki67-positive cells in the SGZ of offspring. Inhibited activation of Shh signaling and decreased levels of its downstream mediators, E2F1 and cyclins, were also observed in pups developmentally exposed to NP. Moreover, we established the in vitro model in the NE-4C cells, a neural precursor cell line, to further investigate the effect of NP exposure on NPCs and the underlying mechanisms. Purmorphamine, a small purine-derived hedgehog agonist, was used to specifically modulate the Shh signaling. Consistent with the in vivo results, exposure to NP reduced cell proliferation by inhibiting the Shh signaling in NE-4C cells, and purmorphamine alleviated this reduction in cell proliferation by restoring this signaling. Altogether, our findings support the idea that developmental exposure to NP leads to inhibition of the NPC proliferation and the NPC pool depletion in the SGZ located in the dentate gyrus. Furthermore, we also provided the evidence that suppressed activation of Shh signaling may contribute to the effects of developmental exposure to NP on the NPC pool.

Nonylphenol (NP), a main byproduct of nonylphenol polyethoxylates (NPEs) degradation, is prevalent across diverse environmental settings. Given its widespread presence, evaluating the ecological risks associated with NP in coastal waters and sediments is essential for the protection of the marine environment. This study evaluates the acute toxicity of NP on ten representative aquatic species from the Bohai Sea, determining the Aquatic Life Criteria (ALC) through two distinct methods. The Criteria Maximum Concentration (CMC) for NP in seawater was established at 12.0 μg/L, with a Predicted No-Effect Concentration (PNEC) for water at 15.2 μg/L and for sediment at 33.3 μg/kg. Additionally, a tiered ecological risk assessment (ERA) of both surface seawater and sediment in the Bohai Sea revealed significant ecological risks at various sediment sites. These results offer crucial insights for assessing the ecological risks to coastal ecosystem and provide foundational data necessary for informed environmental protection and management strategies.

The liver toxicity of alkylphenols (APs) has been demonstrated in animal studies. However, relevant epidemiological evidence is still lacking in humans, especially during pregnancy. We obtained the levels of biochemical indicators of liver function in early (<13 weeks, mean gestation=9.80±1.96 weeks) and late (≥32 weeks, mean gestation = 37.23±2.45 weeks) pregnancies from 219 pregnant women in the Guangxi Zhuang birth cohort from 2015-2017. We also examined the serum levels of APs in these pregnant women in early pregnancy. The present study aimed to investigate the correlations between the exposure of pregnant women to APs and their serum liver function indices. The results of the generalized linear model (GLM) in this study revealed that nonylphenol (NP) was positively correlated with total bilirubin (TBIL) (P=0.04) in early pregnancy, and 4-n-nonylphenol (4-N-NP) was negatively correlated with glutamyl transferase (GGT) (P=0.012). In late pregnancy, NP was positively associated with TBIL (P=0.002), and 4-tert-octylphenol (4-T-OP) was positively correlated with alanine aminotransferase (ALT) (P=0.02). Restricted cubic spline (RCS) results revealed doseresponse relationships between NP and TBIL (Poverall=0.011) and between 4-N-NP and GGT (Poverall=0.007) in early pregnancy. In late pregnancy, there were doseresponse relationships between NP and TBIL (Poverall=0.001) and between 4-T-OP and ALT (Poverall=0.033). There was also a doseresponse relationship between NP volume and GGT with an inverted \'U\' shape (Poverall=0.041, Pnonlinear=0.012). Bayesian kernel machine regression modeling (BKMR) revealed that TBIL increased significantly (P<0.05) with increasing levels of coexposure to APs in both early and late pregnancy. Overall, exposure to APs during pregnancy affects maternal liver function to varying degrees. The present study provides new epidemiological evidence that exposure to alkylphenols in pregnant women interferes with liver function.

Nonylphenol (NP) is a ubiquitous endocrine disruptor that persists in the environment and can significantly contribute to serious health hazards, particularly intestinal barrier injury. Plant essential oils (EOs) have recently gained widespread interest due to their potential for improving intestinal health. However, the precise mechanism and protective effects of EOs ameliorating the intestinal damages induced by NP exposure remain unclear. To clarify the potential mechanism and protective impact of EOs against intestinal injury induced by NP, a total of 144 one-day-old male ducks were randomly allocated to four groups: CON (basal diet), EO (basal diet + 200 mg/kg EOs), NP (basal diet + 40 mg/kg NP), and NPEO (basal diet + 200 mg/kg EOs + 40 mg/kg NP). The data revealed that NP exposure significantly damaged intestinal barrier, as evidenced by a reduction in the levels of tight junction gene expression and an increase in intestinal permeability. Additionally, it disturbed gut microbiota, as well as interfered with tryptophan (Trp) metabolism. The NP-induced disorder of Trp metabolism restrained the activation of aryl hydrocarbon receptor (AhR) and resulted in decreased the expression levels of CYP1A1, IL-22, and STAT3 genes, which were alleviated after treatment with EOs. Taken together, NP exposure resulted in impairment of the intestinal barrier function, disruption of gut microbiota, and disturbances in Trp metabolism. Dietary EOs supplementation alleviated the intestinal barrier injury induced by NP through the Trp/AhR/IL-22 signaling pathway.

The aim of this study is to investigate the role of estrogen receptor β (ERβ) in nonylphenol (NP) - induced depression - like behavior in rats and its impact on the regulation of the TPH2/5-HT pathway. In the in vitro experiment, rat basophilic leukaemia cells (RBL-2H3) cells were divided into the four groups: blank group, NP group (20 μM), ERβ agonist group (0.01 μM), and NP＋ERβ agonist group (20 μM＋0.01 μM). For the in vivo experiment, 72 adult male Sprague-Dawley rats were randomly divided into following six groups: the Control, NP (40 mg/kg) group, ERβ agonist (2 mg/kg, Diarylpropionitrile (DPN)) group, ERβ inhibitor (0.1 mg/kg, 4-(2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl) phenol (PHTPP)) group, NP+ERβ agonist (40 mg/kg NP ＋ 2 mg/kg DPN) group, and NP+ERβ inhibitor (40 mg/kg NP + 0.1 mg/kg PHTPP) group, with 12 rats in each group. Each rat in drug group were given NP by gavage and/or received a single intraperitoneal injection of DPN 2 mg/kg or PHTPP 0.1 mg/kg. Both in vivo and in vitro, NP group showed a decrease in the expression levels of ERβ, tryptophan hydroxylase (TPH1), and tryptophan hydroxylase-2 (TPH2) genes and proteins, and reduced levels of DA, NE, and 5-hydroxytryptophan (5-HT) neurotransmitters. RBL-2H3 cells showed signs of cell shrinkage, with rounded cells, increased suspension and more loosely arranged cells. The effectiveness of the ERβ agonist stimulation exhibited an increase exceeding 60% in RBL-2H3 cells. The application of ERβ agonist resulted in an alleviation the aforementioned alterations. ERβ agonist activated the TPH2/5-HT signaling pathways. Compared to the control group, the NP content in the brain tissue of the NP group was significantly increased. The latency to eat for the rats was longer and the amount of food consumed was lower, and the rats had prolonged immobility time in the behavioral experiment of rats. The expression levels of ERβ, TPH1, TPH2, 5-HT and 5-HITT proteins were decreased in the NP group, suggesting NP-induced depression-like behaviours as well as disturbances in the secretion of serum hormones and monoamine neurotransmitters. In the NP group, the midline raphe nucleus showed an elongated nucleus with a dark purplish-blue colour, nuclear atrophy, displacement and pale cytoplasm. ERβ might ameliorate NP-induced depression-like behaviors, and secretion disorders of serum hormones and monoamine neurotransmitters via activating TPH2/5-HT signaling pathways.

UNASSIGNED: Nonylphenol (NP) is widely recognized as a crucial environmental endocrine-disrupting chemical and persistent toxic substance. The remediation of NP-contaminated sites primarily relies on biological degradation. Compound microbial products, as opposed to pure strains, possess a greater variety of metabolic pathways and can thrive in a wider range of environmental conditions. This characteristic is believed to facilitate the synergistic degradation of pollutants. Limited research has been conducted to thoroughly examine the potential compatibility of compound microbial agents with indigenous microflora, their ability to function effectively in practical environments, their capacity to enhance the dissipation of NP, and their potential to improve soil physicochemical and biological characteristics.
UNASSIGNED: In order to efficiently eliminate NP in contaminated soil in an eco-friendly manner, a simulation study was conducted to investigate the impact of bioaugmentation using the functional compound microbial agent NP-M2 at varying concentrations (50 and 200 mg/L) on the dynamics of the soil microbial community. The treatments were set as follows: sterilized soil with 50 mg/kg NP (CK50) or 200 mg/kg NP (CK200); non-sterilized soil with 50 mg/kg NP (TU50) or 200 mg/kg NP (TU200); non-sterilized soil with the compound microbial agent NP-M2 at 50 mg/kg NP (J50) or 200 mg/kg NP (J200). Full-length 16S rRNA analysis was performed using the PacBio Sequel II platform.
UNASSIGNED: Both the indigenous microbes (TU50 and TU200 treatments) and the application of NP-M2 (J50 and J200 treatments) exhibited rapid NP removal, with removal rates ranging from 93% to 99%. The application of NP-M2 further accelerated the degradation rate of NP for a subtle lag period. Although the different treatments had minimal impacts on the soil bacterial α-diversity, they significantly altered the β-diversity and composition of the bacterial community. The dominant phyla were Proteobacteria (35.54%-44.14%), Acidobacteria (13.55%-17.07%), Planctomycetes (10.78%-11.42%), Bacteroidetes (5.60%-10.74%), and Actinobacteria (6.44%-8.68%). The core species were Luteitalea_pratensis, Pyrinomonas_methylaliphatogenes, Fimbriiglobus_ruber, Longimicrobium_terrae, and Massilia_sp003590855. The bacterial community structure and taxon distribution in polluted soils were significantly influenced by the activities of soil catalase, sucrase, and polyphenol oxidase, which were identified as the major environmental factors. Notably, the concentration of NP and, to a lesser extent, the compound microbial agent NP-M2 were found to cause major shifts in the bacterial community. This study highlights the importance of conducting bioremediation experiments in conjunction with microbiome assessment to better understand the impact of bioaugmentation/biostimulation on the potential functions of complex microbial communities present in contaminated soils, which is essential for bioremediation success.

Nonylphenol (NP) is one of the common pollutants in the environment that have toxic effects on aquatic animals. Nevertheless, little is known about the possible toxicity mechanism of NP on the hepatopancreas of Litopenaeus vannamei. In the present study, the detrimental effects of NP on the hepatopancreas of the L. vannamei were explored at the histological and transcriptomic levels. The findings indicated that after NP exposed for 3, 12, and 48 h, the hepatopancreas histology was changed significantly. Transcriptomic analysis showed that a total of 4302, 3651, and 4830 differentially expressed genes (DEGs) were identified at 3, 12, and 48 h following NP exposure. All these DEGs were classified into 12 clusters according to the expression patterns at different time points. GO and KEGG enrichment analyses of DEGs were also performed, immunological, metabolic, and inflammatory related pathways, including arachidonic acid metabolism (ko00590), the PPAR signaling pathway (ko03320), and the regulation of TRP channels by inflammatory mediators (ko04750) were significantly enriched. Six DEGs were selected for validation by quantitative real-time PCR (qRT-PCR) and the results confirmed the reliability of transcriptome data. All results indicated that NP is toxic to L. vannamei by damaging the histopathological structure and disrupting the biological function. The findings would provide a theoretical framework for lowering or limiting the detrimental impacts of NP on aquaculture and help us to further study the molecular toxicity of NP in crustaceans.

Nonylphenol (NP) is an organic pollutant and endocrine disruptor chemical that has harmful effects on the environment and living organisms. This study looked at whether kidney tissues subjected to increasing doses of nonylphenol generated alterations in histopathologic, pro-inflammatory, and autophagic markers. Fifty rats were divided into five groups of ten each: group I: healthy group, II: control (corn oil), group III: 25 μl/kg NP, group IV: 50 μl/kg NP, group V: 75 μl/kg NP. The kidney tissue samples were obtained for histopathological, immunohistochemical, and biochemical analyses. The histological deteriorations observed in all NP groups included tubular epithelial cell degeneration, inflammation areas, and hemorrhage. The immunohistochemical investigations showed that NP significantly elevated the autophagy markers (Beclin-1, LC3A/B, p62), pro-inflammatory cytokines (TNF-α, IL-6), HIF-1α, and eNOS in group III, IV and V compared with group I and II. The biochemical analysis also revealed that pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) increased in correlation with the NP doses, but only IL-1β reached statistical significance in NP treated rats kidney tissue. The biochemical findings have been confirmed by the histological studies. The damage to renal tissue caused by NP exposure may worsen it by increasing inflammatory and autophagic markers.