Effects Of Nonylphenol Research Articles

Effects of Nonylphenol and Octylphenol on Wastewater Discharge Facilities in Northern Gyeonggi Province

This study examines the emission characteristics of nonylphenol (NP) and octylphenol (OP) in the discharged water of Northern Gyeonggi Province, South Korea, where the textile industry predominates. We evaluated 104 individual wastewater discharge facilities, six public wastewater treatment plants (WWTPs), and the Shincheon River. Our findings reveal that NP and OP concentrations were notably high in the textile industry, with median levels of 0.53 µg/L and 0.43 µg/L, respectively, in individual wastewater discharge facilities. Furthermore, monitoring NP and OP levels in the influent and effluent of WWTPs and river water demonstrated that WWTP effluent has a remarkable impact on NP and OP concentrations in the river. The removal rates of NP and OP in WWTPs averaged 69.6% and 41.8%, respectively, and these rates tended to increase with higher temperatures and influent concentrations. The average concentrations in the Shincheon River were 0.31 µg/L for NP and 0.45 µg/L for OP, slightly exceeding EU standards. It is essential to closely monitor NP and OP levels to protect aquatic ecosystems.

Nonylphenol releases arachidonic acid in rat Sertoli cells via activation of PKA and PLA2.

The endocrine disruptor, nonylphenol (NP) increases 20:4n-6 release in Sertoli cells via PKA/cPLA2 activation. Our data show that lipid metabolism could be a target of NP-induced abnormal reproductive outcomes. Nonylphenol (NP), an endocrine-disrupting chemical, is an environmental contaminant, and many notorious effects on male fertility have been reported in animal models and wild-type species. Here, we evaluated the effects of NP in follicle-stimulating hormone (FSH) signal transduction pathways and lipid metabolism using an in vitro model of rat Sertoli cell (SC) primary culture. Results show that an acute (1 h) SC exposure to NP (10 µM) increased the intra- and extra-cellular concentrations of free fatty acids (FFAs), mainly arachidonic acid (20:4n-6). Phosphatidylinositol seemed to be the major phospholipid source of this 20:4n-6 release by activation of the protein kinase A (PKA)/cytoplasmic phospholipase A2 (cPLA2) pathway. NP also increased diacylglycerols (DAG) levels and the expression (mRNA) of cyclooxygenase 2 (Cox2) and prostaglandin E2 (PGE2) levels. It is noteworthy that accumulation of lipid droplets took place after 24 h NP exposition, which was prevented by both a PKA inhibitor and a PLA2 inhibitor. Like FSH, NP triggers the release of 20:4n-6, which is a substrate for PGE2 synthesis via PKA/PLA2 activation. In addition, NP induces the formation of DAG, which could be required as a cofactor of the PKC-mediated activation of the COX2 inflammatory pathway. Our findings suggest that NP alters lipid homeostasis in SCs by inducing the activation of pro-inflammatory pathways that may trigger adverse effects in testis physiology over time. Concomitantly, the SC enhances the acylation of surplus FFAs (including 20:4n-6) in neutral lipids as a protective mechanism to shield itself from lipotoxicity and pro-inflammatory signals.

Exposure of nonylphenol promoted NLRP3 inflammasome and GSDMD-mediated pyroptosis in allergic rhinitis mice

Studies have confirmed that the intake of nonylphenol (NP) can increase nasal symptoms, eosinophils, and Th2 responses in allergic rhinitis (AR) mice. However, the molecular mechanism of NP exacerbating AR inflammatory response remains unclear. Recent data suggest that NOD-like receptor 3 (NLRP3) inflammasome-mediated pyroptosis contributes to AR development. To investigate the effects of NP on NLRP3 inflammasomes and pyroptosis, an AR mouse model induced by ovalbumin (OVA) was established and treated with 0.5 mg/kg/d NP every other day. Nasal symptoms were evaluated after the final OVA instillation. Mast cells and Eosinophils in the nasal mucosa were observed using toluidine blue and Sirius red staining, respectively. The levels of NLRP3, Caspase-1, ASC, phospho–nuclear factor kappa B (NF-κB) p65, interleukin (IL)-6, TNF-α, IL-18, GSDMD and IL-1β, were assessed by using immunohistochemical staining, ELISA, quantitative real-time PCR, or Western blot. Exposure to NP aggravates AR symptoms and promotes eosinophils, mast cells, and inflammatory factors release, along with significantly increased of NF–κB, NLRP3, Caspase-1, ASC, and GSDMD. It was concluded that NP exposure promotes NLRP3 inflammasome and GSDMD-mediated pyroptosis of the nasal mucosa. Targeted of NLRP3 and GSDMD-mediated pyroptosis may be a novel therapeutic strategy for AR exposed to NP.

Simultaneous determination of the free and total forms of nonylphenol, nonylphenol monoethoxylate, and nonylphenol diethoxylate in human urine by gas chromatography-mass spectrometry.

Nonylphenol (NP), nonylphenol monoethoxylate (NP1EO), and nonylphenol diethoxylate (NP2EO) are widely used in various daily products and have been cataloged as endocrine-disrupting chemicals. Due to their high lipophilicity and low biodegradability, these compounds remain in the environment and enter the human body through the food chain. Growing concerns regarding the potential negative effects of NP, NP1EO, and NP2EO on human health have raised the need for biomonitoring to investigate human exposure to these compounds. In this study, a simultaneous analysis method using solid-phase extraction (SPE) combined with gas chromatography-mass spectrometry (GC-MS) was established by controlling the background contamination of NP, NP1EO, and NP2EO, which are ubiquitous in laboratory environments. The proposed method showed proper linearity of over 0.999 and a recovery greater than 85.8% for all analytes. Accuracy and precision were verified in ranges of 92.97-116.30% and 0.65-9.29%, respectively. The detection limits for NP, NP1EO, and NP2EO were 0.0363μg L-1, 0.0401μg L-1, and 0.0364μg L-1, respectively, which were suitable for determining the trace analytes in human urine. Therefore, this simple and integrated analytical method was applied to measure the free and total forms of the target analytes in 25 human urine samples collected in Korea. Overall, free NP, NP1EO, and NP2EO were detected with average contents of 3.94 ± 4.14μg L-1, 4.63 ± 2.62μg L-1, and 0.293 ± 0.638μg L-1, respectively, and with total NP, NP1EO, and NP2EO contents of 6.14 ± 8.24μg L-1, 5.99 ± 2.91μg L-1, and 0.806 ± 1.10μg L-1, respectively. These data showed that these compounds are prevalent in human urine, and indicate the need for further studies.

Evaluation of the genotoxic effect of nonylphenol applied in different doses on the bone marrow

Nonylphenols are endocrine disrupting toxic compounds and are widely used. For this reason, our study aimed to investigate the genotoxic effect of nonylphenols applied at different doses on mouse bone marrow cells. Groups were classified as control group, the sham administered only group, low dose, medium dose and high dose nonylphenol administered group. After euthanasia, polychromatic erythrocyte/Normochromatic erythrocyte ratio and micronuclear polychromatic erythrocyte count were determined in femur bone marrow cells and analyzed to detect DNA damage. While polychromatic erythrocyte/Normochromatic erythrocyte ratio was found to be lower in the groups treated with different doses of nonylphenol, especially in the group treated with high-dose nonylphenol, this decrease was not statistically significant. When the micronucleated polychromatic erythrocyte values were examined, it was observed that there was a statistically significant increase, especially in the medium and high dose groups compared to the control. High-dose nonylphenol has a toxic effect and may have a long-term genotoxic effect such as cancer development by interacting with genotoxic agents.

Studies of Endocrine Disruptors: Nonylphenol and Isomers in Biological Models.

Certain emerging pollutants are among the most widely used chemicals globally, causing widespread concern in relation to their use in products devoted to cleaniness and asepsis. Nonylphenol ethoxylate (NPEOn) is one such contaminant, along with its degradation product, nonylphenol, an active ingredient presents in nonionic surfactants used as herbicides, cosmetics, paints, plastics, disinfectants, and detergents. These chemicals and their metabolites are commonly found in environmental matrices. Nonylphenol and NPEOn, used, are particularly concerning, given their role as endocrine disruptors chemical and possible neurotoxic effects recorded in several biological models, primarily aquatic organisms. Limiting and detecting these compounds remain of paramount importance. The objective of the present review was to evaluate the toxic effects of nonylphenol and NPEOn in different biological models. Environ Toxicol Chem 2023;42:1439-1450. © 2023 SETAC.

Nonylphenol reduced the number of haploids in in vitro spermatogenesis of the endangered cyprinid Gnathopogon caerulescens

Nonylphenol (NP), an endocrine disrupting chemical, is widely used in industrial and agricultural processes, causing NP influx into aquatic environments. NP induces hormonal imbalance, and male feminization, and reduces germ cell production during spermatogenesis; however, the mechanism by which it affects spermatogenesis remains unknown. Here, we investigated the effect of NP on spermatogenesis in honmoroko (Gnathopogon caerulescens), an endangered fish endemic to Lake Biwa, Japan, using an in vitro differentiation system. We collected spermatogonia from the testes of non-spawning G. caerulescens and subjected them to suspension culture. The spermatogonia differentiated into flagellated spermatozoa in 3 weeks, regardless of the presence of NP. NP concentrations as low as 1 nM caused a decrease in the number of germ cells in a dose-dependent manner, whereas the number of somatic cells decreased only at a high concentration of 1 μM. Flow cytometric analysis revealed that the decrease in germ cell number was attributed to haploids (spermatids and spermatozoa); the number of spermatogonia and spermatocytes was not affected by NP treatment. This result is consistent with the hypothesis that NP might repress the second meiosis or induce apoptosis in haploids. This study demonstrated that the combination of in vitro germ cell differentiation and flow cytometric analysis is useful for evaluating the direct effects of NP on germ cell differentiation in endangered endemic fish.

Role of miR-219a-5p in regulating NMDAR in nonylphenol-induced synaptic plasticity damage

Nonylphenol (NP) is a typical environmental endocrine disruptor with estrogenic effects. It serves as an emulsifier and as the main ingredient of detergents and has become an increasingly common pollutant in both fresh and salt water, vegetables, and fruits. This study aimed to clarify whether NP exposure could lead to cognitive dysfunction and synaptic plasticity impairment, and also explore the mechanism of microRNA (miR)− 219a-5p regulation of N-methyl-D-aspartate receptor (NMDAR) in NP-induced synaptic plasticity impairment in vivo and in vitro. In vivo, 30 male Sprague–Dawley rats were randomly divided into 2 groups: blank control group (pure corn oil) and NP-exposed group [NP 80 mg/(kg·d)], with 15 rats in each group. In vitro, the extracted hippocampal neurons were divided into 6 groups: blank control group, mimics NC group, miR-219 mimics group, NP group (70 μmol/L NP), NP + mimics NC group, and NP + miR-219 mimics group. In vivo, the content of NP in hippocampal tissues after 90 days of NP exposure was significantly higher in the NP-stained group than in the blank control group. NP exposure could lead to a decrease in the ability to learn and memory, ability to remember, and space spatial memory ability in rats. The dendrites in the NP-stained group were disordered, with few dendritic spines and significantly decreased dendritic spine density. The postsynaptic densities were loosely arranged, the thickness and length of the postsynaptic densities shortened, and the length and width of the synaptic gap increased. Glutamine (Glu) and γ-aminobutyric acid (GABA) contents in hippocampal tissues decreased in the NP-stained group. The expression of miR-219a-5p mRNA decreased in the NP-stained group after 3 months of NP exposure. The expression of NMDAR1, NMDAR2A, NMDAR2B, nerve growth–associated protein (GAP-43), and Ca/calmodulin-dependent kinase II (CaMKII) mRNA/proteins decreased in the NP-stained group. In vitro, NMDAR protein expression decreased, while GAP-43 and CaMKII protein expression increased in the miR-219 mimics group compared with the control group. The expression levels of NMDAR and GAP-43 and CaMKII proteins were higher in the NP + miR-219 mimics group compared with the NP group. The levels of neurotransmitters Glu and GABA decreased in the NP and NP + mimics NC groups compared with the blank group. Shortened synaptic active band length, decreased thickness of postsynaptic densities, and shortened length of postsynaptic densities were observed in the NP, NP + mimics NC, and NP + miR-219 mimics groups compared with the blank control group. In vivo, NP exposure reduced learning memory capacity and neurotransmitter content in rats and caused a decrease in dendritic spine density and synaptic number density and a decrease in miR-219a-5p expression. In vitro, high expression of miR-219a-5p inhibited the expression of NMDAR, thus reducing the effect of NP on synaptic plasticity impairment in hippocampal neurons. Our study provided a scientific basis for the prevention of cognitive impairment owing to NP exposure and the development of targeted drug treatment strategies.

Effect of Nonylphenol on the Structure of Adrenal Cortex in F1 Generation Rats

Previous studies, including our own, indicate that distinct morphological changes in rodent adrenal cortex could be induced by exposure of endocrine disrupting chemicals (EDC). In the present study, we conducted histological analyses of adrenocortical substructure using a nonylphenol-treated F1 rat model. The adrenal weight of NP-5000 group was significantly declined in female rats (p<0.001), while the adrenal weights of NP-treated groups were not significantly changed in male rats. The thickness of zona glomerulosa layers of female rats in NP-5000 group was significantly declined (p<0.001) but zona fasciculata layers were not changed. The zona reticularis layers of NP-treated group were significantly thinner than those of control group (NP-50, p<0.05; NP-5000, p<0.01). In male adrenal glands, there was no significant change of zona glomerulosa layers in NP-treated groups while the thickness of zona fasciculata in NP-5000 group was significantly decreased (p<0.01). Like female rats, the thickness of zona reticularis in NP-treated groups was significantly decreased (NP-50, p<0.001; NP-5000, p<0.05). Present study demonstrated that the adrenal histology could be altered by low-dose NP exposure in F1 rats, and the effect might be sexually dimorphic. Further study will be helpful for understanding possible adrenal pathophysiology induced by EDC exposure, and EDC-related sexually dimorphic phenomena in rodent adrenals.

Exploration of interaction property between nonylphenol and G protein-coupled receptor 30 based on molecular simulation and biological experiments

Nonylphenol (NP), a representative of environmental hormones, can cause extensive biological effects in the human body. In this study, we first analyzed the mutual binding modes of NP and G protein coupled estrogen receptor 30 (GPR30) by molecular simulation. The 3D structure of GPR30 was successfully constructed. We found that the binding sites of NP on GPR30 are similar to that of 17β-Estradiol (E2) on GPR30. The GPR30-E2 bond complex is more stable than GPR30-NP bond complex. Next CCK-8 assay was used to detect the regulatory effect of NP on SKBR-3 cell proliferation. When NP and E2 were used alone, low concentration could promote cell proliferation, while high concentration was the opposite. The presence of E2 can promote the cell proliferation effect of NP, and inhibit the inhibitory intensity. NP could promote both the cell proliferation effect and inhibition intensity of E2. Based on our results, we conclude that the binding modes of NP and GPR30 is similar to that of E2 and GPR30. In biology, NP can play estrogen role by activating GPR30 receptor, but it can also produce cytotoxicity at higher concentration.

Nonylphenol exacerbates ovalbumin-induced allergic rhinitis via the TSLP-TSLPR/IL-7R pathway and JAK1/2-STAT3 signaling in a mouse model

Nonylphenol (NP) can be widely used as a plasticizer, surfactant, antioxidant, textile printing, dyeing additive, and pesticide emulsifier. Animal studies have shown that NP aggravates ovalbumin (OVA)-induced allergic rhinitis (AR); however, the exact mechanism underlying its action has not yet been detailed. This study aimed to explore the aggravation of the AR inflammatory response following NP exposure and its possible mechanism. The AR mouse model was constructed using OVA. Under NP exposure, allergic nasal symptoms were observed, eosinophil infiltration was assessed by Sirius red staining, and the levels of IL-4, IL-5, and IL-13 in nasal mucosa samples were detected using cytometric bead array. The mRNA levels of OX40/OX40L and GATA3 in nasal mucosa were detected by qPCR, and the expression levels of the TSLP and JAK1/2-STAT3 signaling pathway components were also identified. Our results suggest that NP exposure exacerbated allergic nasal symptoms and that eosinophils accumulated in nasal mucosa after OVA challenge. The levels of the typical T helper 2 cytokines, as well as the mRNA levels of OX40/OX40L and GATA3, were elevated in the nasal mucosa of OVA-challenged mice exposed to NP. In addition, NP exposure elevated the TSLP, TSLPR, IL-7R, p-JAK1, p-JAK2, and p-STAT3 levels in the nasal mucosa after OVA stimulation. Overall, the present study suggests NP can exacerbate OVA-induced AR inflammatory responses; furthermore, this aggravating effect of NP may be related to the TSLP-TSLPR/IL-7R and JAK1/2-STAT3 signaling pathways.

Toxicity alleviation and metabolism enhancement of nonylphenol in green algae Dictyosphaerium sp. by NaHCO3

Nonylphenol (NP) toxicity limits the improvements in its algal remediation efficiency. This study comprehensively investigated the performance and mechanism of NaHCO3-driving effects on NP-exposed algae. The results showed that NaHCO3 enhanced algal resistance to NP and the corresponding EC50 values increased 1.31–4.25 times. Further, the toxicological effects of NP reduced with increasing pyrenoid volume and chlorophyll and carotenoids production, and decreasing cellular damage degree. Moreover, the concentration of extracellular polymeric substances was enhanced and more NP adsorption sites were formed. Consistently, RNA-seq demonstrated significant expression alterations in genes related to energy metabolism, cellular synthesis, photosynthesis, and carbon fixation. Besides, NP biodegradation rate was increased by 15.2 % and 11.1 % in the 1, and 4 mg/L NP treatments, respectively. Identification of degradation intermediates and their toxicity via Ecological Structure Activity Relationship program showed that NaHCO3 accelerated sequential α-C removal from NP in algae with faster generation of less toxic metabolites, namely, 4-ethylphenol, 4-cresol and 4-hydroxybenzoic acid. This study provides new insights into the role of NaHCO3 in toxicity alleviation and metabolism enhancement of NP in algae and can assist NP bioremediation efforts in aquatic environment.

Effects of nonylphenol on ovarian and testicular tissues in immature rainbow trout (Oncorhynchus mykiss)

Effects of nonylphenol on ovarian and testicular tissues in immature rainbow trout (Oncorhynchus mykiss)

Separate and combined effects of cadmium (Cd) and nonylphenol (NP) on growth and antioxidative enzymes in Hydrocharis dubia (Bl.) Backer.

Cadmium (Cd) is considered a priority pollutant, and nonylphenol (NP) is a common organic pollutant in water environments. However, the ecological risks of combined Cd and NP pollution have not been fully elucidated. In this study, the effects of Cd, NP, and Cd-NP on the growth and physiology of Hydrocharis dubia (Bl.) Backer were studied. The results indicated that Cd-NP joint toxicity is concentration-dependent. The joint toxicity of Cd and NP on H. dubia was antagonistic when the concentrations of Cd + NP were 0.01 + 0.1/1mg/L. At 0.5 + 0.1/1mg/L, Cd and NP had a strong synergistic effect on H. dubia. In addition, plant growth was significantly inhibited, and the chlorophyll contents were significantly reduced under Cd, NP, or Cd-NP exposure. The plant's antioxidant enzyme system was destroyed. The activities of superoxide dismutase (SOD) and catalase (CAT) were significantly decreased under NP-only exposure. The activity of SOD was significantly decreased under Cd-only and under joint exposure. Compound pollution exceeded the oxidative defense capacity of the plants, so the H2O2 content increased significantly. Our results indicated that the ecotoxicity of NP combined with Cd may be exacerbated in aquatic environments and cause obvious damage to H. dubia.

Degradation of the nonylphenol aqueous solution by strong ionization discharge: evaluation of degradation mechanism and the water toxicity of zebrafish.

Nonylphenol (NP) is a typical environmental endogenous disrupter with low concentration and high toxicity. This paper describes the mechanism of NP degradation in solution by strong ionization dielectric barrier discharge (SIDBD). Furthermore, the degradation performance of NP by SIDBD was tested by changing the equipment voltage, the initial concentration of NP in aqueous solution, pH, and inorganic ions. Degradation pathways of NP were detected using a high-performance liquid chromatography-mass spectrometer. The biological effects of NP degradation were assessed by detecting indicators of embryonic development in zebrafish (survival rate, fetal movement, heartbeat, the body length, behavior, deformity) and adult fish (sex differentiation, weight, ovarian testes pathological section analysis). The results showed when the input O2 was 5 L/min and the voltage was 3.2 kV, the degradation efficiency of NP can reach 99.0% after 60 min of experiment. Equipment voltage, initial concentration of NP in solution, pH, inorganic ions and other factors can influence the degradation efficiency of NP by DBD. At the higher concentration of NP, the greater influence on embryonic development in zebrafish was noticed. Although the effects of NP on zebrafish sex differentiation were not obvious, it showed significant male weight inhibition and decrease in sperm number.

Transcriptional expression analysis reveals multiple effects of nonylphenol exposure on scallop immune system

Nonylphenol (NP) is an endocrine disruptor and environmental hormone representing alkylphenol compounds. Marine mollusks are an important source of protein for people worldwide. Many researchers have begun to study the effect of NP on marine mollusks immune system in view of its toxicity; however, the underlying molecular mechanisms require in-depth analysis. In this study, we focused on the transcriptional expression change of immune-related genes and antioxidant enzymes activities variation after NP exposure in a marine bivalve mollusk, Chlamys farreri, to explore the immunomodulatory capacity of NP in marine mollusks. We identified MAVS (Mitochondrial antiviral signaling protein), a key adaptor molecule in the RLR (RIG-I like receptor) pathway, and studied the expression of multiple immune-related genes in response to different concentrations of NP. The key genes involved in RLR/TLR (Toll like receptor) innate immune pathway, apoptosis, and cellular antioxidation mechanism were investigated. Changes in the enzymatic activities of scallop antioxidant enzymes after NP exposure were also examined. The results revealed that the genes expression and the antioxidant enzymes activities show significant changes, thus proving that NP stimulation affects the scallop immune system. Our research results demonstrate the immunomodulatory capacity of NP in marine bivalve mollusks and lay the foundation for further in-depth analysis of the molecular mechanism of NP toxicity.

Mechanisms Mediating the Lipogenic Effect of Nonylphenol in Human Preadipocytes

Mechanisms Mediating the Lipogenic Effect of Nonylphenol in Human Preadipocytes

Effect of Vitamins C and E On Nonylphenol–Induced Dna Damage and Tefu Gene Expression in Drosophila Melanogaster

:Nonylphenol (NP) is one of the major environmental endocrine disrupters that can cause oxidative damage. Vitamin C (ascorbic acid) and vitamin E (α-tocopherol) are powerful antioxidants that could offset the effects of NP and are compounds that should be taken daily. In this study, the potential effects of the separate and combined administration of NP (1 and 10 mg/L) and vitamins C and E (25 mg/L) on DNA damage and telomere fusion (TEFU) gene expression in Drosophila melanogaster, a model organism, were investigated over 40 days. For the NP-administered groups, DNA damage increased while vitamins C and E reduced these effects, especially those induced by a co-administered group of NP and vitamin E. Furthermore, telomerase and DNA damage-associated TEFU gene expression levels increased in the NP-administered groups compared to the control group, while they decreased in the vitamin C and E administered groups. Consequently, it was concluded that vitamin C and E prevents the negative effects of NP on DNA damage.

Nonylphenol regulates TL1A through the AhR/HDAC2/HNF4α pathway in endothelial cells to promote the angiogenesis of colorectal cancer

BackgroundColorectal cancer (CRC) is one of the most malignant cancers worldwide. Nonylphenol (NP) is an endocrine-disruptor chemical and plays an important role in the development of cancers. However, the effects of NP on CRC remain unclear. In this study, we aimed to investigate the potential mechanisms of NP in the pathogenesis of CRC. MethodsThe levels of AhR, TL1A and HDAC2 in CRC tissues and endothelial cells were assessed by RT-qPCR or western blot. CHIP and dual luciferase reporter assays were used to confirm the interaction between AhR and HDAC2, or HNF4α and TL1A. The CCK8, would healing and tube formation assays were conducted to evaluate the proliferation, migration and angiogenesis of HUVECs. Western blot determined HNF4α protein and HNF4α acetylation levels. The secreted TL1A protein was detected by ELISA. The angiogenesis-related factor CD31 was tested by IHC. ResultsThe expression level of AhR was significantly up-regulated in CRC tissues and endothelial cells. Moreover, NP activated the AhR pathway mediated colorectal endothelial cell angiogenesis and proliferation, while TL1A overexpression resisted these effects caused by NP. Besides, NP was found to modulate HNF4α deacetylation through AhR/HDAC2 to inhibit TL1A. Furthermore, in vivo experiments proved that NP regulated CRC growth and angiogenesis via AhR/HDAC2/HNF4α/TL1A axis. ConclusionThis study revealed that NP promoted CRC growth and angiogenesis through AhR/HDAC2/HNF4α/TL1A pathway and could be a new therapeutic target for CRC treatment.

Effect of nonylphenol on the colonic mucosa in rats and intervention with zinc-selenium green tea (Camellia sinensis).

To investigate the effect of nonylphenol (NP) exposure on the colonic mucosa in rats, and the protective effects of Guizhou zinc-selenium tea (Zn-Se tea) on the damage induced by NP, sixty Sprague-Dawley rats were randomly divided into 6 groups (n=10 in each group): control group (corn oil), and rats gavaged with NP at the doses of 0.4mg/kg/d (Low NP group), 4mg/kg/d (Medium NP group), 40mg/kg/d (High NP group), and 40mg/kg NP combined with green tea group at the doses of 0.2g/ml (NP+GT group) and 0.2g/ml Zn-Se tea group (NP+ZST group). NP at 40mg/kg/d was administered to the tea groups for 3months, followed by NP+green tea and NP+Zn-Se tea for 4months, and the rest of the groups were gavaged for 7months. With the increase of NP concentration, NP accumulation in colon gradually increased (P<0.05), colonic villi shortened, tight junctions between cells widened, intestinal integrity was impaired, and goblet cells, intraepithelial lymphocytes and mast cells were significantly lower in NP high-dose group than in control group (P<0.05). Meanwhile, the protein expression of Caspase-1, IL-1β and Pro-IL-1β in NP high-dose group was significantly higher than that in control group (P<0.05). Zn-Se tea increased the number of goblet cells in colon and decreased the accumulation of NP in colon (P<0.05); Zn-Se tea and common green tea decreased the expression of Caspase-1 and Pro-IL-1β protein (P<0.05). NP exposure can destroy intestinal morphology, reduce the number of intestinal immune cells, reduce intestinal immunity and increase the release of inflammatory factors; Guizhou Zn-Se tea has a certain protective effect on colon damage caused by NP.