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ObjectiveTo assess the health risk of dietary exposure to nonylphenol in infants aged 0-36 months through infant formula in Shanghai. MethodsA monitoring of nonylphenol pollution in infant formula was conducted in 2022. A total of 90 samples were obtained from maternal and infant stores， supermarkets， and online stores in Shanghai. Based on the daily consumption data of infant formula， a point assessment method was used to assess the dietary exposure to nonylphenol in infant formula. ResultsThe prevalence of nonylphenol in infant formula retailed in Shanghai was 95.6% （86/90）. The amount of nonylphenol varied from non-detected to 22.70 μg·kg-1， with the mean value of 8.47 μg·kg-1 and the P50 value of 7.77 μg·kg-1. The mean daily nonylphenol exposure （estimated by body weight） from infant formula in infants aged 0-6 months， 7-12 months and 13-36 months in Shanghai was 0.091， 0.068 and 0.054 μg·kg-1， respectively； furthermore， the P95 value of daily exposure （by body weight） was 0.228， 0.152 and 0.119 μg·kg-1， respectively. These amounts were much lower than the tolerable daily intake （TDI） of nonylphenol （by body weight 5 μg·kg-1）. ConclusionThe health risk of daliy nonylphenol intake from infant formula remains low among infants aged 0-36 months in Shanghai.
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Objective:To investigate the influence of nonylphenol (NP) on cytoactive and the expression of G protein-coupled estrogen receptor 30 (GPR30) in human colon cancer SW480 cells.Methods:The experimental study was conducted. The human colon cancer SW480 cells were cultured in vitro. The influence of NP on proliferation, cell cycle, apoptosis and the expression of GPR30 in human colon cancer SW480 cells were analyzed by cell proliferation, cell cycle detection, cell apoptosis and gene expression and protein expression experiments. Cell grouping: SW480 cells cultured with medium were set as the control group, cultured with medium+1×10 ?8 mol/L estradiol were set as the estradiol group, cultured with medium+1×10 ?8 mol/L NP were set as the NP group, cultured with medium+1×10 ?8 mol/L NP+1×10 ?7 mol/L GPR30 specific antagonist G15 were set as the NP+G15 group, respectively. Observation indicators: (1) proliferation index of human colon cancer SW480 cells in the 4 groups; (2) cycle proportion of human colon cancer SW480 cells in the 4 groups; (3) apoptosis index of human colon cancer SW480 cells in the 4 groups; (4) GPR30 messenger RNA(mRNA) expression of human colon cancer SW480 cells in the 4 groups; (5) GPR30 protein expression of human colon cancer SW480 cells in the 4 groups. Measurement data with normal distribution were represented as Mean± SD and one way ANOVA was used for comparison between groups. The least significant difference method was used to test the pairwise comparison. Results:(1) Proliferation index of human colon cancer SW480 cells in the 4 groups. Results of the cell proliferation experiments showed that the proliferation indexes of human colon cancer SW480 cells in the control group, the estradiol group, the NP group and the NP+G15 group were 100.00±0.00, 89.19±4.86, 148.96±6.04 and 120.40±3.39, respectively, showing a significant difference among the 4 groups ( F=21.45, P<0.05). There was a significant difference between the control group and the NP group ( P<0.05), and there was no significant difference between the control group and the estradiol group, between the control group and the NP+G15 group ( P>0.05). (2) Cycle proportion of human colon cancer SW480 cells in the 4 groups. Results of the cell cycle detection experiments showed that the proportions of human colon cancer SW480 cells in the S phase of the cell cycles in the control group, the estradiol group, the NP group and the NP+G15 group were 39.96%±2.02%, 36.67%±0.62%, 43.85%±1.02% and 38.29%±1.42%, respectively, showing a significant difference among the 4 groups ( F=10.08, P<0.05). There were significant differences between the control group and the estradiol group, between the control group and the NP group ( P<0.05), and there was no significant difference between the control group and the NP+G15 group ( P>0.05). (3) Apoptosis index of human colon cancer SW480 cells in the 4 groups. Results of the cell apoptosis experiments showed that the apoptosis indexes of human colon cancer SW480 cells in the control group, the estradiol group, the NP group and the NP+G15 group were 1.67±0.18, 4.80±0.31, 0.75±0.11 and 2.20±0.19, respectively, showing a significant difference among the 4 groups ( F=136.79, P<0.05). There were significant differences between the control group and the estradiol group, between the control group and the NP group ( P<0.05), and there was no significant difference between the control group and the NP+G15 group ( P>0.05). (4) GPR30 mRNA expression of human colon cancer SW480 cells in the 4 groups. Results of quantitative real-time polymerase chain reaction detection showed that the relative expression rates of GPR30 mRNA in human colon cancer SW480 cells of the control group, the estradiol group, the NP group and the NP+G15 group were 1.00±0.00, 0.86±0.05, 1.89±0.27 and 0.64±0.12, respectively, showing a significant difference among the 4 groups ( F=26.61, P<0.05). There were significant differences between the control group and the NP group, between the control group and the NP+G15 group ( P<0.05), and there was no significant difference between the control group and the estradiol group ( P>0.05). (5) GPR30 protein expression human colon cancer SW480 cells in the 4 groups. Results of Western blot detection showed that the relative expression rates of GPR30 protein in human colon cancer SW480 cells of the control group, the estradiol group, the NP group and the NP+G15 group were 1.83±0.16, 1.68±0.15, 3.10±0.30 and 1.26±0.11, respectively, showing a significant difference among the 4 groups ( F=34.05, P<0.05). There were significant differences between the control group and the NP group, between the control group and the NP+G15 group ( P<0.05), and there was no significant difference between the control group and the estradiol group ( P>0.05). Conclusion:Low dose of NP can increase the proliferation index and the proportion of cells in the S phase of the cell cycles, decrease the apoptosis index, and promote the mRNA and protein expression of GPR30 in human colon cancer SW480 cells.
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Environmental endocrine disrupting chemicals are a kind of exogenous chemicals that generally exist in the environment, and can disturb the endocrine homeostasis and adversely affect reproductive, immune, neurological, and other functions after entering the body, among which the damage to the reproductive system is the most significant one. Studies have confirmed that the long-term exposure to environmental endocrine disrupting chemicals have irreversible and harmful effects on primordial germ cell growth, reproductive organ development, and reproductive endocrine regulation, and also have obvious correlations with the occurrence and development of various reproductive system tumors. This paper reviewed various reproductive toxicities induced by common environmental endocrine disrupting chemicals in the developmental and reproductive stages, and associated mechanisms involved in the occurrence and development of reproductive system tumors.
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Aim: The present study was performed to evaluate the genotoxic effect of 4-nonylphenol after acute and subchronic exposure in spleen tissue of Channa punctatus, recovery in DNA damage was also ascertained after 30 days of cessation of exposure.Methodology: Tail length (TL), tail intensity (TI), tail moment (TM), Olive tail moment (OTM) was used as biological indicators of DNA damage. The fish were exposed to different sublethal concentrations of 4-NP for 96 hrs (acute exposure) and for 90 days (sub chronic exposure). Results: Exposed groups showed significantly higher DNA damage in both acute and sub chronic exposure as compared to control groups. In the case of acute exposure, the highest damage was observed at 24 hr of exposure followed by a decline in the value of all the parameters, while in the later hours of exposure these value further increased. On the other hand, in the case of sub-chronic exposure, the highest damage was observed after treatment with 0.10 mg l-1 concentration of 4-NP at 90 days of exposure. Recovery experiment showed a decrease in the values of all the parameter’s studied, however, a significant decrease was observed only at the highest concentration. Interpretation: The results conclude the DNA damaging potential of 4-nonylphenol and highlighted the usage of spleen tissue for genotoxicity testing
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Objective To investigate the effects of nonylphenol (NP) exposure on the activity of SOD and GSH-Px and the content of MDA in gastric tissue of SD rats. Methods Twenty-four clean SD rats were randomly divided into four groups, 6 in each group. The negative control group was given corn oil, and the exposure groups included low, medium and high doses of NP treatment groups. NP was prepared in corn oil and administrated intragastrically. The concentration of NP was 25, 50 and 100 mg/kg, respectively, given once a day. After 42 days of continuous intragastric administration, the animals were sacrificed under anesthesia and gastric tissues were collected. The pathological changes of gastric tissues were observed by HE staining. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and level of malondialdehyde (MDA) in gastric tissues were respectively detected by chemical colorimetry. Results No bleeding or necrosis was found in the gastric mucosa of all groups by naked eye view. Pinhole-sized pigmentation was found in the stomach wall fold and bulge of NP medium dose group, and the number of pigmentation spots was increased significantly in NP high dose group. HE staining showed that the epithelial cells and glands of gastric mucosa of rats in normal group were arranged neatly and intact, and no any defect or abnormality in mucosal myometrium was observed. In the low dose group, hyperemia and edema, and vasodilation in the mucosal glands were observed, while in the medium and high dose groups, the epithelial cells of the gastric mucosa were damaged and exfoliated, the glandular ducts were swollen and congested, and lymphocyte infiltration was observed in the mucosa and interstitium. Compared with the control group, SOD activity in the high dose group was significantly decreased (P0.05). SOD activity decreased gradually with the increase of the dose. Compared with the control group, there was no significant difference in GSH-Px content among the NP exposure groups. Compared with the control group, the MDA content in the low dose group was significantly increased (P<0.05), while there was no significant difference in the medium and high dose groups. Conclusion Short-term exposure to 25mg/kg nonylphenol caused oxidative damage to gastric mucosa.
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PURPOSE: Nonylphenol (NP) is an endocrine disruptor found in products such as cleaners, plastics, and detergents. It exerts actions similar to endogenous 17β-estradiol (E2) and is reported to influence various cancers. However, its role in colon cancer remains elusive. MATERIALS AND METHODS: Colon cancer cell lines COLO 205 and SW480 were employed in our study. The cells were treated with NP or E2 followed by measurement of apoptosis and proliferation using flow cytometry and MTT assays, respectively. G protein–coupled estrogen receptor 30 (GPR30) expression was visualized using immunofluorescence and Western blot. To investigate the underlying mechanism, the expression levels of GPR30, p-protein kinase A (PKA), c-myc, cyclin D1, and ERK1/2 were analyzed using Western blot. Meanwhile, the GPR30 antagonist G15 was utilized to validate the role of GPR30 in colon cancer progression. Finally, the effect of a GPR30 inhibitor on tumor growth was determined in vivo using tumor xenograft mouse models. RESULTS: NP facilitated the proliferation of colon cancer cells and induced apoptosis failure in vitro. Western blot revealed increased GPR30 expression levels in response to NP treatment. Cyclin D1, p-PKA, c-myc, and proliferating cell nuclear antigen, proteins that regulate the cell cycle, were all upregulated by NP, and NP-mediated ERK1/2 activation and subsequent cell proliferation were abrogated by the GPR30 inhibitor G15. Moreover, colon cancer mice that received G15 administration demonstrated impaired tumor growth in vivo. CONCLUSION: Low dose NP promotes the growth of colon tumors through GPR30-mediated activation of ERK1/2 signaling.
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Animals , Mice , Apoptosis , Blotting, Western , Cell Cycle , Cell Line , Cell Proliferation , Colon , Colonic Neoplasms , Cyclin D1 , Detergents , Estrogens , Flow Cytometry , Fluorescent Antibody Technique , Heterografts , In Vitro Techniques , Phosphotransferases , Plastics , Proliferating Cell Nuclear AntigenABSTRACT
Objective To investigate the effects of nonyphenol (NP)exposure during pregnant and lactation period on expression of cytochrome P450 2E1 (CYP2E1) mRNA and protein of hepatic tissues in offspring rats.Methods Pregnant rats were assigned to four groups:the exposure groups received gavage with NP at dose levels of 50 mg · kg-1 · d-1 (low dose group),100 mg · kg-1 · d-1 (medium dose group),200 mg · kg-1 · d-1 (high dose group) and the control group was treated with corn oil alone,NP exposure time was limited from gestational day 6 to postnatal day 21.The newborn rats were sacrificed at 90 days after birth,followed by blood collection and serum separation.Then,serum biochemical indicators of liver function and lipid levels were detected.Glutathione peroxidase (GSH-PX),superoxide dismutase (SOD) activities,malondialdehyde (MDA) level and CYP2E1 mRNA and protein levels were determined in hepatic tissues.Pathologic changes in hepatic tissues were observed with HE staining.Results Compared with the control group,the aspartate aminotransferase (ALT),alanine aminotransferase (AST) levels and AST/ALT ratio of offspring rats in exposure groups were increased in a dose-dependent manner (P＜0.05),as well as serum TG,TC and LDL-C levels were increased (P＜0.05).The liver tissue structure of the control group was normal.The hepatic sinus of the medium dose group was showed mild expansion and inflammatory cellular infiltration.Otherwise,the liver of high dose group had a large amount of lipid droplets.Compared with the control group,SOD and GSH-PX activities were obviously decreased,while MDA level was significantly decreased in each exposure group (P＜0.05).CYP2E1 mRNA and protein expression levels of medium and high dose groups were higher than those in the control group (P＜0.05).Conclusion Exposure to NP during gestation and lactation period can induce lipid metabolism disorders and inflammatory lesions in hepatic tissues of offspring rats,and it maybe associated With up-regulation of CYP2E1 expression.
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Objective To investigate the effects of nonyphenol (NP)exposure during pregnant and lactation period on expression of cytochrome P450 2E1 (CYP2E1) mRNA and protein of hepatic tissues in offspring rats.Methods Pregnant rats were assigned to four groups:the exposure groups received gavage with NP at dose levels of 50 mg · kg-1 · d-1 (low dose group),100 mg · kg-1 · d-1 (medium dose group),200 mg · kg-1 · d-1 (high dose group) and the control group was treated with corn oil alone,NP exposure time was limited from gestational day 6 to postnatal day 21.The newborn rats were sacrificed at 90 days after birth,followed by blood collection and serum separation.Then,serum biochemical indicators of liver function and lipid levels were detected.Glutathione peroxidase (GSH-PX),superoxide dismutase (SOD) activities,malondialdehyde (MDA) level and CYP2E1 mRNA and protein levels were determined in hepatic tissues.Pathologic changes in hepatic tissues were observed with HE staining.Results Compared with the control group,the aspartate aminotransferase (ALT),alanine aminotransferase (AST) levels and AST/ALT ratio of offspring rats in exposure groups were increased in a dose-dependent manner (P＜0.05),as well as serum TG,TC and LDL-C levels were increased (P＜0.05).The liver tissue structure of the control group was normal.The hepatic sinus of the medium dose group was showed mild expansion and inflammatory cellular infiltration.Otherwise,the liver of high dose group had a large amount of lipid droplets.Compared with the control group,SOD and GSH-PX activities were obviously decreased,while MDA level was significantly decreased in each exposure group (P＜0.05).CYP2E1 mRNA and protein expression levels of medium and high dose groups were higher than those in the control group (P＜0.05).Conclusion Exposure to NP during gestation and lactation period can induce lipid metabolism disorders and inflammatory lesions in hepatic tissues of offspring rats,and it maybe associated With up-regulation of CYP2E1 expression.
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Objective · To compare urine sample collection methods for measuring urinary concentrations of phenolic endocrine disrupting chemicals including bisphenol A (BPA),triclosan (TCS),and 4-n-nonylphenol (4-n-NP) in pregnant women.Methods· Urine samples were collected from women at late pregnancy by two methods:urine catheter and collection bag (n=176),urine collecting containers made of polypropylene (PP) (n=642).Urinary concentrations of BPA,TCS and 4-n-NP were measured with high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS)method.Confirmation experiment used PP containers,urine catheter and collection bags,as well as low-density polyethylene (LDPE) tubes and glass containers as both negative controls to collect urine samples from each of the 5 women.Results · Geometric mean (GM) of urinary BPA concentration collected by urine catheter and collection bags was 82.5 ng/mL (95％ CI 71.4-95.4 ng/mL),which was 63 times higher than that from PP containers (GM 1.3 ng/mL;95％ CI 1.3-1.5 ng/mL).Concentrations of urinary 4-n-NP and creatinine were similar between two collection methods.Confirmation experiment showed that urinary BPA concentration collected by urine catheter and collection bags was much higher than those collected by other three methods.Conclusion· In collection of urine samples for measuring phenolic chemicals,PP urine collection container as well as LDPE containers are adequate for use in epidemiologic studies,but urine catheter and collection bag is not.
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The current study aimed to investigate the effects of perinatal exposure to nonylphenol (NP) on delivery outcome of pregnant rats and subsequent inflammatory hepatic injury in newborn rats. The pregnant rats were divided into 2 groups: control group (corn oil) and NP exposure group. Thirty-four pregnant rats were administered NP or corn oil by gavage from the sixth day of pregnancy to 21 days postpartum, with blood samples collected at 12 and 21 days of pregnancy and 60 days after delivery. The NP concentration was measured by HPLC, with chemiluminescence used for detection of estrogen and progesterone levels. Maternal delivery parameters were also observed. Liver and blood of the newborn rats were collected and subjected to automatic biochemical detection of liver function and blood lipid analyzer (immunoturbidimetry), and ultrastructural observation of the hepatic microstructure, with the TNF-α and IL-1β hepatic tissue levels evaluated by immunohistochemistry. Compared with the control group, the pregnant and postpartum serum NP and estradiol levels of the mother rats in the NP group were significantly increased, together with lowered progesterone level, increased number of threatened abortion and dystocia, and fewer newborn rats and lower litter weight. Serum and hepatic NP levels of the newborn rats measured 60 days after birth were significantly higher than those of the control group, as well as lower testosterone levels and increased estradiol levels. When observed under electron microscope, the hepatocyte nuclei of the control group were large and round, with evenly distributed chromatin. The chromatin of hepatocytes in the NP group presented deep staining of the nuclei, significant lipid decrease in the cytoplasm, and the majority of cells bonded with lysate. The results of immunohistochemistry showed that there was almost no TNF-α or IL-1β expression in the hepatocytes of the control group, while the number of TNF-α-, PCNA-, and IL-1β-positive cells in the NP group was increased, with higher integral optical density than the control group. Compared to the control group, the serum levels of alanine aminotransferase, aspartate aminotransferase, triglyceride and low-density lipoprotein in the newborn rats of the NP group were significantly increased. There was no significant difference in the serum level of high-density lipoprotein or cholesterol between the groups. Perinatal exposure to NP can interfere with the in vivo estrogen and progesterone levels of pregnant rats, resulting in threatened abortion, dystocia and other adverse delivery outcomes. High liver and serum NP levels of the newborn rats led to alteration of liver tissue structure and function. The NP-induced hepatotoxicity is probably mediated by inflammatory cytokines TNF-α and IL-1α.
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Animals , Female , Rats , Chemical and Drug Induced Liver Injury/etiology , Phenols/toxicity , Animals, Newborn , Chemical and Drug Induced Liver Injury/pathology , Disease Models, Animal , Interleukin-1/analysis , Prenatal Exposure Delayed Effects/chemically induced , Rats, Sprague-Dawley , Tumor Necrosis Factor-alpha/analysisABSTRACT
Objective To observe the effects of nonylphenol(NP)on the intracellular calcium concentration changes and cell proliferation,and the involvement of GPR30 receptor in H9c2 cell. Methods The intracellular calcium concentration changes were recorded by using intracellular calcium determination method and cell proliferation was observed by MTT method in H9c2 cell. Results NP(1×10-10 mol/L)increased the intra?cellular calcium concentration changing amplitude and promoted the proliferation of H9c2 cells,while NP(1×10-6 mol/L)decreased intracellular calcium concentration changing amplitude and suppressed cell proliferation. G15 could block the promoting effect of 1×10-10 mol/L NP on the intracel?lular calcium concentration and cell proliferation,but could not block the inhibition of 1×10-6 mol/L NP on the intracellular calcium increase and cell proliferation. Conclusion The results indicate that NP affect rapid calcium signal changes and cell proliferation in non?monotonic dose dependent manner,and its mechanism may be due to the different involvement of GPR30 receptor in different concentrations.
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OBJECTIVES: This study aimed to estimate the effects of 4-nonylphenol (NP), a ubiquitously present surfactant in aquatic environments, on the anti-oxidant systems of the liver in the Far Eastern catfish Silurus asotus. METHODS: Changes in biochemical parameters involved in glutathione (GSH)-related and other anti-oxidant systems were analyzed following 4 weeks of 4-NP administration (0.1 and 1.0 mg/kg diet) via a formulated diet to catfish. RESULTS: 4-NP exposure induced an elevation in hepatic lipid peroxide levels and an accompanying decrease in reduced state GSH after 2 weeks, suggesting pro-oxidant effects of the chemical in catfish. This oxidative stress was associated with an inhibition of the GSH-utilizing enzyme glutathione peroxidase at the same time point. This inhibition was restored after 4 weeks. The activities of other anti-oxidant enzymes, i.e., glutathione reductase, superoxide dismutase and catalase were increased after 4 weeks. These enzyme increases occurred more strongly at the higher 4-NP concentration (1.0 mg/kg diet). CONCLUSIONS: 4-NP given to catfish at 0.1 to 1.0 mg/kg diet, concentrations relevant to environmental levels, depletes the endogenous anti-oxidant molecule GSH and temporarily inhibits GSH-related anti-oxidant enzymes. Such declines in anti-oxidant capacity and elevated oxidative stress seem to be compensated eventually by subsequent activation of various anti-oxidant enzyme systems.
Subject(s)
Catalase , Catfishes , Detergents , Diet , Glutathione , Glutathione Peroxidase , Glutathione Reductase , Liver , Oxidative Stress , Superoxide DismutaseABSTRACT
OBJECTIVES: This study aimed to estimate the effects of 4-nonylphenol (NP), a ubiquitously present surfactant in aquatic environments, on the anti-oxidant systems of the liver in the Far Eastern catfish Silurus asotus. METHODS: Changes in biochemical parameters involved in glutathione (GSH)-related and other anti-oxidant systems were analyzed following 4 weeks of 4-NP administration (0.1 and 1.0 mg/kg diet) via a formulated diet to catfish. RESULTS: 4-NP exposure induced an elevation in hepatic lipid peroxide levels and an accompanying decrease in reduced state GSH after 2 weeks, suggesting pro-oxidant effects of the chemical in catfish. This oxidative stress was associated with an inhibition of the GSH-utilizing enzyme glutathione peroxidase at the same time point. This inhibition was restored after 4 weeks. The activities of other anti-oxidant enzymes, i.e., glutathione reductase, superoxide dismutase and catalase were increased after 4 weeks. These enzyme increases occurred more strongly at the higher 4-NP concentration (1.0 mg/kg diet). CONCLUSIONS: 4-NP given to catfish at 0.1 to 1.0 mg/kg diet, concentrations relevant to environmental levels, depletes the endogenous anti-oxidant molecule GSH and temporarily inhibits GSH-related anti-oxidant enzymes. Such declines in anti-oxidant capacity and elevated oxidative stress seem to be compensated eventually by subsequent activation of various anti-oxidant enzyme systems.
Subject(s)
Catalase , Catfishes , Detergents , Diet , Glutathione , Glutathione Peroxidase , Glutathione Reductase , Liver , Oxidative Stress , Superoxide DismutaseABSTRACT
Objective To observe the effect of nonylphenol (NP) on plasma and urine 5-hydroxytryptamine (5-HT) levels and expression of 5-HT and of 5-HT2A receptor in the platelets of rats, so as to explore the toxic mechanisms of NP on 5-HT and 5-HT2A receptor.
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OBJECTIVES: Heat shock protein 90 (HSP90) is a highly conserved molecular chaperone important in the maturation of a broad spectrum of protein. In this study, an HSP90 gene was isolated from Asian paddle crab, Charybdis japonica, as a bio-indicator to monitor the marine ecosystem. METHODS: This work reports the responses of C. japonica HSP90 mRNA expression to cellular stress by endocrine disrupting chemicals (EDCs), such as bisphenol A (BPA) and 4-nonylphenol (NP) using real-time. reverse transcription polymerase chain reaction. RESULTS: The deduced amino acid sequence of HSP90 from C. japonica shared a high degree of homology with their homologues in other species. In a phylogenetic analysis, C. japonica HSP90 is evolutionally related with an ortholog of the other crustacean species. The expression of HSP90 gene was almost distributed in all the examined tissues of the C. japonica crab but expression levels varied among the different body parts of the crabs. We examined HSP90 mRNA expression pattern in C. japonica crabs exposed to EDCs for various exposure times. The expression of HSP90 transcripts was significantly increased in C. japonica crabs exposed to BPA and NP at different concentrations for 12, 24, 48 and 96 hours. The mRNA expression of HSP90 gene was significantly induced in a concentration- and time-dependent manner after BPA or NP exposures for 96 hours. CONCLUSIONS: Taken together, expression analysis of Asian paddle crab HSP90 gene provided useful molecular information about crab responses in stress conditions and potential ways to monitor the EDCs stressors in marine environments.
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Humans , Amino Acid Sequence , Asian People , Ecosystem , Endocrine Disruptors , Gene Expression , Heat-Shock Proteins , Human Body , Molecular Chaperones , Polymerase Chain Reaction , Reverse Transcription , RNA, MessengerABSTRACT
A simple analytical method by means of on-line solid phase extraction followed liquid chromatography-tandem mass spectrometry ( SPE-LC-MS/MS) was developed for the simultaneous quantitation of 4 endocrine disruptors ( triclosan, triclocarban, bisphenol A and nonylphenol) in dairy products. Infant formula and milk samples were dissolved in acetic acid buffer and hydrolyzed by β-glucuronidase/arylsulfatase. Acetonitrile was used as the extract. Then, the mixture was freeze-centrifuged for 10 min and the supernatant was diluted with water, and analyzed via on-line SPE-LC-MS/MS. The sample extracts were concentrated by an Xbridge C8 cartridge and separated on a BEH C18 column with a gradient mobile phase of methanol and water; then analyzed by triple quadrupole mass spectrometry. Mass acquisition was conducted under negative electrospray ionization mode. Quantification was performed by isotopic internal standard calibration. Acceptable linearity (R2>0. 99) was achieved over the range of 0. 005-5. 0 μg/L, with limits of quantification of 0. 03-1. 0μg/kg. Average recoveries of four target compounds (spiked at three concentration levels) ranged from 80. 2%-106. 7%,with relative standard deviation less than 15%. Due to its rapidity, simplicity, and high sensitivity, the method is suitable for the analysis of endocrine disruptors in dairy products. It has been applied in the analysis of raw milk and milk products collected in Beijing. As a result, nonylphenol was found with a high detectable frequency.
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Bisphenol A [2,2-bis(4-hydroxyphenyl)propane] (BPA), 4-nonylphenol (NP) and di(2-ethylhexyl)phthalate (DEHP), and its metabolite mono-2-ethylhexyl phthalate (MEHP) are chemicals found in plastics, which act as endocrine disruptors (EDs) in animals, including human. EDs act like hormones in the endocrine system, and disrupt the physiologic function of endogenous hormones. Most people are exposed to different endocrine disruptors and concern has been raised about their true effect on reproductive organs. In the testis, they seem to preferentially attack developing testis during puberty rather than adult organs. However, the lack of information about the molecular mechanism, and the apparently controversial effect observed in different models has hampered the understanding of their effects on mammalian spermatogenesis. In this review, we critically discuss the available information regarding the effect of BPA, NP and DEHP/ MEHP upon mammalian spermatogenesis, a major target of EDs. Germ cell sloughing, disruption of the blood-testis-barrier and germ cell apoptosis are the most common effects reported in the available literature. We propose a model at the molecular level to explain the effects at the cellular level, mainly focused on germ cell apoptosis.
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Animals , Humans , Male , Air Pollutants, Occupational/adverse effects , Air Pollutants, Occupational/toxicity , Apoptosis/drug effects , Benzhydryl Compounds/adverse effects , Benzhydryl Compounds/toxicity , Endocrine Disruptors/adverse effects , Endocrine Disruptors/toxicity , Infertility, Male/chemically induced , Phenols/adverse effects , Phenols/toxicity , Plasticizers/toxicity , Spermatogenesis/drug effects , Apoptosis/physiology , Germ Cells/drug effects , Plasticizers/adverse effects , Plasticizers/chemistry , Spermatogenesis/physiology , Testis/drug effectsABSTRACT
Alkylphenol polyethoxylates is a group of estrogenic compounds. Natural or synthetic types of these compounds react with the endocrine system by binding hormone receptors, resulting in interference with their action, which is why they are called endocrine disrupting chemicals. Among their hydrolytic products are nonylphenols (NP), which are considered pollutants of aquatic environments. The objective of this study was to evaluate the pathological alterations on liver tissue of fish exposed to these compounds for long durations, starting from beginning of life and during the period of sexual maturity. Tilapia fish were obtained from Abhur fish farms, reared in the laboratory in special basins, and divided into two groups. The first maternal group was untreated and their larvae were divided into three sub-groups: control; exposed to 15μg/L; and exposed to 30 μg/L. The second maternal group was divided into 2 sub-groups: with larvae exposed to 15μg/L; and with their larvae exposed to 30 μg/L. Larvae and mother exposed to different concentrations of NP (15 and 30 μg/L) showed an increased accumulation of NP in both livers and muscles compared to the control group due to bioaccumulation. Tissue section examinations of the treated group (15 μg NP /L) showed disruption of liver architecture, with lyses, loss of nuclei, necrosis, and fatty infiltration. The changes were more marked in tissues exposed to (30 μg NP /L). Although this pollution was not lethal, its effect may be reflected in vital activities and in the economy.
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Animals , Female , Male , Environmental Exposure/adverse effects , Liver/drug effects , Phenols/toxicity , Seawater/chemistry , Tilapia , Water Pollutants, Chemical/toxicity , Endocrine System/drug effects , Liver/chemistry , Liver/pathology , Models, Animal , Reproduction/physiology , Saudi Arabia , Sexual Maturation/drug effects , Sexual Maturation/physiology , Water Pollutants, Chemical/analysisABSTRACT
Nonylphenol ethoxylates (NPEOs), which are widely used for industrial and domestic purposes, exert adverse effects on wildlife after being used and discharged into the environment. However, their ultimate biodegradability and biodegradation pathway remains unclear. In this study, the aerobic degradability of nonylphenol ethoxylates (NPEOs) by the acclimated microorganisms in active sludge was examined using shaking-flask tests. The degradation of benzene rings in NPEOs was determined using UV spectroscopy and high performance liquid chromatography (HPLC). Results showed that more than 80 percent of benzene rings were removed after 8-10 days of degradation, and the majority of NPEOs were also removed after 9 days of degradation, indicating NPEOs and the benzene rings could be ultimately degraded by microorganisms in acclimated active sludge. Electrospray ionization-mass spectroscopy (ESI-MS) analysis of biodegradation intermediates indicate that stepwise omega, beta-oxidation of EO chains or fission of EO chains, and further omega, beta-oxidation of alkyl-chain for short-EO-chain NPEOs constitute the main pathway in the early stage, and complete biodegradation occur when the benzene rings in these molecules are opened in the later stage.
Subject(s)
Biodegradation, Environmental , Ethylene Glycol , Phenols , Chromatography, High Pressure Liquid , Spectrometry, Mass, Electrospray IonizationABSTRACT
Objective To explore the influence of nonylphenol(NP) on the filial generation rats spatial learning and memory capacity which were exposed to the parent rat during its pregnancy. Methods At the first day of the pregnancy, the rats were divided into four groups, which were orally administered with NP at doses of 0,50, 100 and 200 mg/kg,respectively, on gestational days 9～15. Cognitive function was tested by Morris water maze and step-down test. The ultrastructure of hippocampus tissues were observed by electronic microscope.Result The escape latency extended ((61.14±5.92) s) and erroring time increased ((4.57±1.13)times) in Morris water maze, and step down latency extended ((37.5±6.3)s), step through latency shortened((97.8±11.0)s) and erroring time increased ((3.0±1.4) times) in step down test in the N P 200 mg/kg treated groups (P<0 05). The correspond indexes were separately (35.85±4. 29) s, (2.57±0.97) time, (27.1±3.8) s,(172.0±89.2)s and(0.9±0.7)time in control group. Compared to the control group, there were significant differences in the results of the water maze test and step-down test between NP 200 mg/kg and the control group (P <005). The changes of the uhrastructure were found among the hippocampus neurons of NP 200 mg/kg group that characterized with chromatin condensed,clumped in circa-nuclei and mitochondrial tumefaction and vacuolization.Conclusion Exposures to NP during gestation might decreased abilities of spatial learning and memory capacity on F1 rats significantly.