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Background Dibutyl phthalate (DBP) is a common plasticizer in daily life and has been proved to be related to the exacerbation of allergic asthma. Domestic and foreign studies have shown that lipid peroxidation is closely related to the severity of asthma, which can be used as a basis for the diagnosis and treatment of asthma. Whether DBP can induce lipid peroxidation in allergic asthma remains to be further studied. Objective To investigate whether DBP aggravates allergic asthma by inducing lipid peroxidation in allergic asthma mice. Methods Eighty male BALB/c mice were randomly divided into 4 groups, namely control group, DBP group (40 mg·kg−1), 50 μg ovalbumin (OVA) group (allergic asthma model group), and DBP+OVA group. The DBP group and the DBP+OVA group were given DBP by gavage from Day 1 to 28, and the OVA group and the DBP+OVA group were sensitized by intraperitoneal injection of OVA, once every 3 d, a total of 5 injections, from Day 9 to 21. From Day 29 to 35, the OVA group and the DBP+OVA group were challenged by OVA atomization. After the exposure, samples of blood and lung were collected. The airway hyperresponsiveness of mice was observed by lung function analysis. The serum contents of immunoglobulin E (IgE), OVA-specific immunoglobulin E (OVA-IgE), and lung homogenate levels of interleukin 4 (IL-4) were detected by enzyme-linked immunosorbent assay (ELISA) to evaluate airway allergic inflammation. The pathological changes of lung tissues were observed after hematoxylin-eosin (HE) staining and collagen fiber (Masson) staining. The contents of reactive oxygen species (ROS), lipid ROS, glutathione peroxidase 4 (GPX4), reduced glutathione (GSH), malondialdehyde (MDA), and 4-hydroxynonenal (4-HNE) in lung homogenates were detected by ELISA to evaluate lipid peroxidation. Results The results of lung function analysis showed that compared with the control group, the inspiratory resistance (Ri) and expiratory resistance (Re) of the OVA group and the DBP+OVA group were increased, and the lung compliance (Cldyn) was decreased. The DBP + OVA group was more severe, and the difference between the OVA group and the DBP + OVA group was statistically significant (P<0.05 or P<0.01). Compared with the control group, the contents of IgE, OVA-IgE, and IL-4 in the OVA group and the DBP+OVA group were increased (P<0.05 or P<0.01), which indicated more severe allergic airway inflammation. The HE sections of the OVA group and the DBP+OVA group showed inflammatory cell infiltration around the airway, airway wall hyperplasia and thickening, and severe airway deformation, and the presentation of the DBP+OVA group was the most serious. After Masson staining, the OVA group and the DBP+OVA group showed depositions of a large number of collagen fibers, and the blue collagen fibrosis in the DBP+OVA group was even more serious. ROS, lipid ROS, MDA, and 4-HNE levels increased and GSH and GPX4 levels decreased in the OVA and DBP+OVA groups (P<0.05 or P<0.01), with the most severe effect in the DBP+OVA group. Conclusion DBP may induce lipid peroxidation in mice allergic asthma by producing excessive ROS which may aggravate the allergic asthma in mice.
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Abstract To evaluate the release of bisphenol-A glycidyl methacrylate (BisGMA), triethylene glycol dimethacrylate (TEGDMA), bisphenol A (BPA), and phthalates of the composite resin used in the bonding of spurs applied in the treatment of children with anterior open bite and its effects on human keratinocytes. Methodology Saliva samples of 22 children were collected before spur attachment (baseline) and 30 minutes (min) and 24 hours (h) after spur bonding. Analysis was performed using high-performance liquid chromatography (HPLC) coupled to tandem mass spectrometry (HPLC-MS/MS) and gas chromatography coupled to mass spectrometry (GC-MS). Standardized resin increments were added to three different dilutions of the cell culture medium. Keratinocytes (HaCaT) were cultivated in the conditioned media and evaluated for cell viability (MTT) and cell scratch assay. Results The levels of BisGMA (1.74±0.27 μg/mL), TEGDMA (2.29±0.36 μg/mL), and BPA (3.264±0.88 μg/L) in the saliva after 30 min, in comparison to baseline (0±0 μg/mL, 0±0 μg/mL, and 1.15±0.21 μg/L, respectively), presented higher numbers. After 24 h, the levels of the monomers were similar to the baseline. Phthalates showed no significant difference among groups. HaCat cells showed increased viability and reduced cell migration over time after exposure to methacrylate-based resin composites. Conclusion Resin composites, used to attach spurs in children with anterior open bite during orthodontic treatment, release monomers after polymerization and can influence the behavior of human keratinocytes, even at very low concentrations. Orthodontists should be aware of the risks of the resinous compounds release and preventive procedures should be held to reduce patient exposure.
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Background Di(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) are representative environmental endocrine disruptors of phthalate esters (PAEs). Some studies have shown that PAEs exposure may have an impact on lipid metabolism. Objective To investigate the effects of DEHP and/or DBP on lipid metabolism in rats and their possible mechanisms of action. Methods Thirty-six weaned healthy SD male rats, 3 weeks old, weighing 50-70 g, were divided into four groups, i.e., a corn oil control group, a DEHP (750 mg·kg−1) group, a DBP (500 mg·kg−1) group, and a DEHP+DBP (750 mg·kg−1+500 mg·kg−1) group. The rats were exposed to DEHP and/or DBP by oral gavage for 8 weeks, and weighed once a week. The rats were anesthetized 24 h after the last dose, and blood was taken from the apical part of the heart. Serum high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), and triglyceride (TG) were detected. Liver tissues and perigenital adipose tissues were collected, weighed, and one portion of the tissues was fixed in 10% neutral formalin for pathomorphological observation, and another portion was used for mRNA detection of lipid metabolism-related genes such as Janus kinase 3 (JAK3), signal transducer and activator of transcription 5b (STAT5b), and peroxisome proliferator-activated receptor γ (PPARγ). Results During the DEHP and/or DBP exposure period, the rats in all groups were free to eat and drink without death or injury observed. Compared with the control group: The body weight gain in the DEHP+DBP group was lower at all time points from the 2nd week onwards (P<0.05); the liver organ coefficients of the DEHP and the DEHP+DBP groups were higher (P<0.05); the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). Compared with the DEHP+DBP group: The body weight gains in the DEHP group at the 2nd, 4th, 5th, and 8th weeks were higher (P<0.05), and the body weight gains in the DBP group were higher at all time points except the 1st week (P<0.05); the liver organ coefficients in the DEHP group and the DBP group were lower (P<0.05); the serum TG level in the DEHP group was higher(P<0.05), and the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). The pathomorphological results of liver tissues showed that the hepatocytes in the DEHP, DBP, and DEHP+DBP groups were disordered with loss of cord-like arrangement, swelling (suggesting change of cell proliferation), and presented bilirubin pigmentation. The pathomorphological results of rat perigenital adipose tissues showed had irregular alignment, sizes, and arrangement of adipocyte in the DEHP, DBP, and DEHP+DBP groups. The results of rat liver lipid metabolism-related gene mRNA levels showed that the liver JAK3, STAT5b, and PPARγ mRNA levels in the DEHP, DBP, and DEHP+DBP groups were lower than those in the control group (P<0.05); the rat liver PPARγ mRNA levels in the DEHP and DBP groups were lower than those in the DEHP+DBP group (P<0.05). Conclusion DEHP and/or DBP can inhibit the increase of body weight to varying degrees, induce inflammatory damage to liver tissues, and cause abnormal lipid metabolism in rats, and the associated mechanism may be related to inhibiting the activation of JAK3/STAT5b/PPARγ signaling pathway in rat liver tissues.
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Aim To explore the antagonistic effect of nimodipine (Nim) on dibutyl phthalate (DBP)-in-duced learning and memory impairment in KM mice. Methods Thirty-six male KM mice were treated with saline (control), 50 mg • kg-1 DBP, 2 mg • kg-1 Nim, and DBP + Nim lasted for 28 days. The latency of KM mice in each group was measured. Levels of calmodulin (CaM), calmodulin/calmodulin-dependent protein kinase II ( CaMKII ) , protein kinase C (PKC) , cytochrome C (Cyt C) and caspase-3 in hippocampus of KM mice in each group were detected. And expressions of ERK1/2 and p-ERKl/2 were evaluated. In addition, the pathological changes of hipp-ocampal CAI region were also analyzed by HE, Nissl staining, and TUNEL assay. Results Compared with 50 mg • kg-1 DBP group, the learning and memory im-pairment of KM mice in DBP + Nim group was alleviated, the pathological damage and apoptosis in CA1 region of hippocampus were reduced, the levels of PKC, Cyt C, caspase-3 and p-ERKl/2 decreased, while the levels of CaM and CaMKII increased accordingly (P < 0.05). Conclusions DBP affects Ca2 +-related proteins and up-regulates p-ERKl/2 expression, inducing hippocampal neuronal damage and apoptosis, whereas Nim can improve DBP-induced learning and memory impairment in KM mice, which may be related to the ability of Nim to reduce the levels of p-ERKl/2 and caspase-3 in brain tissues of mice after DBP exposure by blocking DBP-induced Ca2+ concentration.
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To establish a model of ocular apoptosis in zebrafish by using dibutyl phthalate(DBP), and accordingly to evaluate the activity of anti-ocular apoptosis drugs. Methods Zebrafish embryos (30 hpf) were treated with DBP(0. 1, 10, 50, 100 jxmol L " 1) for 18 h and 42 h, and the survival rate was calculated. Then zebrafish embryos (30 or 54 hpf) were incubated with DBP(0. 1, 1 , 5 , 10, 50 |j.mol L 1) for 18 h under direct or indirect light conditions, and visualized under microscope, then the ocular apoptosis was assessed by AO staining. Furthermore, modeled zebrafish was treated with N-acetyl-L-cysteine(NAC) or ginsenoside Rgl, and the effects on ocular apoptosis were observed. Results There was no mortality in zebrafish at concentrations below 10 |j,mol L"1 after modeling with DBP for 18 h and 42 h. The survival rate of zebrafish was significantly reduced with a concentration above 50 |xmol L"1 (P < 0 . 0 1) . Furthermore, obvious ocular apoptosis was found at 30 hpf after 18 h with DBP(10 (unol L"1) (P < 0. 0 1) . The zebrafish showed spontaneous apoptosis of the ocular cells at 72 h, which was not associated with light conditions. Effect of NAC or ginsenoside Rgl was observed on decreasing ocular apoptosis in zebrafish (P < 0. 05) . Conclusions DBP can be used to rapidly and efficiently establish a model of ocular apoptosis in zebrafish, which can be used for rapid evaluation of drug activity-.
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Objective To identify a strain screen which utilize dibutyl phthalate (DBP) as the sole carbon source and to explore the optimal conditions for the degradation of DBP. Methods The solid leachate was inoculated in minimal salt medium (MSM) supplemented with DBP as the sole carbon and energy source to isolate the targeted strain. The strain was identified through colony phenotype, transmission electron microscope and 16SrDNA gene sequence analysis. The targeted strain was inoculated to the above medium with different pH and temperature. The optimal temperature and pH of the microbial degradation of DBP were studied with determination of the DBP residue and bacterial biomass. Results One bacterial strain named L6 was isolated from the solid with adding DBP as the sole carbon source. Based on its morphology, physiochemical characteristics, and 16SrDNA sequence, the strain was identified as Methylobacterium sp. The optimal pH and temperature for its biodegradation activities were 7 and 30℃, respectively. The targeted strain could degrade 85% of 800 mg/L DBP within 120 hours. Conclusion Based on the high removal rate, the isolated Methylobacterium sp. L6 has a potential for bioremediation technology of DBP pollution.
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Objective: To further study the chemical constituents of Stelleropsis tianschanica. Methods: The constituents were isolated and purified by silica gel chromatography repeatedly, and the structures were identified by spectra analysis and chemical methods. Results: Twelve compounds including five lignans and three diphenylpentane derivatives were obtained, and named as kusunokinin (1), pluviatolide (2), dibutyl phthalate (3), dipropyl phtalate (4), p-dihydroxybenzene (5), daphneolon (6), 2(S)- hydroxy-1-(4-hydroxy phenyl)-5-phenyl-1-pentanone (7), (2R,3R)-1,5-diphenylpentane-2,3-diol (8). lariciresinol (9), isolariciresinol (10), matairesinol (11), and 4α,5βH-guai-9,7(11)-dien-12,8-olide-12,8α-diol (12). Conclusion: Compounds 1-12 are all obtained from the plant of S. tianschanica and the genus Stelleropsis Pobed. for the first time.
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Objective: To study the antipyretic and anti-inflammatory constituents from the active fraction of Reduning Injection (RI). Methods: The active fraction of RI was screened by the LPS-induced mouse endotoxin shock model. The chemical constituents were isolated by chromatography on silica gel, ODS, Sephadex LH-20, Toyopearl HW-40 columns, reverse phase MPLC, and HPLC repeatedly, and their structures were identified by spectral data and physicochemical property. Results: The 95% ethanol eluate of RI on the macroporous adsorption resin column was proved to be the antipyretic and anti-inflammatory active fraction of RI. Fourteen compounds were isolated and identified as dibutyl phthalate (1), isovanillic acid (2), acetovanillone (3), phenylpropionic acid (4), geniposide (5), jasmigeniposide B (6), geniposidic acid (7), genipin-1-β-D-gentiobioside (8), 6″-O-trans-p-coumaroylgenipin gentiobioside (9), 6″-O-trans-feruloylgenipin gentiobioside (10), 6″-O-trans-sinapoylgenipin gentiobioside (11), jasmigeniposide A (12), 6″-O-trans-cinnamoylgenipin gentiobioside (13), and 2'-O-trans-caffeoylgardoside (14). Conclusion: Compounds 1-4 and 13 are reported from RI for the first time; And UPLC analyses and literature data showe that compounds 5 and 7-13 are originated from Gardenia jasminoides.
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The magnetic molecularly imprinted polymers (MMIPs), based on the surface of magnetic nanoparticles being modified by surface grafting, have been successfully synthesized, with dibutyl phthalate (DBP) as template molecule, ethylene glycol dimethacrylate (EGDMA) as cross-linking agent and azobisisobutyronitrile (AIBN) as initiator. Scanning electron microscopy (SEM), transmission electron microscope (TEM), and elemental analysis were employed to characterize the MMIPs. The structure and magnetic properties of the MMIPs were investigated by means of X-ray diffraction and vibrating sample magnetometer. The BET surface area shows that MMIPs is 380 m2/g and MNIPs is 324 m2/g. A series of static adsorption experiments were conducted to analyze its adsorption performance, which followed pseudo-second-order model by the kinetic analysis with correlation coefficient (R2) 0.9797, and Sips equation with correlation coefficient (R2) 0.999 by the isothermal analysis. The imprinting factors of diallyl phthalate (DAP), DBP and di-2-ethylhexyl phthalate (DEHP) were 1.53, 2.21 and 1.39 respectively, showing that MMIPs had better recognition performance for DBP. The experiment of regeneration recycles with five times showed the regeneration ability of DBP was only reduced by 12.3％.
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<p><b>Objective</b>To study the possible pathogenesis of infertility caused by dibutyl phthalate (DBP) and investigate the effects of Yishen Shengjing Capsules (YSC, kidney-tonifying and essence-producing capsules) on DBP-induced reproductive function injury and its possible action mechanisms in male Wistar rats.</p><p><b>METHODS</b>Models of DBP-induced reproductive function injury were made in 80 male Wistar rats and another 20 were used as blank controls. After modeling, the model rats were randomly divided into a model control, a high-dose YSC, a medium-dose YSC, and a low-dose YSC group. Four weeks after intervention, all the animals were sacrified for observation of the histomorphologic changes in the testis under the light microscope, measurement of sperm concentration, motility and abnormality, and determination of the levels of serum testosterone (T), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) by radioimmunoassay.</p><p><b>RESULTS</b>Compared with the blank controls, the model rats showed obvious pathological changes in testicular histomorphology, significantly decreased sperm concentration and motility, increased sperm abnormality, reduced contents of serum T and LH, and elevated the level of serum FSH (P<0.01). After 4 weeks of medication, the animals of the high-, medium-, and low-dose YSC groups, in comparison with the model controls, exhibited different degrees of recovery from testicular histomorphological damage, remarkably increased sperm concentration and motility, decreased sperm abnormality, elevated levels of serum T and LH, and reduced content of serum FSH (P<0.01). There were statistically significant differences in all the parameters above between the high-dose YSC and medium- and low-dose YSC groups (P<0.01).</p><p><b>CONCLUSIONS</b>DBP reduces sperm motility and concentration, increases sperm abnormality, causes damage to the morphological structure of the rat testis, decreases the contents of serum T and LH, and elevates the level of the serum FSH. Yishen Shengjing Capsules can improve DBP-induced productive function injury, increase sperm motility and concentration, decrease sperm abnormality, elevate the level of serum T and LH, reduce the content of serum FSH, improve the morphological structure of the testis, and thus promote the reproductive function of the male rat.</p>
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OBJECTIVE: To screen small molecule metabolites of dibutyl phthalate( DBP) in the rat plasma using ~1H nuclear magnetic resonance( NMR) technology; and to clarify the changes of metabolites and possible mechanism in metabolic regulation of DBP in rats from the molecular level and the aspects of material and energy metabolism. METHODS: According to random number table method,twenty-four specific pathogen free SD male rats were divided into four groups: control group,low dose group,middle dose group and high dose group with the given dose of 0,500,1 000 and1 500 mg / kg of body mass,respectively. After giving DBP of gavage once a day for two weeks,the plasma samples were obtained,and ~1H NMR spectra was recorded. The plasma metabonomic profiles were analyzed using pattern recognition.Difference metabolites were screened by principal components analysis,partial least squares-discriminate analysis and orthogonal partial least squares-discriminate analysis. Biomarkers was screened by variable importance in the projection norm. RESULTS: There were changes of twelve important metabolites in the plasma metabonomic profiles between DBP treatment groups and control group. The differences of metabolites had dose-effect relationship. Plasma levels of high density lipoprotein cholesterol, low density lipoprotein cholesterol, hydrobutyrate, glycoprotein, citric acid, glucose,creatine phosphate,unsaturated fatty acid,tyrosine and phenylalanine were reduced( P < 0. 05),while lactic acid and pyruvic acid were increased( P < 0. 05). CONCLUSION: DBP induces the metabolic disorders including amino acid metabolism,lipid metabolism and energy metabolism.
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Objective: To study the chemical constituents in Sappan Lignum (the core material of Caesalpinia sappan). Methods: The chemical constituents of Sappan Lignum were isolated by different column chromatographic techniques, including silica gel and Sephadex LH-20 columns. The structures of these compounds were identified by a comprehensive analysis on the spectroscopic data. Results: Fifteen compounds were isolated from the EtOAc extract of Sappan Lignum. The compounds were identified as protosappanin A (1), 3,7-dihydroxychroman-4-one (2), 7,3',4'-trihydroxy-3-benzyl-2H-chromene (3), bonducellin (4), 3'-deoxysappanol (5), 3'-deoxy-4-O-methylepisappanol (6), 3-deoxysappanchalcone (7), 3,8,9-thihydroxy-6H-benzo[c] chromen- 6-one (8), 3,9-dihydroxy-8-methoxydibenzo [b, d] pyran-6-one (9), (-)-syringaresinol (10), dibutyl phthalate (11), β-sitosterol (12), β-daucosterol (13), stigmasterol (14), and 1-heneicosanol (15). Conclusion: Compounds 9, 11, and 12 are first isolated from the plants of Caesalpinia Linn. and compound 4 is first isolated from this plant.
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Objective: To study the chemical constituents in fermented mycelium of endophytic fungus Arthrinium sp. A092 from Uvaria microcarpa. Methods: The compounds were isolated and purified by chromatography on silica gel, Sephadex-LH20 columns, HPLC, and so on. Their structures were identified on the basis of physicochemical properties and spectroscopic data. All compounds were tested for their cytotoxic activities against four tumor cell lines HepG-2, MCF-7, NCI-H460, and SF-268. Results: Ten compounds were isolated from the mycelial extract and identified as 3,4,5-trimethyl-6-methoxy-8-hydroxyisocoumarin (1), decarboxycitrinone (2), 4-hydroxy-17R-methylincisterol (3), 4-hydroxy-3-methoxybenzoic acid (4), dibutyl phthalate (5), flemingipanic acid (6), indole- 3-carboxy acid (7), ergosterol peroxide (8), p-hydroxybenzoic acid (9), and 4-hydroxybenzal-dehyde (10). Compounds 3 exhibited the inhibitory activity against SF-268 and MCF-7 with IC50 values of 63.8 and 57.2 μmol/L, respectively. Compounds 8 exhibited the inhibitory activity against SF-268, MCF-7, and NCI-H460 with IC50 values of 50.6, 32.3, and 39.0 μmol/L, respectively. Conclusion: Compound 1 is a new compound named arthrinisocoumarin A. Compounds 3-5 and 7-10 are isolated from the fungus of Arthrinium sp. for the first time. Compounds 3 and 8 show the moderated cytotoxic activities against SF-268, MCF-7, and NCI-H460.
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Objective: To optimize the matrix proportion of SIS hot melt pressure sensitive adhesive suit for hydrophilic material releasing. Methods: By orthogonal test method, taking adhesiveness and hydrophilic drug release rate as factors, and C5 petroleum resin hydrogenate, lanoline styrene-isoprene-styrene (SIS) triblock copolymer, ethyl acrylate-methyl methacrylate-trimethylamino (RLPO), liquid paraffin, dibutyl phthalate (DOP), polyethylene glycol (PEG) 400, and Antioxidant 1010 as materials, the matrix proportion was optimized. Results: The optimized formulation was as follows: SIS-C5 petroleum resin hydrogenate-SIS-RLPO-DOP-PEG 400-Antioxidant 1010 was 3:4:6:6:5:1:0.1. The adhesiveness was proper and shows more release rate for hydrophilic material. Conclusion: The SIS hot melt pressure sensitive adhesive shows good property and is suitable to prepare transdermal patch.
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Objective:To evaluate the effects of dibutyl phthalate on rat sperm production and quality. Methods:Totally 150 male rats were randomly divided into the low dose group (50 mg·kg-1), the middle dose group (200 mg·kg-1), the high dose group (1 000 mg·kg-1 ) , the blank control group and the solvent control group ( peanut oil as the control) with 30 ones in each. After continu-ous administration for every 30 days, 10 rats from each group were anatomized, the weight of testes and epididymides were determined, and one side of epididymis was used to carry out the sperm analysis including counting, survival rate and morphology. Results:After intragastric administration for 90 days, the sperm count and survival rate, the weight of testis and epididymis and organ coefficient in the middle dose group and high dose group were decreased significantly(P<0. 05 or 0. 01). Conclusion:The long-term administration of dibutyl phthalate at high dose exhibits notable toxicity on rat reproductive function.
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The objective of the present study was to evaluate the effect of different plasticizers on the ethylcellulose coatings of capsules and its timed release characteristics. Various plasticizers such as dibutyl phthalate (DBP), triacetin (TA), glycerol, triethyl citrate (TEC), polyethylene glycol-4000 and polyethylene glycol-6000 (PEG) were studied. The physicochemical properties of the casted polymeric films such as mechanical resistance, water uptake and dry weight loss were determined. Also the type and concentration of plasticizer on timed release of the capsule was studied. The drug release was found to be strongly dependent on the type of plasticizer and was in the order of GY>TA>PEG 6000>PEG 4000>TEC>DBP. Capsules coated with hydrophobic DBP (5%) showed good release with a lag time of 6 ± 0.5 h. DBP provided mechanically resistant coatings on the capsule and remained within the polymeric films without leaching upon exposure to the release media which helped in maintaining the lag time.
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Objective: To study the chemical constituents of Gastrodia elata. Methods: The constituents were isolated by various chromatographies, including preparative TLC, silica gel, Sephadex LH-20, and ODS columns, and their structures were elucidated on the basis of their physicochemical properties and spectral data. Results: Eleven compounds were isolated from 70% EtOH fraction eluted from resin column and their structures were identified as gastrodin (1), 4-hydroxybenzyl alcohol (2), 4-hydroxybenzoic acid (3), 4-hydroxybenzaldehyde (4), 4-hydroxybenz-yl methyl ether (5), parishin (6), 4-(methylsulfinylmethyl) phenol (7), dibutyl phthalate (8), dioctyl phthalate (9), 4, 4'-dihydroxydiphenyl methane (10), and grossamide (11). Conclusion: Compound 7 is a new natural product, and compounds 9 and 11 are isolated from the plants of Orchidacee for the first time.
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OBJECTIVES: Although phthalates like dibutyl phthalate (DBP) and di-2-ethylhexyl phthalate (DEHP) are commonly used as plasticizers and their metabolites are especially suspected of reproductive toxicity, little is known about occupational exposure to those phthalates. The aim of this study was to assess the utility of measuring the metabolite concentrations of DBP and DEHP in serum and urine samples as an indicator of occupational exposure to those phthalates. METHODS: Phthalate metabolites were analyzed by using column-switching high-performance liquid chromatography tandem mass spectrometry (LC-MS/MS). RESULTS: We detected phthalate metabolites in serum and urine matrices at approximately 10-fold lower than the limit of detection of those metabolites in the same matrix by LC-MS/MS without column switching, which was sufficient to evaluate concentrations of phthalate metabolites for industrial workers and the general population. CONCLUSION: The accuracy and precision of the analytical method indicate that urinary metabolite determination can be a more acceptable biomarker for studying phthalate exposure and adverse health outcomes.
Subject(s)
Humans , Biomarkers , Chromatography, Liquid , Dibutyl Phthalate , Diethylhexyl Phthalate , Limit of Detection , Occupational Exposure , Phthalic Acids , Plasticizers , Plastics , Tandem Mass SpectrometryABSTRACT
Objective To develop a method for the determination of DBP and DEHP in cosmetics by GC-MS. Methods The samples was extracted by methanol or acetic ether, DBP and DEHP were separated by GC and determined by MS. Results The linear range, regression equation of calibration curve and correlation coefficient were 0.5-100.0 ?g/ml, y=2?106 x-2?106, 0.999 6 for DBP respectively and 5.5-110.0 ?g/ml, y=988 223 x-7?106, 0.995 9 for DEHP respectively. Based on threefold ratio of signal and noise, as the sample was 1.0 and 0.2 g respectively, the volume was 10.0 ml, the detection limits were 1.0 and 5.0 mg/kg respectively for both DBP and DEHP. The recovery rates were 90.8%-119.0% for DBP and 90.4%-115.3% for DEHP. Relative standard deviations were 4.8%-9.8% for DBP and 6.0%-8.6% for DEHP. Conclusion This method is sensitive, accurate and high reproducible, and was applicable to the determination of DBP and DEHP in the cosmetics.
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Toxic effects of ozone, 4-(N-methyl-N-nitrosamino)-1-(3- pyridyl)-1-butanone (NNK), and/or dibutyl phthalate (DBP) were examined through NF-kappaB, AP-1, Nrf2, and osteopontin (OPN) in lungs and livers of B6C3F1 mice. Electrophoretic mobility shift assay (EMSA) indicated that mice treated with combination of toxicants induced high NF-kappaB activities. Expression levels of p105, p65, and p50 proteins increased in all treated mice, whereas IkB activity was inhibited in NNK-, DBP-, and combination-treated ones. All treated mice except ozone-treated one showed high AP-1 binding activities. Expression levels of c-fos, c-jun, junB, jun D, Nrf2, and OPN proteins increased in all treated mice. Additive interactions were frequently noted from two-toxicant combination mice compared to ozone-treated one. These results indicate treatment of mixture of toxicants increased toxicity through NF-kappaB, AP-1, Nrf2, and OPN. Our data could be applied to the elucidation of mechanism as well as the risk assessment of mixture-induced toxicity.