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OBJECTIVE: To investigate the hepatotoxicity induced by subchronic crotonaldehyde exposure in male rats and analyze its possible mechanism. METHODS: The specific pathogen-free male Wistar rats were randomly divided into control group, low-, medium-and high-dose crotonaldehyde groups, with 10 rats in each group. The crotonaldehyde solution at doses of 0.0, 2.5, 4.5, and 8.5 mg/kg body weight were given by intragastric administration, once a day, 5 days per week, and continuous for 90 days. The body weight of the rats were weighed during the exposure period. After the exposure, the liver organ coefficients and histopathological changes of the rats were observed. The activities of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) and the level of total bilirubin(TBIL) in the serum of rats were determined by colorimetry. The levels of malondialdehyde(MDA) and reduced glutathione(GSH), and the activities of glutathione peroxide(GSH-Px) and superoxide dismutase(SOD) were determined by colorimetry. The levels of interleukin(IL)-1β, IL-6, tumor necrosis factor alpha(TNF-α) and interferon-γ(IFN-γ) was detected by enzyme-linked immunosorbent assay. RESULTS: At the end of exposure, the increment of body mass of rats in the low-, medium-and high-dose crotonaldehyde groups was lower than that in the control group(P<0.05). The organ coefficients of rats in the middle-and high-dose groups were lower than that in the control group(P<0.05). The liver tissues of the three doses crotonaldehyde groups showed varying degrees of inflammatory cell infiltration. The activities of ALT, AST and the level of TBIL in the serum of rats increased with the increase of the crotonaldehyde exposure dose(P<0.01). With the increase of the crotonaldehyde dose, the level of MDA in rat liver tissue increased(P<0.01), and the level of GSH and the activities of GSH-Px and SOD decreased(P<0.01). The levels of IL-1β, IL-6, TNF-α and IFN-γ in rat liver tissues increased(P<0.05). CONCLUSION: Crotonaldehyde exposure can cause liver tissue damage in rats. Its mechanism of action may be related to the changes of oxidative balance and upregulation of the expression of inflammatory factors in liver tissue. These changes have the dose-effect relationship.
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OBJECTIVE: To observe the effect and mechanism of crotonaldehyde sub-chronic exposure-induced pyroptosis in pulmonary inflammatory reaction in male rats. METHODS: Specific pathogen-free male Wistar rats were randomly divided into control group and low-, medium-and high-dose groups, with 10 rats in each group. Rats were treated with crotonaldehyde at concentrations of 0.0, 2.5, 4.5, and 8.5 mg/kg body weight by intra-gastric administration, once per day for 120 consecutive days. Rats′ body mass was recorded during exposure. After exposure, the rats were sacrificed, and the lung tissues were isolated. The relative expression of reactive oxygen species(ROS) in lung tissues was detected by fluorescent probes at the end of crotonaldehyde exposure. The fluorescent staining of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3) and Caspase-1 in lung tissues was observed by immunofluorescence microscope. The protein expression of NLRP3, apoptosis-associated spot-like protein(ASC), Caspase-1 precursor(pro-Caspase-1), Caspase-1, interleukin(IL)-1β and IL-18 in lung tissues was determined by Western blotting. RESULTS: At the end of exposure, the body weight gain of rats decreased with the increasing doses of crotonaldehyde(P<0.01). Among them, the body weight gain in the medium-and high-dose groups was lower than that of the control group(P<0.05). After exposure, the lung tissue of each group showed severe inflammatory change with the increasing doses of crotonaldehyde. Immunofluorescence staining showed that the expression of NLRP3 and Caspase-1 in the lung tissues of rats increased in a dose-dependent manner. The relative expression of ROS and the protein of NLRP3, ASC, pro-Caspase-1, Caspase-1, IL-1β and IL-18 in lung tissue of each group increased with the dose of crotonaldehyde(P<0.01). The above indexes of lung tissue in the medium-and high-dose groups were higher than that in the control group(P<0.05). CONCLUSION: Sub-chronic exposure to crotonaldehyde may cause pyroptosis by up-regulating ROS expression in the lung tissues of rats. The up-regulation of Caspase-1 classic dependent pathway leads to pyroptosis, thereby causing inflammatory responses in the lungs.
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OBJECTIVE: To observe the conditions of sub-chronic crotonaldehyde exposure-induced pulmonary inflammation,oxidative stress and apoptosis in male rats,and to explore the related mechanisms. METHODS: The specific pathogen free Wistar male rats were randomly divided into control group,low-,medium-and high-dose crotonaldehyde groups,with 10 rats in each group. Rats were treated with crotonaldehyde at the concentrations of 0. 0,2. 5,4. 5 and 8. 5 mg/kg body weight by intra-gastric administration,once per day for 120 consecutive days. After the end of treatment,rats were sacrificed,the lungs were weighed and histopathological examination was performed. The levels of malondialdehyde( MDA),superoxide dismutase( SOD) and glutathione peroxidase( GSH-Px) in the serum of rats were determined by colorimetry. The relative expression of reactive oxygen species in lung tissues was detected by fluorescence probe. The apoptosis rate was detected by Tunel staining. The relative expression of B-cell lymphoma( Bcl)-2,Bcl-2 associated X protein( Bax) and cysteine aspartic acid protease-3( Caspase-3) proteins in lung tissue was detected by western blotting.RESULTS: The body weight of the rats in the high-dose group began to decrease after 30 days of exposure( P < 0. 05),and the body weight in the low-and medium-dose groups began to decrease at 90 days exposure( P < 0. 05),when compared with that of the control group at the same time. The body weight of the high-dose group was lower than that of the low-and medium-dose groups began to decrease at 90 days exposure( P < 0. 05). After exposure,the lung tissue of the three doses groups showed different degrees of inflammatory change in a dose-effect relationship. The level of serum MDA in rats increased with the treatment of crotonaldehyde( P < 0. 01). The activities of serum SOD and GSH-Px decreased with the treatment of crotonaldehyde( P < 0. 01). The relative expression of ROS and apoptosis rate in rat lung tissue increased with the treatment of crotonaldehyde( P < 0. 01). The relative expression of Bcl-2 protein and the ratio of Bcl-2/Bax in the lung tissue of rats decreased with the treatment of crotonaldehyde( P < 0. 01). The relative protein expression of Bax and Caspase-3 increased with the treatment of crotonaldehyde( P < 0. 01). CONCLUSION: Crotonaldehyde sub-chronic exposure can cause apoptosis in lung tissue by altering the oxidative balance,leading to inflammatory pathological changes in the lung.
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Objective@#To investigate the effect of subchronic exposure to crotonaldehyde on reproductive damage and oxidative stress in male rate.@*Methods@#Forty male SPF Wistar rats were randomly divided into four group: a control group and 3 exposure groups, 10 per group. The rats in each group were continuously administrated with crotonaldehyde (normal saline) for 1 time/d. For 128 d, the doses were 0.0, 2.5, 4.5, 8.5 mg/kg. After the end of the exposure, the body weight, the weight of the testis and epididymis was measured, and calculating organ coefficient. The left spermatozoon tail was used to determine sperm motility, number and testicular tissue marker enzyme activity : LDH, SDH, ACP, γ-GT; blood biochemical related index concentration: FSH, LH, T; oxidative stress-related indicator concentrations: MDA, SOD, GSH-Px and CAT.@*Results@#Compared with the control group, the weight gain, testicular and epididymis weight, and organ coefficient of the rats in the 4.5 and 8.5 mg/kg groups were decreased, the difference was statistically significant (P<0.05) . In the exposed group, the testicular tissue volume was reduced, the color was dark, and the number of germ cells in some seminiferous tubules was reduced. Compared with the control group, the sperm count and sperm motility of the 4.5 and 8.5 mg/kg groups were significantly lower (P<0.05) ; compared with the control group, 4.5 and 8.5 mg/kg. The activities of serum ACP, LDH, SDH and γ-GT in the exposed group were significantly lower (P<0.05) . Compared with the control group, the serum levels of T in the 8.5 mg/kg group were decreased. The levels of LH and FSH in the 4.5 and 8.5 mg/kg exposure groups were significantly lower (P<0.05) . Compared with the control group, the rats in the 4.5 mg/kg and 8.5 mg/kg exposure groups were compared. The activity of MDA in serum increased, SOD, GSH-Px and CAT activity decreased, the difference was statistically significant (P<0.05) .@*Conclusion@#Crotonaldehyde may cause subchronic reproductive damage and oxidative damage in rats by altering the hormone of the reproductive system, the expression of antioxidant enzymes, and destroying the oxidative balance of the rat.
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Objective@#To observe the lung injury of male rats induced by sub-chronic exposure to crotonaldehyde, and to explore the possible mechanism of injury.@*Methods@#Forty SPF male Wistar rats were randomly divided into control group and 3 groups in each group, and each group received 0.0, 2.5, 4.5, 8.5 mg/kg body weight crotonaldehyde solution for continuous intragastric administration. 120 d, once a day. After the end of the exposure, the body weight of the rats was measured, and the lung tissues were quickly separated after cervical dislocation. The organ coefficients were calculated and histopathological examination was performed to determine malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione. Peroxidase (GSH-Px) content; ELISA was used to measure interleukin (IL) -6, IL-1β, and tumor necrosis factor (TNF) -α in lung tissues.@*Results@#Compared with the control group, the weight gain of the rats in the 4.5 and 8.5 mg/kg exposure groups was small, and the lung weight and organ coefficient of the exposed group decreased, the difference was statistically significant (P<0.05). In the exposed group, the lung tissue structure was disordered, the alveolar wall was thickened, and inflammatory cell infiltration was observed. Compared with the control group, the MDA activity in the serum of the rats in the 4.5 mg/kg and 8.5 mg/kg groups increased, and the SOD and GSH-Px activities decreased, the difference was statistically significant (P<0.05). TNF-α levels in the lung tissues of rats exposed to 4.5 mg/kg and 8.5 mg/kg, and levels of (IL) -6 and IL-1β in the lungs of rats in the 2.5, 4.5, and 8.5 mg/kg groups. Significantly increased, the difference was statistically significant (P<0.05) .@*Conclusion@#Crotonaldehyde may induce inflammatory and oxidative stress damage in rats by up-regulating the expression of inflammatory factors in lung tissue and changing the oxidative balance.
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OBJECTIVE: To establish a method for detecting triphenyl phosphate( TPP) in the workplace air by gas chromatography. METHODS: TPP in the air of workplace was collected with glass fiber filter paper,desorbed with ether,separated by HP-5 gas chromatographic column,and detected by flame photometric detector. RESULTS: This method has good linear range of 12. 50-800. 00 mg/L,with the correlation coefficient of 0. 999 9. The detection limit was 0. 78 mg/L,and the minimum detectable concentration was 0. 09 mg/m3(sample volume was 45 L). Desorption efficiency was 97. 2%-99. 4%; standard recovery rate was 99. 5%-100. 3%. The within-run relative standard deviation( RSD) was 2. 7%-3. 4%and the between-run RSD was 1. 4%-3. 2%. The sampling efficiency was 99. 6%-100. 0%. The samples could be stored at room temperature for at least 14 days. CONCLUSION: The method is simple,accurate and highly sensitive for detecting TPP in workplace air.
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Objective@#To observe the effect of long term crotonaldehyde exposure on heart damage in male rats, and to explore the possible mechanism of toxic action.@*Methods@#24 specific pathogen free healthy male wistar rats were randomly divided into 4 groups with 6 rats in each group. Rats were treated with with 8.5, 4.5, 2.5 and 0.0 mg/kg body weight crotonaldehyde by gavage, once a day for consecutive 150 days. After the last treatment, they were anesthetized and collected blood samples by cardiac puncture. The heart was rapidly separated after cervical dislocation. The cardiac organ coefficient was calculated and the histopathology changes in heart were observed by HE staining. At the same time, the activities of creatine kinase (CK) , lactate dehydrogenase-L (LDH-L) in serum were determined by automatic biochemical analyzer. Moreover, the levels of cardiac troponin (cTnT) , Angiotensin Ⅱ (Ang Ⅱ) , Brain natriuretic peptide (BNP) , Aldosterone (ALD) and interleukin (IL) -6, 8, 1β, interferon (IFN) -γ and tumor necrosis factor (TNF) -α in heart were determined by enzyme linked immunosorbent assay.@*Results@#At the 90d, 120 d, and 150 d exposure, compared with the control group, the body weight gain in 4.5 and 8.5 mg/kg groups were decreased. Moreover, the heart weight in 4.5 and 8.5 mg/kg groups, and heart coefficient in 8.5 mg/kg group were decreased (P<0.05) . With the increasing dosage of crotonaldehyde, the degree of pathological changes in the heart of exposed rats were aggravated. The major pathological changes of heart in 4.5 and 8.5 mg/kg groups could be summarized as lymphocyte infiltration, abnormal cardiac muscle fiber arrangements, necrosis and fibrous connective tissue hyperplasia. Compared with the control group, the serum CK activity in 4.5 mg/kg group, CK and LDH-L activitivies in 8.5 mg/kg group were increased (P<0.05) ; Compared with the control group, the levels of ALD and ANGII in the heart of 4.5 and 8.5 mg/kg groups were increased, BNP level were decreased, and cTNT level in 8.5 mg/kg group were increased (P<0.05) . Compared with the control group, the levels of IL-1β、IL-6、IL-8 in 4.5 mg/kg group and IL-1β、IL-6、IL-8、TNF-α、IFN-γ in 8.5 mg/kg group were increased (P<0.05) .@*Conclusion@#Crotonaldehyde could up-regulate cardiac inflammatory cytokines and alter the balance ofangiotensin-aldosterone-brain natriuretic peptide causing heart damage.
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Objective@#To establish a method for the determination of diethyl phthalate by gas chromatography in the air of workplaces.@*Methods@#Diethyl phthalate in the air of workplace was collected throμgh glass fiber filter, eluted with methylbenzene, and detected by gas chromatography coupled with FID detectors.@*Results@#The linear range of diethyl phthalate determined by this method was 14.0~1 400 μg/ml, y=2.09801x-3.66229, and the coefficient correlation was 0.999 99. The detection limit was 1.10 μg/ml, and the minimum detection concentration was 0.18mg/m3 (collected sample volume was 30 L) . The within-run precisions were 1.04%~2.75%, and the between-run precisions were 0.34%~1.30%. The recovery rates were 98.72%~103.21%, and sampling efficiency was 97.2%~100.0%. The elution efficiencies were 97.25%~98.68%. The samples could be stored at room temperature for 15 days.@*Conclusion@#The indicators established in this study were conformed with the requirements of GBZ/T210.4-2008, "The Guidelines for the Development of Occupational Hygiene Standards Methods Part 4: Determination of Chemical Substances in the Air of Workplaces" . Diethyl phthalate in the workplace air could be rapidly collected, accurate separated and determinated. This method is applicable to the determination of diethyl phthalate in the workplace air.
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Objective@#To put forward the suggestion of the occupational contact limit of tributyl phosphate in the air of the workplace.@*Methods@#Data of production and usage, workers' basic information, occupational history, and physical examinations were collected, and the environmental and individual levels of exposure were monitored using fixed-point and individual sampling. The results of the questionnaire and health examination were statistically analyzed using exact probability method of Fisher in the workers exposed to tributyl phosphate and the control group.@*Results@#The results showed that tributyl phosphate was widely distributed in the workplace of production and using enterprises, and the concentration of tributyl phosphate in packaging area was highest at 2.47 mg/m3, and in feeder nose was highest at 2.13 mg/m3. The discomfort symptoms were classified and results showed that tributyl phosphate exposure group of 136 people, all symptoms of 128 people, accounting for 94.44% of the total, the remaining 5.56% of the staff report had psychiatric symptoms or lethargy and irritability skin itching, the control group had no symptoms. There is or not discomfort symptoms in the tributyl phosphate exposure group and the control group was compared with the exact probability of Fisher, and the difference was statistically significant (P<0.05) . The results of healthy physical examination of workers exposed to tributyl phosphate and control group were statistically analyzed by the exact probability method of Fisher. The results showed that there was no significant difference in the results of routine internal medical examination, nervous system examination, skin examination, five senses examination, blood routine, urine routine, lung ventilation, and X ray chest fluoroscopy between the tributyl phosphate exposure group and the control group (P<0.05) .@*Conclusion@#The workplace permissible time-weighted tributyl phosphate and short-term exposure limit concentrations in China were set at 2.5 mg/m3 and 5 mg/m3, respectively.
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Objective@#To observe the effect of crotonaldehyde long-term exposure on kidney injury in male rats, and to explore the specific mechanism of toxic action.@*Methods@#32 specific pathogen free healthy adult male wistar rats were randomly divided into 4 groups with 8 rats in each group: high-, moderate-, low-dose groups and a control group. Rats were treated with 8.5, 4.5, 2.5 and 0.0 mg/kg body weight crotonaldehyde by gavage, once a day for consecutive 128 days. After the last treatment, they were sacrificed and separated bilateral kidney. Kidney organ coefficients were calculated and the histopathology changes in kidney were observed by HE staining. The activities of malondialdehyde (MDA) , superoxide dismutase (SOD) , glutathion peroxidase (GSH-Px) and the levels of malaondialdehyde uric acid (UA) , urea nitrogen (BUN) , creatinine (CR) in serum were determined in the same time. Moreover, the levels of interleukin (IL) -6, 8, interferon (IFN) -γ and tumor necrosis factor (TNF) -α in kidney were determined by enzyme linked immunosorbent assay.@*Results@#Bilateral kidneys in the 8.5 mg/kg group were reduced in size and dark in color. Under the microscope, the major pathology changes of kidneys could be summarized as summarized as protein cast renal tubule, inflammatory cells and lymphocytes infiltration among kidney cortex. Compared with the control group, the weight gain of rats in 8.5 mg/kg group were smaller, and the weight and organ coefficient of kidney in each groups were significant decreased (P<0.05) . With the increasing dosage of crotonaldehyde, the serum BUN and UA levels in 8.5, 4.5 mg/kg groups, CR level in 8.5 mg/kg group were significant increased (P<0.05) .Compared with the control group, the serum MDA level in 8.5 mg/kg group was significant increased (P<0.05) . However, serum SOD activity in 8.5 mg/kg group and GSH-PX activity in 8.5, 4.5 mg/kg groups was significant decreased (P<0.05) . With the increasing dosage of crotonaldehyde, there are upward trend in the kidney IL-6, IL-8, TNF-α, IFN-γ, β-2 microglobulin levels. Compared with the control group, IL-6, TNF-α, IFN-γ, β-2microglobulin levels in 8.5, 4.5 mg/kg groups and IL-8 level in 8.5 mg/kg group in kidney were significant increased (P<0.05) .@*Conclusion@#Crotonaldehyde could develop the inflammatory factors levels and change the oxidation balance condition in the kidney of male rats, causing the inflammatory and oxidative injures of renal tissues.
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OBJECTIVE: To formulate a limit of occupational benzoquinone in the air of workplace. METHODS: According to GBZ/T 210. 1-2008 Guide for Establishing Occupational Health Standards--Part 1: Occupational Exposure Limits for Airborne Chemicals in the Workplace,the relevant literatures on toxicology,epidemiology and foreign occupational exposure limit for benzoquinone were collected and analyzed. A benzoquinone production enterprise was selected as the research subject. Occupational hygiene investigation and occupational epidemiological investigation were carried out. The occupational exposure limit of benzoquinone in the air of workplace was assessed. RESULTS: The literature data analysis results showed that benzoquinone is a highly toxic substance,has strong stimulated effect on human respiratory tract,eyes and skin. The occupational exposure limit of benzoquinone in the workplace air in the United States of America,Germany and Australian is 0. 400 mg/m~3. In the benzoquinone production enterprise,the median of concentration-time weighted average of benzoquinone exposed workers( exposure group) was 0. 100 mg/m~3. The median of concentration-short term exposure limit in the workplace air was 0. 160 mg/m~3. There was no significant difference on the abnormal detection rate of conjunctivitis,dermatitis,and abnormal liver B type and abnormal kidney B type ultrasound between the exposure group and the control group( P > 0. 05). There was no significant difference on the serum liver function and renal function indexes between the two groups( P > 0. 05). The results of blood routine examination in the two groups were within the normal reference range. CONCLUSION: It is suggested that the permissible concentration-time weighted average of benzoquinone in the workplace air should be set at 0. 400 mg/m~3 in China.
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OBJECTIVE: To observe the levels of four hydroxylated metabolites of polycyclic aromatic hydrocarbons(PAHs)in the urine of coke workers and its influencing factors.To explore the feasibility of using PAHs as biomarkers for exposure of coke oven emissions(COEs).METHODS: A cross-sectional survey was used to compare 261 coke oven workers in a coke oven plant as exposure group with 111 workers without COEs exposure in an oxygen making plant as control group.Ultra high liquid chromatography-mass spectrometry was used to detect four hydroxylated metabolites of PAHs,including1-hydroxypyrene(OHP),1-hydroxynaphthalene(OHN),2-OHN and 3-hydroxyphenanthrene,in urine of these two groups.RESULTS: The levels of four hydroxylated metabolites of PAHs in urine in exposure group were higher than that of the control group(P<0.01).The levels of urinary 1-OHP,1-OHN,2-OHN were followed by the sequence of bottomoven,side-oven,and top-oven subgroups among the exposure group(P<0.05).The multiple linear regression results indicated that the levels of urinary 1-OHP,1-OHN,2-OHN were correlated with COEs exposure(P<0.05),after adjusting the confounding factors of gender,age,length of service,smoking status and alcohol drinking status.The levels of urinary 1-OHP,1-OHN,2-OHN of the exposure group increased with the increase of COEs exposure levels showing a dose-effect relationship(P<0.01).The levels of 1-OHN and 2-OHN were associated with smoking apart from COEs exposure(P<0.01).CONCLUSION: The urinary 1-OHP can be used as a reliable biomarker for the evaluation of internal exposure to COEs.The 1-OHN and 2-OHN can be used as adjuvant biomarkers.
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Objective@#To establish a practical method forsampling and detectingtributyl phosphate intheworkplace.@*Methods@#The samples were extracted by glass fiber membrane, eluted with ether, separated by gas chromatography, and detected by flame photometric detector.@*Results@#There were good linear relationship in the minimum detection concentration was 7.2-720.0 μg/ml, and the correlation coefficient was 0.999 92. The detection limit was 0.86 μg/ml, and the minimum detection concentration was 0.14 mg/m3 (sample volume was 30 L) . Recovery rates were 99.8%-100.2%. The with-in relative standard deviations were 4.0%-5.4% and the between relative standard deviations were 2.0%-5.5%, and average samplingefficiency was about 99.1%-100.0%.@*Conclusion@#This method conforms with the requirements of "Standardization of Methods for Determination of Toxic Substance in Workplace" . Tributyl phosphate in air could be determined accurately using this method.
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Objective@#To explore the effect of occupational exposure to glyphosate on hepatorenal function.@*Methods@#526 workers who were occupationally exposed to glyphosate from 5 glyphosate-producing factories were selected as cases; and another 442 administrative staffs who were not exposed to glyphosate were selected as controls from April to November, 2014. All the subjects accepted occupational health examination. The concentration level of glyphosate in the air of workshop was detected and the time weighted average concentration (TWA) was calculated. And analyze the difference of hepatorenal fuction between case group and control group.@*Result@#The age of the subjects in the case and control groups were separately (35.6±10.3), (34.3±9.7) years old, with the length of working for (6.5±5.7), (7.7±6.8) years. The TWA of glyphosate in the case group was between <0.03-48.91 mg/m3, with the geometric mean at 3.78 mg/m3. The overall rates of abnormal hepatic and renal function in the case group were 14.4% (76 cases) and 16.2% (85 cases), respectively; while those were 5.0% (22 cases) and 4.8% (21 cases), respectively in control group, and the difference showed statistical significance (P<0.05). When TWA reached <0.03-6.00 mg/m3, the difference of hepatorenal fuction between case group and control group showed statistical significance, and the rates of abnormal hepatic and renal function was 8.0% (36/447) and 9.8% (44/447) respectively in case group. When cumulative exposure level reached <1.56-68.64 g, the difference of hepatorenal fuction between case group and control group showed statistical significance, and the rates increased to 9.2% (37/404) and 10.4% (42/404) respectively in group of cases.@*Conclusion@#Glyphosate can affect the hepatic and renal function among occupational exposure population, and there was an association between the effect and the exposure dose.
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<p><b>OBJECTIVE</b>To analyze the expression levels of heat shock protein70 (HSPs70) and HSPs70 mRNA in different exposure to manganese, and research the neuroprotective effect on the career exposure to manganese.</p><p><b>METHODS</b>From 2008 to 2009, with cross-sectional study design, and in a locomotive and rolling stock works, by stratified random sampling method, the exposed sample consisted of 180 welders from different welding shops and 100 unexposed in the last three years, non-welder controls with age-matched workers of similar socioeconomic status from the same industry. The control workers had not been exposed to neurotoxic chemicals. The mRNA expressions of four different metabolic enzyme were detected by SYBR Green I quantitative real-time polymerase chain reaction. The expression levels of the two enzymes mRNA in different exposure to manganese were analyzed. The expressions of HSPs70 were detected by Western blot. The concentration of air manganese was determined by GFAAS. The average concentration of 8 h time (8h-TWA) was used to express the level of individual exposure to manganese, according to the air manganese workplace occupational exposure limit (8h-TWA=0.15 mg/m3), the exposed group is divided into high exposed group (>0.15 mg/m3) and low exposure group (<0.15 mg/m3).</p><p><b>RESULTS</b>The individuals exposed to manganese dose of exposed group ((0.25±0.31) mg/m3) was higher than the control group ((0.06±0.02) mg/m3) (t=6.15, P=0.001); individuals exposed to manganese dose of high exposure group for (0.42±0.34) mg/m3, which was higher than low exposure group (0.09±0.07) mg/m3 (t=9.80, P=0.001). HSPs70 mRNA and protein of exposure group (5.65±0.21, 3.26±0.15) were higher than the reference group (0.41±0.03, 1.32±0.12) (t=18.91, t=8.68, P=0.001). HSP70 mRNA and protein of high exposure group (6.48±0.37, 3.67±0.26) were higher than the low exposure group (5.15±0.23, 3.02±0.19) (t=3.24, t=2.01, P=0.003, P=0.043).</p><p><b>CONCLUSION</b>The expression of peripheral blood lymphocytes HSPs70 level and HSPs70 mRNA workers exposed to manganese increased and protect nerve cells from related to Mn stimulation induced lipid peroxidation damag.</p>
Subject(s)
Humans , Cross-Sectional Studies , HSP70 Heat-Shock Proteins , Manganese , Occupational Exposure , RNA, Messenger , WeldingABSTRACT
Objective To establish an HPLC-FLD method for simultaneous determination of homovanillic acid(HVA) and vanilmandelic acid(VMA) in human urine.Methods After being filtered with 0.45 ?m membrane,the samples of urine were injected directly into an ODS column(250 mm?4.6 mm,5.0 ?m) at the room temperature.The samples of urine were carried with the mobile phase comprised of methanol-0.1mol/L phosphate buffered solution(20:80,V/V).The flow rate was 1 ml/min,the injection volume was 10 ?l,the detection was taken at ?ex=277 nm,?em=320 nm.Results The determination was finished in 15 min,the retention time was 3.18 min for VMA and 6.72 min for HVA respectively.The detection limit of HVA was 0.15 ?g/ml,the linear range was 0-25 ?g/ml,the recovery rates were between 84.53%-106.1%,the relative standard deviation(RSD)