OBJECTIVETo investigate the effects of carbon disulfide (CS(2)) inhalation on the lipid levels of ApoE knockout gene mice and C57BL/6J mice.

METHODSFifty-one male ApoE gene knockout mice were randomly divided into four groups: CS(2)-exposed normal diet group, CS(2)-unexposed normal diet group, CS(2)-exposed high-fat diet group, and CS(2)-unexposed high-fat diet group. Fifty male C57BL/6J mice were divided into four groups in the same way. The exposed groups received 1000 mg/m3 CS(2) by static inhalation (5h/d, 5d/w) for four weeks. The weight of each mouse was determined and recorded once a week. On the 14th day of exposure, six mice in each group were randomly selected to measure serum total cholesterol (TC) levels. On the 28th day of exposure, the serum levels of TC and low-density lipoprotein (LDL) in the remaining mice were measured.

RESULTSThe mean weight gain of exposed groups was less than that of the unexposed groups. On the 14th and 28th days of experiment, the TC levels of the CS2-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P < 0.01 for both). On the 14th day of experiment, the TC levels of the CS(2)-unexposed high-fat diet group were significantly higher than those of the CS(2)-unexposed normal-diet group among C57BL/6J mice group (P < 0.05). On the 28th day of experiment, the LDL levels of the CS(2)-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P = 0.003).

CONCLUSIONCS(2) exposure, high-fat diet, and ApoE gene knockout can elevate blood lipids in mice, thus increasing the risk of atherosclerosis.

Administration, Inhalation ; Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; Body Weight ; Carbon Disulfide ; toxicity ; Diet, High-Fat ; adverse effects ; Gene Knockout Techniques ; Lipid Metabolism ; drug effects ; Lipids ; blood ; Lipoproteins, LDL ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout

OBJECTIVETo study the influences of carbon disulfide (CS2) exposure on fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice.

METHODSTwenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m(3)) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy.

RESULTSThere were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.045 0). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.045 2). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.044 7).

CONCLUSIONExposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.

Administration, Inhalation ; Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; Carbon Disulfide ; toxicity ; Diet, High-Fat ; Fatty Acids ; chemistry ; Lipid Metabolism ; drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout

OBJECTIVETo investigate atmospheric mercury concentration in the workplace and urinary mercury concentration in workers exposed to mercury in a thermometer factory, and to determine the levels and influencing factors of urinary Β₂-microglobulin (Β₂-MG) and retinol-binding protein (RBP) in these workers.

METHODSAn occupational health survey of the workplace was completed according to relevant national occupational health standards. Questionnaire survey and occupational health examination were conducted in 178 workers exposed to mercury in the factory. Statistical analysis was accomplished using SPSS 19.0.

RESULTSIn the workplace, atmospheric mercury concentration was out of limits at seven of eight detection points expressed by short-term exposure limit; it was out of limits at all the eight detection points shown by time-weighted average. Statistically significant difference in atmospheric mercury concentration was found among different detection points (F = 138.714, P < 0.001). The geometric mean of urinary mercury concentration measured in 154 workers was 171.607 µg/g. There were 127 workers with urinary mercury concentration exceeding the standard (82.5% over-standard rate). Significant difference in urinary mercury concentration was shown in the workers among different positions (χ² = 44.531, P < 0.01). Urinary mercury concentration was positively correlated with atmospheric mercury concentration (r = 0.624, P < 0.01). The mean urinary Β₂-MG level measured in 148 workers was 0.142 mg/L, and seven workers had urinary Β₂-MG levels greater than 0.3 mg/L (4.7% abnormal rate). The mean urinary RBP level measured in 153 workers was 0.485 mg/L, and 19 workers had urinary RBP levels greater than 0.7 mg/L (12.4% abnormal rate). Ordinal logistic regression showed that age >34 years (OR = 4.88, 95%CI: 2.24∼10.62) and length of service >15 years (OR = 2.50, 95%CI: 1.06-5.92) were risk factors for increased urinary Β₂-MG level. Age >45 years (OR = 7.52, 95%CI: 2.50∼22.65) was a risk factor for increased urinary RBP level.

CONCLUSIONIn the thermometer factory under study, atmospheric and urinary mercury concentrations both seriously exceeded the standards, which were harmful to the health of workers. High atmospheric mercury concentration, old age, and long length of service were risk factors for increased urinary Β₂-MG and RBP levels in workers exposed to mercury.

Adult ; Environmental Exposure ; Humans ; Kidney ; drug effects ; Kidney Diseases ; chemically induced ; Mercury ; analysis ; toxicity ; Occupational Exposure ; Risk Factors ; Threshold Limit Values ; Time Factors ; Workplace

OBJECTIVETo find out and analyze differentially expressed miRNAs in the plasma of benzene exposed workers, and explore the potential roles of plasma miRNAs in the development of hematologic toxicity induced by benzene exposure.

METHODSBy individual matching, low blood cell group, unstable blood cell group and normal group of 10 benzene exposed workers in each group were taken as subjects. Microarray was used to find out differentially expressed miRNAs among three groups. Three miRNAs validated by real-time quantitative PCR. Target genes of 9 miRNAs with the high abundance and significant difference were predicted using Target scan, Picture and miRanda softwares. David 6.7 online platform was used to perform GO term enrichment and KEGG pathway analysis of those targets.

RESULTSMicroarray screened out that 138 miRNAs were differentially expressed. Three significant classes of differentially expressed miRNAs were found with the cluster analysis. The detected expressions of miR-638, let-7f-5p and miR-223-3p by relative RT-qPCR was consistent with the microarray date. Pathway analysis showed that the most enriched pathway was focal adhesion, with 6 potential functional targets, including SOS₂, VCL, CCND2, COL4A6, IGF1 and MAPK1.

CONCLUSIONWe have identified the plasma miRNA profile in benzene exposed workers, and further analysis indicates that focal adhesion-associated miRNAs play a potential role in hematologic toxicity induced by benzene exposure.

Adult ; Benzene ; adverse effects ; Female ; Humans ; Male ; MicroRNAs ; genetics ; Middle Aged ; Occupational Exposure ; adverse effects ; Oligonucleotide Array Sequence Analysis ; Young Adult