[Effect of carbon disulfide exposure on fatty acid metabolism in ApoE knockout and C57BL/6J mice].

OBJECTIVE: To study the influences of carbon disulfide (CS2) exposure on fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice. METHODS: Twenty-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. RESULTS: There 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). CONCLUSION: Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.

[Screening and analysis of plasma microRNA profile in benzene exposed workers].

OBJECTIVE: To 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. METHODS: By 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. RESULTS: Microarray 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. CONCLUSION: We 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.

[Effects of carbon disulfide inhalation on lipid levels of ApoE gene knockout mice and C57BL/6J mice].

OBJECTIVE: To investigate the effects of carbon disulfide (CS(2)) inhalation on the lipid levels of ApoE knockout gene mice and C57BL/6J mice. METHODS: Fifty-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. RESULTS: The 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). CONCLUSION: CS(2) exposure, high-fat diet, and ApoE gene knockout can elevate blood lipids in mice, thus increasing the risk of atherosclerosis.

[Early changes in renal injury parameters and their influencing factors in workers exposed to mercury].

OBJECTIVE: To 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. METHODS: An 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. RESULTS: In 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. CONCLUSION: In 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.

[Association between single nucleotide polymorphisms of PON2 gene and susceptibility to occupational noise-induced deafness among Chinese Han population exposed to high noise levels].

OBJECTIVE: To investigate the association between the single nucleotide polymorphisms (SNPs) of paraoxonase-2 (PON2) gene and the susceptibility to occupational noise-induced deafness among Chinese Han population exposed to high noise levels [>85 dB (A)]. METHODS: A case-control study was conducted in Chinese Han population exposed to high noise levels. The subjects were divided into case group (n = 127) and control group (n = 136) according to the Diagnostic criteria of occupational noise-induced deafness (GBZ 49-2007). The case group was composed of 127 workers with a mean binaural high-frequency hearing threshold not less than 40 dB, as measured using an electro-audiometer, while the control group was composed of 136 workers with a mean binaural high-frequency hearing threshold less than 40 dB, as measured using the electro-audiometer, who were on shift in the same position as the cases and matched with them for age, sex, and years of noise exposure. Peripheral venous blood (2 ml) was collected from each subject during physical examination to extract genomic DNA, and genotypes were identified using a TaqMan probe. RESULTS: PON2 genotypes rs7493 CG+GG, rs7785846 CT+TT, rs12026 CG+GG, and rs7786401 GT+TT were the risk factors for occupational noise-induced deafness, and the adjusted odds ratios (95%confidence intervals) were 5.87 (3.11∼11.07), 5.92 (3.10∼11.32), 5.53 (2.93∼10.45), and 5.93 (3.10∼11.34), respectively. In addition, the higher the noise exposure levels, the higher the risk of developing occupational noise-induced deafness among the individuals carrying mutant genotypes. CONCLUSION: PON2 genotypes rs7493 CG+GG, rs7785846 CT+TT, rs12026 CG+GG, and rs7786401 GT +TT may be associated with the susceptibility to occupational noise-induced deafness among Chinese Han population exposed to high noise levels, and the effects of mutant genotypes and noise exposure levels may be mutually enhanced.

PON2 and ATP2B2 gene polymorphisms with noise-induced hearing loss.

BACKGROUND: Noise-induced hearing loss (NIHL) is a complex disease induced by a combination of genetic and environmental factors. Paraoxonase2 (PON2) gene involved in the regulation of reactive oxygen species, and affecting the vulnerability of cochlea to NIHL, and ATPase, calcium-transporting, plasma membrane 2 (ATP2B2) gene which encodes plasma membrane calcium-transporting ATPase isoform 2 (PMCA2) are the candidate genes relating to the attack of NIHL. In this study, we investigated whether ATP2B2 and PON2 polymorphisms were associated with NIHL in Chinese of Han nationality population. METHODS: We performed a case-control study between six single nucleotide polymorphisms (SNPs) (rs1719571, rs3209637 and rs4327369 within ATP2B2, rs12026, rs7785846 and rs12704796 within PON2) and NIHL in 454 subjects. All the SNPs were genotypes, using the TaqMan MGB probe assay. Odds ratios (ORs) were calculated with 95% confidence intervals (95% CIs) with logistic regression analysis to test the level of association for SNPs. RESULTS: In our study, 221 subjects with hearing loss and 233 subjects without hearing loss were recruited. The frequencies of the CG and CG + GG genotype of rs12026 (PON2) conferred risk factors for NIHL with adjusted OR values of 2.62 (95% CI, 1.69-4.06) and 2.48 (95% CI, 1.63-3.78), respectively. This kind of significance was also found at locus rs7785846, where genotypes CT and CT + TT were the risk types, with adjusted ORs of 2.52 (95% CI, 1.62-3.93) and 2.35 (95% CI, 1.54-3.58), respectively. We performed stratified analysis per noise exposure level, when it came to rs7785846 and rs12026 in the >92 dB(A) noise exposure group, the subjects who carried heterozygote were of significantly (P<0.01) higher susceptibility to NIHL than homozygote carriers. By contrast, no significantly higher risk was found for any rs12704796 genotypes or any genotypes in ATP2B2 (P>0.05), which may suggest that these SNPs did not have significant effects on noise susceptibility across noise exposure. CONCLUSIONS: Our research suggested that PON2 might play a role in the etiology of NIHL in Chinese of Han nationality population.

A functional Ser326Cys polymorphism in hOGG1 is associated with noise-induced hearing loss in a Chinese population.

DNA damage to cochlear hair cells caused by 8-oxoguanine (8-oxoG) is essential for the development of noise-induced hearing loss (NIHL). Human 8-oxoG DNA glycosylase1 (hOGG1) is a key enzyme in the base excision repair (BER) pathway that eliminates 8-oxoG. Many epidemiological and functional studies have suggested that the hOGG1 Ser326Cys polymorphism (rs1052133) is associated with many diseases. The purpose of this investigation was to investigate whether the hOGG1 Ser326Cys polymorphism in the human BER pathway is associated with genetic susceptibility to NIHL in a Chinese population. This polymorphism was genotyped among 612 workers with NIHL and 615 workers with normal hearing. We found that individuals with the hOGG1 Cys/Cys genotype had a statistically significantly increased risk of NIHL compared with those who carried the hOGG1 Ser/Ser genotype (adjusted OR=1.59, 95% CI=1.13-2.25) and this increased risk was more pronounced among the workers in the 15- to 25- and >25-year noise exposure time, 85-92 dB(A) noise exposure level, ever smoking, and ever drinking groups, similar effects were also observed in a recessive model. In summary, our data suggested that the hOGG1 Cys/Cys genotype may be a genetic susceptibility marker for NIHL in the Chinese Han population.

Association between paraoxonase 2 gene polymorphisms and noise-induced hearing loss in the Chinese population.

OBJECTIVES: The aim of the present study was to investigate whether PON2 gene polymorphisms (rs7493, rs12026, rs12704796, rs7785846 and rs7786401) are associated with susceptibility to noise-induced hearing loss (NIHL) in the Chinese population. METHODS: A case-control study was conducted using 615 cases selected without any restriction in age or sex and 644 controls who were matched with the cases in terms of age, gender and the intensity and duration of exposure to noise. Information on these subjects was gathered by questionnaires that were administered through face-to-face interviews by trained interviewers. RESULTS: We found that the rs7493 CG + GG genotype (OR=1.36, 95% CI, 1.08-1.72), rs12026 CG + GG genotype (OR=1.34, 95% CI, 1.06-1.70), rs7785846 CT + TT genotype (OR=1.36, 95% CI, 1.07-1.71) and rs7786401 GT + TT genotype (OR=1.33, 95% CI, 1.05-1.68) were risk factors for NIHL. CONCLUSIONS: PON2 gene polymorphisms may be associated with susceptibility to NIHL in the Chinese population

On-line coupling of sequential injection lab-on-valve to differential pulse anodic stripping voltammetry for determination of Pb in water samples.

Sequential injection lab-on-valve (LOV) was first proposed for analyzing ultra-trace amounts of Pb using differential pulse anodic stripping voltammetry (DPASV) with a miniaturized electrochemical flow cell fabricated in the LOV unit. Deposition and stripping processes took place between the renewable mercury film carbon paste electrode and sample solution, the peak current was employed as the basis of quantification. The mercury film displayed a long-term stability and reproducibility for at least 50 cycles before next renewal, the properties of integrated miniature LOV unit not only enhanced the automation of the analysis procedure but also declined sample/reagent consumption. Potential factors that affect the present procedure were investigated in detail, i.e., deposition potential, deposition time, electrode renewable procedure and the volume of sample solution. The practical applicability of the present procedure was demonstrated by determination of Pb in environmental water samples.