To investigate hematopoiesis and cytogenetics changes in staff of interventional radiology.A total of 121 intervention radiation workers, 245 common radiation workers and 100 medical personnel (healthy control) without exposure to radiation were enrolled in the study. The peripheral lymphocyte chromosomal aberrations and micronucleus were detected, and the result of white blood cells examination was analyzed.Compared with common radiation group and healthy control group, decreases in white blood cells count, neutrophil ratio, and increase in lymphocyte ratio were observed in intervention radiation group (all<0.05). Intervention radiation group had higher chromosome aberration rate and micronuclear rate than common radiation group and healthy control group (all<0.05). Most common chromosome aberrations were dicentric chromosome, acentric ring, fragments and minute chromosome. Abnormal rates in chromosome aberration and micronucleus rates were increased with the rise of length of service, but no statistically significant difference was observed (>0.05).Long term exposure to ionizing radiation may lead to changes in the human hematopoietic system and cause human chromosome aberration, and the severity of such injuries may be associated with the dose of ionizing radiation.
Adult ; Chromosome Aberrations ; radiation effects ; Dose-Response Relationship, Radiation ; Female ; Hematopoiesis ; radiation effects ; Humans ; Leukocyte Count ; statistics & numerical data ; Leukocytes ; pathology ; radiation effects ; Lymphocytes ; pathology ; radiation effects ; ultrastructure ; Male ; Micronuclei, Chromosome-Defective ; radiation effects ; Occupational Exposure ; adverse effects ; Radiation Exposure ; adverse effects ; statistics & numerical data ; Radiation, Ionizing ; Radiologists ; statistics & numerical data ; Time Factors

OBJECTIVETo investigate the effect of CCM3 gene defection on lead induced cell genotoxicity in mouse embryonic fibroblasts.

METHODSC57 female mice were mated with CCM3 gene heterozygous male mice. E13.5 embryos were taken to isolate primary mouse embryonic fibroblasts. After genotyping, wild type and heterozygous cells were treated with different doses of lead acetate. Cell viability, genotoxicity and protein expression were detected by MTS assay, CB micronucleus method and Western blot, respectively.

RESULTSMouse embryonic fibroblasts with lead acetate treatment for 24 h, wild-type cells 100.00 µmol/L lead acetate-treated group (69.16±1.36) and the control group (100.00±2.33) compared to cells decreased by 30%, CCM3 heterozygous type cell 100.00 µmol/L lead acetate-treated group (87.16±5.50) and the control group (100.00±2.06) compared to cells decreased by 13%, the difference was statistically significant (F values were 98.59, 82.63, P<0.001). Lead acetate treatment after 48 h, wild-type cells 100.00 µmol/L lead acetate-treated group (51.99±5.62) and the control group (100.00±3.11) compared to cells decreased by 50%, heterozygous type cells 100.00 µmol/L lead acetate treatment group (66.33±4.06) and the control group (100.00±5.72) compared to cells decreased by 35%, the differences were statistically significant (F values were 82.63, 36.86, P < 0.001). The results of CBMN test showed that with increased dose, micronucleus cell rate of two genotypes showed an increasing trend, in the wild-type cells, the micronucleus cell rate (/1 000) for the control group, 29.6±2.2, 6.25 µmol/L dose group 47.3±6.6, 25 µmol/L dose group 55.5±9.1, 100.00 µmol/L dose group 66.8±3.5; heterozygous cells micronucleus cell rate (/1 000) for the control group, 35.3±5.6, 6.25 µmol/L dose of 50.0±8.3, 25.00 µmol/L dose group 57.0±8.5, 100.00 µmol/L dose group 58.8±2.1. Micronucleus cell rates (/1 000) were significant differences, in 100.00 µmol/L dose groups of two genotypes. Western blot results showed that wild-type cells CCM3 expression 100.00 µmol/L lead acetate-treated group (0.70±0.03) was 1.32 times higher than the control group (0.53±0.07), heterozygous cells CCM3 expression 100.00 µmol/L lead acetate-treated group (0.48±0.02) was 1.77 times higher than control group that of 0.27±0.04, there was statistically significant difference (F values were 14.77, 25.74, P < 0.001); wild-type cells γ-H2AX expression 100.00 µmol/L lead acetate-treated group (0.69±0.03) was 1.06 times higher than the control group (0.65±0.07), heterozygous cells γ-H2AX expression 100.00 µmol/L lead acetate-treated group (0.99±0.04) was 1.55 times higher than the control group CCM3 expression levels (0.64±0.06), there was statistically significant difference (wild-type cells: F = 7.08, P = 0.012, heterozygous type cell: F = 13.49, P = 0.002).

CONCLUSIONCCM3 gene may play a role in lead-induced genetic toxicity of mouse embryonic fibroblasts, CCM3 gene-lead interactions effects on mouse embryonic fibroblasts cell toxicity.

Animals ; Apoptosis Regulatory Proteins ; DNA Damage ; Embryo, Mammalian ; Female ; Fibroblasts ; Genotype ; Male ; Membrane Proteins ; Mice ; Mice, Inbred Strains ; Micronuclei, Chromosome-Defective ; Organometallic Compounds ; Proto-Oncogene Proteins

OBJECTIVETo explore the genotoxic effects of oral-exposed TiO2 nanoparticles on bone marrow cells in young rats.

METHODSTwenty-eight SD male young rats (4 weeks old) were randomly divided into 4 groups, which were exposed to TiO2 nanoparticles ((75 ± 15) nm, anatase) through intragastric administration at 0, 10, 50 and 200 mg/kg body weight (bw) every day for 30 days. The bone marrow cells were collected for micronuclei and γ-H2AX immunofluorescence analysis.

RESULTSThe percentage of γ-H2AX foci-positive cells (37.4 ± 10.0)% in the 50 mg/kg bw dose group were significantly higher than that in the control group (19.8 ± 3.1)% (t value was -17.59, P < 0.01). No significantly difference was found in polychromatic erythrocyte/normochromatic erythrocyte (PCE/NCE) ratio and PCE micronucleus rate between three experimental groups and control group.

CONCLUSIONTiO2 nanoparticles can increase the frequency of DNA double-strand breaks in bone marrow cells, but has no effect on micronucleus of bone marrow cells in young rats.

Animals ; Bone Marrow Cells ; DNA Damage ; Histones ; Male ; Micronuclei, Chromosome-Defective ; Nanoparticles ; Rats ; Titanium

OBJECTIVETo evaluate the effects of polymorphisms in XRCC1 and APE1 genes on vinyl chloride (VC)-induced chromosomal damage in peripheral lymphocytes.

METHODSIn this study, 317 workers occupationally exposed to VC were recruited from a factory in Shandong Province, China. The micronucleus (MN) frequency in peripheral lymphocytes was used as an indicator of chromosomal damage. Polymerase chain reaction-restriction fragment length polymorphism and created restriction site combined with restriction fragment length polymorphism were used to determine the five single nucleotide polymorphisms in XRCC1 and APE1 genes in the base excision repair pathway. The association of chromosomal damage with these polymorphisms and the haplotype of XRCC1 was analyzed using Poisson regression and PHASE 2.0.2.

RESULTSIt was found that among the VC-exposed workers, individuals with XRCC1 polymorphisms (-77C/T, Arg194Trp, Arg280His, and Arg399Gln) had a significantly higher MN frequency than those with homozygous wild-type genotypes, with frequency ratios (FR) as follows, respectively: FR = 1.21, 95%CI: 1.05∼1.39 (P < 0.05); FR = 1.14, 95%CI: 1.00∼1.38 (P < 0.05); FR = 1.26, 95%CI: 1.11∼1.44 (P < 0.05); FR = 1.23, 95%CI: 1.08∼1.46 (P < 0.05). APE1 Asp148Glu was found of no significant relationship with MN frequency. Haplotype analysis of XRCC1 demonstrated that the MN frequencies in subjects with CTAA/CTAA and CCAA/CTAA were significantly higher than that in those with TCGG/TCGG (FR = 1.19, 95%CI: 1.02∼1.32, P < 0.05; FR = 1.41, 95%CI: 1.02∼1.87, P < 0.05). Furthermore, association was found between accumulated exposure to VC and XRCC1 polymorphisms (-77C/T, Arg194Trp, Arg280His, and Arg399Gln) after adjustment for age, sex, drinking, and smoking.

CONCLUSIONVC can induce chromosomal damage even when the exposure level is lower than the national occupational health standard of China (PC-TWA: 10 mg/m(3)); the polymorphisms in XRCC1 and APE1 are associated with chromosomal damage induced by VC.

Adult ; DNA-(Apurinic or Apyrimidinic Site) Lyase ; genetics ; DNA-Binding Proteins ; genetics ; Female ; Haplotypes ; Humans ; Male ; Micronuclei, Chromosome-Defective ; Middle Aged ; Occupational Exposure ; adverse effects ; Polymorphism, Restriction Fragment Length ; Vinyl Chloride ; poisoning ; X-ray Repair Cross Complementing Protein 1 ; Young Adult

OBJECTIVEUsing the stable HSPA1A (HSP70-1) promoter-driven luciferase reporter HepG2 cells (HepG2/HSPA1A cells) to assess the overall toxicity of coke oven emissions.

METHODSThe stable HepG2/HSPA1A cells were treated with different concentrations of coke oven emissions (COEs) collected from the top, side, and bottom of a coke oven battery for 24 h. After the treatments, luciferase activity, cell viability, malondialdehyde (MDA) concentration, Olive tail moment, and micronuclei frequency were determined, respectively.

RESULTSThe bottom COEs induced significant increases (P < 0.01) in relative luciferase activity up to 1.4 times the control level at 0.15 µg/L. The low dose of side COEs (0.02 µg/L) led to a significant increase (P < 0.01) in relative luciferase activity that progressively increased to 2.1 times the control level at 65.4 µg/L. The top COEs produced a strong dose-dependent induction of relative luciferase activity up to over 5 times the control level at the highest concentration tested (202 µg/L). In HepG2/HSPA1A cells treated with the bottom COEs, relative luciferase activity was positively correlated with MDA concentration (r = 0.404, P < 0.05). For the three COEs samples, positive correlations were observed between relative luciferase activity and Olive tail moment and micronuclei frequency.

CONCLUSIONThe relative luciferase activity in HepG2/HSPA1A cells can sensitively reflect the overall toxicity of COEs. The stable HepG2/HSPA1A cells can be used for rapid screening of the overall toxicity of complex air pollutants in the workplace.

Coke ; toxicity ; Genes, Reporter ; HSP70 Heat-Shock Proteins ; genetics ; Hep G2 Cells ; Humans ; Luciferases ; genetics ; Malondialdehyde ; analysis ; Micronuclei, Chromosome-Defective ; Occupational Exposure ; Promoter Regions, Genetic ; Toxicity Tests

OBJECTIVETo study the protective effect of an extract of Guipi Pill () against radiation-induced damage.

METHODSA total of 100 Kunming mice were randomly divided into normal group, model group, positive drug group (treated with radioprotective agent "523", 5 mg/kg at 24 h before irradiation) and two treatment groups, with 20 mice in each group. The extract of water extraction-alcohol precipitation (WAP) from Guipi Pill were administered orally to the mice in the two treatment groups at the dose of 500 and 1,000 mg/kg, respectively, for 6 days prior to whole body radiation (8 Gy). Fifty mice with 10 in each group were used to observe the survival rate 30 days after radiation. The other 50 mice with 10 in each group were sacrificed on day 10 after radiation (6 Gy) in order to take blood, liver and unilateral femur.

RESULTSPretreatment prior to irradiation with WAP resulted in a significantly higher 30-day survival rate of mice after exposure to a potentially lethal dose of 8-Gy radiation. WAP could significantly increase the total white blood cell count and DNA content of bone marrow, and it also increased the activity of various antioxidant enzymes, such as superoxide dismutase, catalase, total antioxidant capacity and glutathione peroxidase in liver tissue of mice, which were reduced by radiation treatment. Maleic dialdehyde level and bone marrow micronucleus rate were significantly reduced by WAP, which were increased after 6-Gy radiation.

CONCLUSIONWAP of Guipi Pill could increase the 30-day survival rate and the antioxidant capacity as well as protect bone marrow in mice. WAP of Guipi Pill is an effective radioprotective agent.

Animals ; Antioxidants ; metabolism ; Bone Marrow ; pathology ; Chemical Precipitation ; DNA ; metabolism ; Drugs, Chinese Herbal ; therapeutic use ; Leukocyte Count ; Liver ; metabolism ; pathology ; radiation effects ; Male ; Mice ; Micronuclei, Chromosome-Defective ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Protective Agents ; pharmacology ; therapeutic use ; Radiation Injuries, Experimental ; blood ; drug therapy ; prevention & control ; Survival Analysis ; Water

OBJECTIVETo explore the relationship between the polymorphisms of DNA repair gene (XRCC1 194, 280 and 399) and the chromosomal damage induced by benzene.

METHODSThe chromosomal damage of the peripheral lymphocytes in 459 workers occupationally exposed to benzene and 88 non-exposed controls were detected with cytokinesis-block micronucleus (CBMN) assay. PCR-RFLP technique was used to measure polymorphisms in XRCC1 194, 280 and 399.

RESULTSIt was found that the MN frequency (2.12‰ ± 1.88‰) of the exposed group was significantly higher than that (1.19‰ ± 1.68‰) of the control group (P < 0.05), in the exposed group, the MN frequency (3.00‰ ± 2.76‰) of older workers (> 35 years) was significantly higher than that (2.02‰ ± 1.71‰) of younger workers (≤ 35 years) (P < 0.05). The effect of genetic polymorphisms of XRCC1 on CBMN was not found. The haplotypes AAA/BAA, AAB/AAB, ABA/ABA, ABB/ABB could associated with the increased frequencies of total micronucleus (P < 0.05).

CONCLUSIONBenzene exposure could result in chromosome damage. Age of workers and diplotypes of XRCC1 could associated with chromosomal damage induced by benzene.

Adult ; Benzene ; adverse effects ; DNA Damage ; drug effects ; genetics ; DNA-Binding Proteins ; genetics ; Humans ; Micronuclei, Chromosome-Defective ; Micronucleus Tests ; Occupational Exposure ; Polymorphism, Single Nucleotide ; X-ray Repair Cross Complementing Protein 1 ; Young Adult

OBJECTIVETo investigate cytotoxicity and genotoxicity of benzo(a)pyrene (B(a)P) by 16HBE-CYP1A1 cells which are human bronchial epithelial cell with CYP1A1 transformed.

METHODSExpression of CYP1A1 and mEH of cell models were tested by real-time quantitative polymerase chain reaction. Cells were treated with 0, 1, 5, 10 and 20 micromol/L B(a)P for 24 h. Adverse effects of B(a)P were tested by cytokinesis-block micronucleus (CBMN) cytome assays. Cytotoxicity was assessed by the nuclear division index (NDI), frequency of necrotic and apoptotic cells. Genetic damages were assessed by frequencies of CBMN, nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs).

RESULTSHigh levels of CYP1A1 and mEH were found in 16HBE-CYP1A1 cells (relative mRNA content was 7.8 x 10(-4) and 0.030 respectively). In 16HBE-CYP1A1 cells, NDI were decreased in 1, 5, 10 and 20 micromol/L B(a)P treated groups, 1.92 +/- 0.04, 1.71 +/- 0.01, 1.61 +/- 0.04, and 1.41 +/- 0.01, respectively; and lower than control group (2.08 +/- 0.03). Compared with control group ((82.67 +/- 6.66)%), the binucleated cells ratios were decreased, (76.33 +/- 3.51)%, (66.33 +/- 0.58)%, (51.67 +/- 1.53)% and (39.0 +/- 1.0)% respectively.Necrotic cells ratios were (1.93 +/- 0.42)%, (2.20 +/- 0.53)%, (8.07 +/- 0.90)% and (15.27 +/- 2.80)%, respectively, higher than control group ((0.47 +/- 0.11)%). The differences were significant (F values were 899.94, 303.33, 240.87, P < 0.01). Apoptotic cells were increased at lower groups and decreased to normal at higher groups treated by B(a)P. They were (1.20 +/- 0.53)%, (2.00 +/- 0.20)%, (1.47 +/- 0.12)%, (1.20 +/- 0.00)% and (1.20 +/- 0.00)%, respectively. Analysis on biomarkers of genetic damage, the significant dose-effect relationship were observed in NPBs and NBUDs (F values were 50.23, 121.09, P < 0.01, respectively). Frequencies of NPBs were (4.67 +/- 2.89) per thousand, (7.33 +/- 1.53) per thousand, (10.67 +/- 2.08) per thousand and (11.00 +/- 1.00) per thousand respectively. Frequencies of NBUDs were (2.33 +/- 0.58) per thousand, (4.00 +/- 1.00) per thousand, (5.00 +/- 1.00) per thousand, and (7.67 +/- 1.16) per thousand respectively. However, the dose-relationship of CBMN last only to 10 micromol/L B(a)P treated groups in 16HBE-CYP1A1 cells, and frequencies of CBMN were (8.33 +/- 3.21) per thousand, (14.67 +/- 1.15) per thousand, respectively. Frequency of CBMN was (16.67 +/- 2.88) per thousand in 20 micromol/L B(a)P treated group, lower than 10 micromol/L B(a)P treated group ((17.67 +/- 2.08) per thousand). In 16HBEV control cells, the cytotoxicity was found only in higher B(a)P treated groups and frequencies of CBMN, NPBs and NBUDs were increased also. While no significant differences were observed between 5, 10, 20 micromol/L B(a)P treated groups (they were (6.37 +/- 2.08) per thousand, (9.33 +/- 1.52) per thousand, (9.33 +/- 3.21) per thousand; (4.33 +/- 1.53) per thousand, (6.00 +/- 2.65) per thousand, (5.33 +/- 1.53) per thousand and (2.33 +/- 0.58) per thousand, (3.33 +/- 1.16) per thousand, (3.67 +/- 1.16) per thousand, respectively).

CONCLUSIONSThe genetic damages were more severe after treated with activated B(a)P, which may be induced by decreased NDI, increased necrotic cells and inhibition of apoptosis.

Apoptosis ; drug effects ; Benzo(a)pyrene ; toxicity ; Cell Division ; drug effects ; Cell Line, Transformed ; DNA Damage ; Humans ; Micronuclei, Chromosome-Defective

Adult ; Chromosome Aberrations ; drug effects ; Ethylene Oxide ; poisoning ; Humans ; Lymphocytes ; drug effects ; pathology ; Male ; Micronuclei, Chromosome-Defective ; drug effects

OBJECTIVETo explore a flow cytometry (FCM)-based method for discriminating aneugen- or clastogen-induced micronuclei.

METHODSCells were stained with anti-CD71-FITC and PI, and the PI fluorescent signal intensity of micronucleated reticulocyte (MN-RET) in the peripheral blood of NIH mouse treated with COL or CP was detected by flow cytometry.

RESULTSThe ratio of the median of the intensity of MN-RET fluorescent signals to that of nucleated cell was low in the cyclophosphamide treated mouse, while the median was high in the colchicine treated mouse.

CONCLUSIONThe flow cytometry-based micronucleus assay can be used to discriminate primarily smaller MN induced by the clastogen exposure from the larger MN induced by an aneugen.

Animals ; Colchicine ; toxicity ; Cyclophosphamide ; toxicity ; Flow Cytometry ; methods ; Male ; Mice ; Micronuclei, Chromosome-Defective ; Mutagens ; toxicity ; Reticulocytes ; drug effects ; ultrastructure