DNA Damage ; drug effects ; Formaldehyde ; toxicity ; Mutagenicity Tests

Animals ; Coal Tar ; toxicity ; Comet Assay ; DNA Damage ; drug effects ; Mice ; NIH 3T3 Cells ; drug effects

Animals ; Comet Assay ; DNA Damage ; drug effects ; Lymphocytes ; drug effects ; Male ; Organometallic Compounds ; toxicity ; Rats

OBJECTIVETo detect the DNA damage of the nurses occupationally exposed to anticancer drugs and to assess the exposure level using Comet assay.

METHODSSixteen nurses occupationally exposed to anticancer drugs were selected as exposure group, the average exposure period was 5.6 years, and the average exposure dose was to prepare 7.8 portions of anticancer drugs daily. Meanwhile, sixteen nurse students were selected as control group. The DNA migration of the peripheral lymphocytes of both groups was detected using comet assay.

RESULTSThe comet length was 46.27 microns in exposure group, which was significantly higher than that of control group (26.78 microns, P < 0.01). Also the percentage of long tailed nucleus (LTN) of exposure group was 64.83%, which was significantly higher than that of control group (4.87%, P < 0.01).

CONCLUSIONSThere was DNA damage in the nurses occupationally exposed to antineoplastic drugs.

Antineoplastic Agents ; adverse effects ; DNA Damage ; Humans ; Lymphocytes ; drug effects ; Nurses ; Occupational Exposure ; adverse effects

OBJECTIVETo investigate the effects of hydroquinone (HQ) on expression of Polymerase eta (Pol eta) and DNA damage in human hepatic cells (L-02), and to explore the role and possible mechanism of Pol eta involved in the process of DNA damage-tolerance.

METHODSAfter L-02 hepatic cells were exposed to HQ with various concentrations (0, 5, 10, 20, 40, 80 and 160 micromol/L) for 24 h, cell survival rate was detected by MTT assay; DNA impairment was detected by single cell gel electrophoresis (SCGE); Real-time fluorescent quantitative PCR and Western blotting methods were used to measure the expression of Pol eta at the mRNA and protein level in L-02 hepatic cells exposed to HQ with various concentrations (0, 5, 10, 20, 40, 80 and 160 micromol/L).

RESULTSMTT assay showed that HQ with concentrations from 0 to 80 micromol/L had little effect on the survival rate of L-02 (P>0.05); whereas the survival rate of the group of 160 micromol/Lwas significantly higher than that of the control (P<0.01) after being treated with HQ for 24 h; the higher dose of HQ presented, the more degrees of DNA damage were produced. It was found that HQ in a low concentration (1-80 micromol/L) could induce the expression of Pol eta which was in proportion to the increasements of HQ concentration; the expression levels of mRNA and protein were reached to the maximum when treated with 80 micromol/L; the expression of Pol eta decreased (the relative quantity values were 2.32 +/- 0.16 and 1.20 respectively) once the concentration of HQ exceeded 160 micromol/L as compared with the group of 80 micromol/L, but it was higher than that of the control.

CONCLUSIONThis study suggested that Pol eta might involve in the process of DNA damage-tolerance induced by HQ in the hepatic cells.

Cell Survival ; drug effects ; Cells, Cultured ; DNA Damage ; drug effects ; DNA Repair ; DNA-Directed DNA Polymerase ; metabolism ; Hepatocytes ; drug effects ; metabolism ; Humans ; Hydroquinones ; adverse effects ; Mutagens

OBJECTIVETo study DNA damage of workers occupationally exposed to lead with flow cytometer assay.

METHODSThe lymphocytes were obtained from 41 workers occupationally exposed to lead (comparable group) and another 50 from control group. Flow cytometer (FCM) assay was used to detect DNA damage.

RESULTSDNA damage rate and geometric mean fluorescence intensity in the comparable group were significantly higher than those in the control group (P<0.05). There were no significant differences in the DNA damage and geometric mean fluorescence intensity between different age groups (P>0.05). The differences in correlation analysis between blood lead, urine lead, delta-ALA and DNA damage rate were not significant (P>0.05). The correlation analysis showed no statistical significance between concentration of blood lead, urine lead, delta-ALA and geometric mean fluorescence intensity (P>0.05). There was positive correlations not only between the high concentration of blood lead, delta-ALA and damage rate of DNA, but also between the high concentration of blood lead and geometric mean fluorescence intensity. The coefficient r showed statistical significance (P<0.05).

CONCLUSIONOccupational lead exposure can cause DNA damage. Gamma H2AX flow cytometer assay is a sensitive, objective and effective method for detection of DNA damage of peripheral blood lymphocytes.

DNA Damage ; drug effects ; Flow Cytometry ; Humans ; Lead ; adverse effects ; Lymphocytes ; drug effects ; Occupational Exposure ; adverse effects

Cells, Cultured ; Comet Assay ; DNA Damage ; drug effects ; Dose-Response Relationship, Drug ; Humans ; Lymphocytes ; drug effects ; Styrene ; adverse effects

OBJECTIVETo study the effect of polychlorinated biphenyl, Aroclor1254 on benzo (a) pyrene [B (a) P]-induced DNA damage in HepG2 cells.

METHODSHepG2 cells were pretreated with Aroclor1254 (11.5, 23 and 46 micromol/L) for 24 hours and then exposed to B (a) P (50 micromol/L). DMSO (10 ml/L) was used as solvent control. Single cell gel electrophoresis (SCGE) and high-performance liquid chromatography-electrochemical detection (HPLC-EC) assays were applied to detect DNA single-strand breaks and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in HepG2 cells, respectively.

RESULTSAverage Oliver tail moment (OTM) and 8-OHdG level in HepG2 cells were significantly increased in B (a) P treated group (1.66 +/- 0.21), (23.31 +/- 6.02) 8-OHdG/10(6)dG than that in solvent control (0.79 +/- 0.15), (12.31 +/- 3.24) 8-OHdG/10(6)dG, respectively. In Aroclor 1254 treated group (11.5, 23.0, 46.0 micromol/L), average OTM were 0.88 +/- 0.20, 1.01 +/- 0.15 and 1.10 +/- 0.16, and 8-OHdG levels were (19.57 +/- 7.57), (22.80 +/- 9.16) and (31.74 +/- 9.25) 8-OHdG/10(6)dG, respectively. A concentration of 46 micromol/L Aroclor1254 caused a significant increase of 8-OHdG level as compared with the solvent control. After pretreatment of HepG2 cells with Aroclor1254 (11.5, 23.0 and 46.0 micromol/L), B (a) P induced more DNA strand breaks (OTM: 2.14 +/- 0.22, 2.43 +/- 0.32 and 2.71 +/- 0.31) and 8-OHdG [(32.50 +/- 3.81), (49.23 +/- 16.66) and (60.36 +/- 18.04) 8-OHdG/10(6)dG] in HepG2 cells than B (a) P alone.

CONCLUSIONAroclor1254 might enhance B (a) P-induced DNA damage in HepG2 cells, which should imply a synergistic effect of Aroclor1254 on the genotoxicity of B (a) P.

Benzo(a)pyrene ; toxicity ; Cell Line, Tumor ; DNA Damage ; drug effects ; Drug Synergism ; Humans ; Polychlorinated Biphenyls ; toxicity

OBJECTIVETo study the effects of indium exposure on the relative content of mitochondrial ND1 gene in lymphocytes.

METHODSVenous blood was obtained from 14 healthy workers and anticoagulated with heparin. Blood lymphocytes were separated and divided into three tube cultures. For two tubes in the exposed group, indium chloride was added to final concentrations of 0.2 mmol/L and 0.8 mmol/L, respectively. For one tube in the control group, an equal volume of normal saline solution was added. After incubation for 72 h, the relative content of mitochondrial gene in each group was determined using quantitative real-time PCR.

RESULTSLymphocytes exposed to 0.8 mmol/L indium chloride had a significantly higher relative content of mitochondrial gene than those exposed to 0.2 mmol/L indium chloride and those in the control group (P < 0.05, P < 0.05).

CONCLUSIONLymphocytes exposed to a high concentration of indium and its compounds have an elevated relative content of mitochondrial ND1 gene, indicating increased oxidative DNA damage induced by exposure to a high concentration of indium and its compounds.

DNA Damage ; drug effects ; DNA, Mitochondrial ; genetics ; Humans ; Indium ; toxicity ; Lymphocytes ; drug effects ; NADH Dehydrogenase ; genetics ; Occupational Exposure

The defect or block of apoptosis is an important factor involved in the drug resistance of tumor cells. Blm gene plays a great role in DNA damage and repair. This study was aimed to explore the relationship of blm gene expression with cell cycle and apoptosis after Jurkat DNA damage. The apoptosis rate and change of cell cycle were detected by flow cytometry, the expression level of blm mRNA in Jurkat cells was determined by semi-quantitative RT-PCR. The results indicated that after induction with 0.4 g/L of mitomycin C (MMC) for 24 hours the apoptosis rate of Jurkat cells were (11.42±0.013)%, and (66.08±1.60)% Jurkat cells were arrested in G2/M phase. After induction for 48 hours, the apoptosis rate of Jurkat cells declined from (11.42±0.013)% to (8.08±0.27)%, and cell count of Jurkat cells arrested in G2/M phase decreased from (66.08±1.60)% to (33.96±1.05)%. When induced with 0.4 g/L of MMC for 24 hours, the apoptosis rate of fibroblasts and the percentage of fibroblasts in G2/M, G0-G1 and S phase all showed no significant change until 48 hours. The range of apoptosis rate and the change of cell percentage in three phases were significantly different between Jurkat cells and fibroblasts (p<0.01). Expression level of blm mRNA in Jurkat cells was remarkably higher than that in normal fibroblasts (p<0.01), at 48 hours expression level of blm mRNA was remarkably higher than that at 24 hours. The 2 groups showed clear difference of blm mRNA expression after treated by MMC (p<0.01). It is concluded that the blm gene may play a significant role in repair of DNA damage of Jurkat cells after MMC induction. Abnormal expression of blm is correlated to the drug resistance of leukemia cells.
Apoptosis ; Cell Cycle ; DNA Damage ; drug effects ; DNA Repair ; drug effects ; Humans ; Jurkat Cells ; Mitomycin ; pharmacology ; RecQ Helicases ; genetics