Chinese herbal medicine for carriers of the hepatitis B virus: an updated systematic review and meta-analysis.

More than a third of the world's population is infected with the hepatitis B virus (HBV) and 5% are thought to be HBV carriers, putting them at risk of developing serious liver diseases. The treatment of liver diseases with Chinese herbal medicines (CHM) dates back 2,500 years and the aim of this analysis was to evaluate the efficacy and safety of CHM for HBV carriers compared to Western medicine (WM) or placebo and to summarize the most commonly used herbs. Several databases, such as Pubmed, Embase and the Chinese database CNKI, were used to evaluate randomized, controlled trials (RCTs) focused on CHM treatment for HBV carriers up to 2013. We performed a systematic review and meta-analysis on the herbs and their effect on hepatitis B viral proteins (HBeAg, HBsAg) and HBV DNA. Subgroups were examined based on the study design and pooled risk ratios (RRs) were estimated with 95% confidence intervals (CIs). For the meta-analysis, we focused on 11 out of 52 RCTs (Jadad ≥ 2) and found that CHM was more effective than placebo for HBeAg seroconversion when combined with WM (RR 4.67, 95% CI 1.36-15.98; P = 0.01; P = 39%); Radix Astragali was the most commonly used herb. Those that received CHM were more prone to adverse events; however, they were mild and reversible. The risk of bias was assessed with regards to blinding, incomplete outcome data and publication bias. It should be noted that, due to the poor methodological quality of the studies and the small number of RCTs, the results cannot fully support the use of CHM in the treatment of HBV carriers. To conclude, CHM may be used to treat HBV carriers, but rigorously designed RCTs with long-term follow-ups are required to further evaluate the benefits and safety of CHM.

Comparison of isocentric C-arm 3-dimensional navigation and conventional fluoroscopy for C1 lateral mass and C2 pedicle screw placement for atlantoaxial instability.

STUDY DESIGN: A retrospective study. OBJECTIVE: The aim of the study was to compare the precision of C1 lateral mass and C2 pedicle (C1LM-C2P) screw fixation for atlantoaxial instability using the isocentric C-arm 3-dimensional (Iso-C 3D) navigation versus conventional fluoroscopy. SUMMARY OF BACKGROUND DATA: The Iso-C 3D navigation has been widely used in spinal surgeries in recent years. The advantages of this navigation system compared with conventional fluoroscopy in C1LM-C2P screw fixation for atlantoaxial instability are not known. METHODS: Twenty-four patients diagnosed with atlantoaxial instability were treated with C1LM-C2P screw fixation in this study. The navigation group included 12 patients and the other 12 patients were in the conventional fluoroscopy group. The clinical and radiographic results were recorded and compared between the 2 groups. Patients were followed up with clinical examination and radiographs at a mean of 10.8 months. RESULTS: There were no significant differences between groups in the mean age, gender, and causes of atlantoaxial instability. Operative time was 130 ± 5.4 minutes in the navigation group versus 145 ± 6.5 minutes in the conventional fluoroscopy group. The mean blood loss in the navigation group was 304.2 ± 47.9 mL relative to 462.5 ± 55.4 mL in the conventional fluoroscopy group. The radiation time was significantly reduced using 3D navigation (47.5 ± 1.5 s vs. 64.0 ± 3.0 s). 95.8% (46/48) of 3D navigated screws and 83.3% (40/48) of fluoroscopy screws had no pedicle perforation. Each patient showed evidence of solid fusion after 6 months on cervical plain radiographies. CONCLUSION: On comparing the 2 imaging techniques, it was found that using Iso-C 3D navigation can significantly improve the accuracy of screw placement and decrease intraoperative fluoroscopic time and blood loss. This study demonstrates that Iso-C 3D navigation is a safe and effective means of guiding C1LM-C2P screw fixation for atlantoaxial instability.

Inhibition of hepatitis C virus replication by single and dual small interfering RNA using an HCV-infected cell model.

Dual siRNA against different regions of gene in hepatitis C virus (HCV) synergistically inhibited replication of HCV RNA. An HCV-infected cell model was established, and HCV RNA and core protein were detected by RT-PCR and Western blot, respectively. Four HCV-specific siRNAs (siCore, siNS3, siNS4B, siNS5B) were designed and transfected into HCV-infected Huh7.5.1 cells. The antiviral efficacies of the siRNAs were compared using real time PCR and agarose gel electrophoresis. HCV replication in infected cells was inhibited by IFNα-2b in a dose-dependent manner. Synergistic inhibition effects were achieved with combination treatment of any two of the siRNAs (siCore, siNS3 and siNS5B) at low doses (0.1 and 10 nM), as compared to single siRNA treatment (P < 0.05). Furthermore, CCK-8 assay showed no toxicity of the siRNAs to Huh7.5.1 cells. These findings indicate a promising new therapeutic approach for treatment of HCV.

An investigation of oxidative DNA damage in pharmacy technicians exposed to antineoplastic drugs in two Chinese hospitals using the urinary 8-OHdG assay.

OBJECTIVE: To investigate oxidative DNA damage in pharmacy technicians preparing antineoplastic drugs at the PIVAS (Pharmacy Intravenous Admixture Service) in two Chinese hospitals. METHODS: Urinary 8-OHdG served as a biomarker. 5-Fluorouracil (5-FU) concentrations in air, masks and gloves were determined. The spill exposure of each PIVAS technician to antineoplastic drugs was investigated. Eighty subjects were divided into exposed group I, II, and control group I, II. RESULTS: 5-FU concentration ratios for gloves and masks in exposed group I were significantly higher than those in exposed group II (P<0.05 or P<0.01). The average urinary 8-OHdG concentrations in exposed group I, control group I, exposed group II, and control group II were 14.69±0.93, 10.68±1.07, 10.57±0.55, and 11.96±0.73 ng/mg Cr, respectively. Urinary 8-OHdG concentration in exposed group I was significantly higher than that in control group I or that in exposed group II (P<0.01). There was a significant correlation between urinary 8-OHdG concentrations and spill frequencies per technician (P<0.01). CONCLUSION: There was detectable oxidative DNA damage in PIVAS technicians exposed to antineoplastic drugs. This oxidative DNA damage may be associated with their spill exposure experience and contamination of their personal protective equipment.

[Inhibition of hepatitis C virus replication by small interfering RNA in cells infected by HCV].

OBJECTIVE: To investigate the inhibitive effects of small interfering RNA (siRNA) on hepatitis C virus (HCV) replication in cells infected by HCV in vitro. METHODS: The HCV RNA transcripts prepared by pFL-JC1 were transfected into Huh-7.5.1 cells. Na ve Huh-7.5.1 cells were incubated with the supernatants of transfected cells and the expression of HCV core protein in infected cells was detected by indirect immunofluorescence. The infected cells were transfected with 4, 40 and 200 nmol/L of NS5B siRNA for 24 h, 48 h and 72 h, respectively. The normal Huh-7.5.1 cells were transfected with 4, 40 and 200 nmol/L of NS5B siRNA. Group of blank, lipofectamine 2000, unrelated siRNA and IFNα-2b (1000 IU/ml) served as controls. The HCV RNA and PKR mRNA levels were examined by quantitative RT-PCR. RESULTS: The HCV core protein in HCV infected cells was detected. Compared with control groups, the HCV RNA levels in infected cells significantly decreased when transfected with 40 and 200 nmol/L of siRNA for 24 h; 4, 40 and 200 nmol/L of siRNA for 48 h and 72 h (P<0.05). The HCV RNA levels in infected cells treated with IFNα-2b (1000 IU/ml) for 24 h, 48 h and 72 h were significantly lower than those in control groups (P<0.05 or P<0.01). The PKR mRNA levels in Huh-7.5.1 cells transfected with siRNA of three concentrations did not have significant difference, as compared with control groups (P>0.05). CONCLUSION: siRNA against HCV NS5B region can effectively inhibit HCV replication in HCV infected cells, but can not activate the dsRNA-dependent protein kinase (PKR).

[Analysis of new pneumoconiosis cases during 2006-2009 in Zhejiang province].

OBJECTIVE: To analyze the characteristics of pneumoconiosis cases in Zhejiang province and to provide the evidence for pneumoconiosis control and prevention measures in Zhejiang province. METHODS: The data of new pneumoconiosis cases were from national surveillance system of occupational disease in Zhejiang province during 2006-2009, and were analyzed for distribution, age, exposure duration, pneumoconiosis phases and enterprise types. RESULTS: During 2006-2009, 819 new pneumoconiosis cases (173, 157, 209 and 280 cases, respectively) were reported, 86.9% cases suffered from silicosis. Most of pneumoconiosis cases were distributed in Ningbo, Wenzhou areas and in building materials, machinery, coal, geological and mining, light industries and construction enterprise. The average ages of new pneumoconiosis cases were (47.8 +/- 10.0), (52.5 +/- 13.1), (55.5 +/- 11.2) and (55.9 +/- 12.2) years old, respectively and showed a significant increase trend (P<0.05). The average exposure duration of new pneumoconiosis cases were (12.4 +/- 8.6), (12.9 +/- 9.4), (12.4 +/- 8.6) and (15.7 +/- 10.0) years. The average exposure duration of phase I, phase II, phase III new pneumoconiosis cases were (14.3 +/- 9.87), (12.4 +/- 8.7) and (11.4 +/- 7.1) years, respectively and there were significant differences (P<0.05). CONCLUSION: New pneumoconiosis cases in Zhejiang province are increasing year by year, the main type of pneumoconiosis is silicosis, the distribution of pneumoconiosis cases is associated with the areas and enterprises, and the exposure duration of new pneumoconiosis cases is relatively shorter.

[Investigation on occupational exposure to 5-fluorouracil in pharmacy intravenous admixture service of a hospital].

OBJECTIVE: To investigate the level of occupational exposure to 5-fluorouracil (5-Fu) in the pharmacy intravenous admixture service (PIVAS) of a hospital, and identify the sources of 5-Fu contamination. METHODS: The 5-Fu concentrations in air, on the surface of different areas in PIVAS and personal protective equipments were detected using UV-vis spectrophotometry. RESULTS: The 5-Fu in air could not be detected. The 5-Fu concentrations on five different surfaces of biological safety cabinets were (22.00 +/- 6.35), (13.99 +/- 2.46), (14.13 +/- 0.72), (7.25 +/- 1.19) and (9.87 +/- 1.23) ng/cm2, respectively, which were significantly higher than those [(3.14 +/- 0.04), (5.43 +/- 0.65), (2.26 +/- 0.17), (2.26 +/- 0.17) and (3.63 +/- 0.46) ng/cm2] of corresponding controls (P < 0.05 or P < 0.01). The 5-Fu concentrations of the floor under cabinets [(18.19 +/- 5.22) ng/cm2], the floor in front of cabinets [(10.25 +/- 2.57)ng/cm2], the office floor [(11.64 +/- 2.53) ng/cm2], the terrace floor [(99.89 +/- 14.06 ) ng/cm2], the floor beside trash can in dressing room [(24.54 +/- 0.23) ng/cm2] were significantly higher than those of control [(3.36 +/- 0.11 ) ng/cm2] (P < 0.05 or P < 0.01). The 5-Fu concentrations of the tables in preparation room [(7.22 +/- l.04) ng/cm2] and the tables in office [(11.81 +/- 1.18) ng/cm2] were significantly higher than those of control [(5.56 +/- 0.14) ng/cm2] (P < 0.05 or P < 0.01). The 5-Fu concentrations of the indoor handle in preparation room were significantly higher than those of controls (P < 0.05 or P < 0.01). 5-Fu concentrations on the surfaces of outdoor handle and floor beside door in preparation room were not significantly increased compared with controls (P > 0.05). The 5-Fu concentrations on the surfaces of infusion bags, transfer box, transfer trays were significantly higher than those of controls (P < 0.05). The differences of 5-Fu concentrations between outer and inner masks and controls were not significant (P > 0.05). The 5-Fu concentrations of gloves of preparing and checking staffs were significantly higher than those of controls (P < 0.05 or P < 0.01). CONCLUSION: The preparing and checking process of 5-Fu and the treatment of medical wastes are major sources of 5-Fu contamination.

[Genotoxicity of organic bentonite particles in vitro].

OBJECTIVE: To study the genotoxicity induced by organic bentonite particles in vitro. METHODS: Human B lymphoblast cells (HMy2.CIR) were exposed to organic bentonite particles at the doses of 0, 1.88, 3.75, 7.50 and 15.00 µg/ml for 24, 48 and 72 h, calcium sulfate (30 µg/ml) and SiO2 (30 and 240 µg/ml) served as negative and positive controls, respectively. The genotoxicity of organic bentonite particles and soluble fraction was detected using comet assay and Cytokinesis-block micronucleus (CBMN) assay. RESULTS: The results of comet assay indicated that % tail DNA increased with the exposure doses and time in organic bentonite group, % tail DNA at the dose of 15.00 µg/ml for 24 h, 48 h and 72 h in organic bentonite group were 3.20 ± 0.19, 4.63 ± 0.88 and 9.49 ± 1.31 respectively which were significantly higher than those in calcium sulfate group (1.40 ± 0.11, 1.37 ± 0.22 and 0.90 ± 0.16) and those in 30 µg/ml SiO2 group (1.83 ± 0.21, 1.41 ± 0.27 and 2.48 ± 0.25) (P < 0.01). The results of CBMN assay showed that micronucleus frequencies (MNF) in organic bentonite group (except for 1.88 µg/ml for 24 h) were significantly higher than those in 30 µg/ml calcium sulfate group (MNF for 24, 48 and 72 h were 1.33‰ ± 0.58‰, 1.33‰ ± 1.15‰ and 1.33‰ ± 0.58‰) and those in 30 µg/ml SiO2 group (2.00‰ ± 0.00‰, 1.68‰ ± 0.58‰ and 2.33‰ ± 0.58‰) (P < 0.01). The results of two assays demonstrated that the soluble fraction of organic bentonite did not induce the genotoxicity. CONCLUSION: The organic bentonite dusts can induce the genotoxicity in vitro, which may be from the particle fraction.

[Comparative study of cytotoxicity induced by two kinds of bentonite particles in vitro].

OBJECTIVE: To study comparatively the cytotoxicity induced by acid bentonite and organic bentonite. METHODS: The cytotoxicity of two kinds of bentonite was detected using CCK8 assay, neutral red uptake (NRU) assay, lactate dehydrogenase (LDH) leakage assay, apoptosis assay and hemolysis assay. In hemolysis assay human erythrocytes served as target cells and were exposed to the two kinds of bentonite at the doses of 0, 0.3125, 0.6250, 1.2500 and 2.5000 mg/ml for ten min. In other four assays, human B lymphoblast cells (HMy2.CIR) served as target cells and were exposed to the two kinds of bentonite at the doses of 0, 10, 20, 30, 60, 120 and 180 microg/ml for four h. RESULTS: In hemolysis assay, the hemolysis rates induced by two kinds of bentonite at all doses were significantly higher than that of control (P<0.05); in CCK-8 assay, the cellular activities in acid bentonite group at the doses > or =30 microg/ml and in organic bentonite group at the doses > or =20 microg/ml were significantly lower than that of control (P<0.01); the similar results appeared in NRU assay and LDH assay, and the dose-effect relationship was observed in above 4 assays. In apoptosis assay, the early apoptosis cell rates in acid bentonite group at the dose of 180 microg/ml and in organic bentonite group at the doses of 120,180 microg/ml were significantly higher than that of control (P<0.05). Moreover, the results of five in vitro assays indicated the cytotoxicity induced by organic bentonite was higher than that induced by acid bentonite. CONCLUSION: Two kinds of bentonite could induce cytotoxicity, such as apoptosis and damage of cell membrane. The cytotoxicity of organic bentonite is higher than that of acid bentonite due to the different industrial treatment and characteristics of two kinds of bentonite particles.

[Cyto-genotoxicity induced by cigarette smoke condensates in human peripheral blood lymphocytes in vitro].

OBJECTIVE: To investigate the cyto-genotoxicity of cigarette smoke condensates (CSCs) in human peripheral blood lymphocytes with different assays in vitro. METHODS: Human lymphocytes were exposed to particle matter of cigarette smoke combined with or without S9 mixtures at doses of 25, 50, 75, 100 and 125 microg/ml for 3 h. The cytotoxicity induced by CSCs was detected by CCK-8 assay. The DNA damage, DNA repair (repair time: 30, 60, 90, 120 and 240 min, respectively) and the somatic cell mutations induced by 75 microg/ml CSCs were measured by comet assay, hprt gene and TCR gene mutation tests, respectively. RESULTS: CCK-8 assay indicated that the cell viability decreased with CSCs doses. At the doses of 100, 125 microg/ml, the cell viability of CSCs +S9 group was significantly higher than that of CSCs -S9 group (P < 0.05, P < 0.01). In comet assay, DNA damage significantly increased in a dose-dependent manner, as compared with controls (P < 0.01). Moreover, there was significant difference between -S9 group and +S9 group (P < 0.05, P < 0.01). The Mf-TCR at each dose group was significantly higher than that of controls (P < 0.05, P < 0.01). The Mf-hprt at high-dose groups were significantly higher than that of controls (P < 0.01), and significant difference of Mf-TCR and Mf-hprt at high doses of CSCs between -S9 group and +S9 group (P < 0.05, P < 0.01). The DNA damage induced by CSCs +S9 or CSCs -S9 could be repaired, but DNA repair speed was different between -S9 group and +S9 group (P < 0.05, P < 0.01). CONCLUSION: CSCs may induce cyto-genotoxicity in human peripheral blood lymphocytes in vitro, but S9 mix could reduce the toxicity of CSCs and impact DNA repair speed.

Response of lymphocytes to radiation in untreated breast cancer patients as detected with three different genetic assays.

OBJECTIVE: To detect the response of lymphocytes to radiation in untreated breast cancer patients with three different genetic assays. METHODS: Blood samples were collected from 25 untreated patients and 25 controls. Each blood sample was divided into two parts: one was irradiated by 3-Gy X-ray (irradiated sample), the other was not irradiated (non-irradiated sample). The radiosensitivity of lymphocytes was assessed by comet assay, cytokinesis-block micronucleus (CBMN) assay and 6-TG-resistant cells scored (TG) assay. RESULTS: The baseline values of micronucleated cell frequency (MCF) and micronucleus frequency (MNF) in the patients were significantly higher than those in the controls (P < 0.01), and 3-Gy X-ray induced genetic damage to lymphocytes in the patients increased significantly as compared with that in the controls as detected with the three genetic assays (P < 0.01). The proportion of radiosensitive cases in the patient group was 48% for the mean tail length (MTL), 40% for the mean tail moment (MTM), 40% for MCF, 44% for MNF, and 48% for mutation frequencies of the hprt gene (Mfs-hprt), respectively, whereas the proportion of radiosensitive cases in the control group was only 8% for all the parameters. CONCLUSION: The difference in the lymphocyte radiosensitivity between the breast cancer patients and the controls is significant. Moreover, there are wide individual variations in lymphocyte radiosensitivity of patients with breast cancer. In some cases, the radiosensitivity of the same patient may be different as detected with the different assays. It is suggested that multiple assays should be used to assess the radiosensitivity of patients with breast cancer before therapy.

[Mutagenic, carcinogenic and teratogenic effects induced by radiofrequency electromagnetic field of mobile phone].

OBJECTIVE: The extensive use of mobile phones causes increasing public concern on health effects of exposure to radiofrequency (RF) electromagnetic fields. Conflicting results are found in publications on the mutagenic, carcinogenic and teratogenic effects of RF electromagnetic fields. The overwhelming findings do not support the assumption that RF exposure may induce mutagenic, carcinogenic or teratogenic effects. However, health effects from low level RF exposure need to be further studied.

[Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and DNA damage in lens epithelial cells by noise magnetic fields].

OBJECTIVE: To investigate whether the exposure to the electromagnetic noise can block reactive oxygen species (ROS) production and DNA damage of lens epithelial cells induced by 1800 MHz mobile phone radiation. METHODS: The DCFH-DA method and comet assay were used respectively to detect the intracellular ROS and DNA damage of cultured human lens epithelial cells induced by 4 W/kg 1800 MHz mobile phone radiation or/and 2 muT electromagnetic noise for 24 h intermittently. RESULT: 1800 MHz mobile phone radiation at 4 W/kg for 24 h increased intracellular ROS and DNA damage significantly (P<0.05). However, the ROS level and DNA damage of mobile phone radiation plus noise group were not significant enhanced (P>0.05) as compared to sham exposure group. CONCLUSION: Electromagnetic noise can block intracellular ROS production and DNA damage of human lens epithelial cells induced by 1800 MHz mobile phone radiation.

[Influence of 1.8 GHz microwave on DNA damage induced by ultraviolet C ray].

OBJECTIVE: To study whether 1.8 GHz microwaves (MW) (SAR, 3 W/kg) exposure can influence DNA damage induced by ultraviolet ray (UV). METHODS: The lymphocytes were obtained from three young healthy donors. The cells were exposed to 254 nm UV at the doses of 0.25, 0.50, 0.75, 1.00, 1.50 and 2.00 J/m(2). The lymphocytes were also exposed to 1.8 GHz MW (SAR, 3 W/kg) for 0, 1.5 and 4.0 h. The combination exposure of UV plus MW was conducted. The treated cells were incubated for 0, 1.5 and 4.0 h. Finally, comet assay was used to detect DNA damage of above treated lymphocytes. RESULTS: The difference of DNA damage induced between MW group and control group was not significant (P>0.05). the MTLs induced by UV were (1.71+/-0.09), (2.02+/-0.08), (2.27+/-0.17), (2.27+/-0.06), (2.25+/-0.12), (2.24+/-0.11)microm, respectively, which were significantly higher than that of control [(0.96+/-0.05) microm], (P<0.01). MTLs of some sub-groups in combination exposure groups at 1.5 h incubation were significantly lower than those of corresponding UV sub-groups (P<0.01 or P<0.05. However, MTLs of some sub-groups in combination exposure groups at 4.0 h incubation were significantly higher than those of corresponding UV sub-groups (P<0.01 or P<0.05). CONCLUSION: The exposure to 1.8 GHz (SAR, 3 W/kg) MW for 1.5 and 4.0 h can not enhance significantly human lymphocyte DNA damage. But MW can reduce or enhance DNA damage of lymphocytes induced by UV at 1.5 h and 4.0 h incubation in comet assay in vitro, respectively.

[DNA damage and repair induced by acute exposure of microwave from mobile phone on cultured human lens epithelial cells].

OBJECTIVE: To investigate the effects of acute exposure of low-power 217 Hz modulated 1. 8 GHz microwave radiation on the DNA damage of human lens epithelial cells (hLECs) and repair. METHODS: Cultured hLECs were exposed to 217 Hz modulated 1. 8 GHz microwave radiation at SAR (specific absorption rate) of 1. 0, 2. 0, 3. O0 and 4. 0 W/kg for 2 hours in an sXc-1800 incubator and irradiate system, the DNA single strand breaks were detected with comet assay ( single-cell gel electrophoresis) in sham-irradiated cells and irradiated cells incubated for varying periods: 0, 30 and 60 minutes after irradiation. Images of comets were digitized and analyzed using an Imagine-pro plus software, and the indexes used in this study were tail length (TL) and tail moment (TM). BrdU was added into the medium with additional one hour incubation after radiation, the cell proliferation rate was determined using a BrdU-kit. RESULTS: The difference of DNA-breaks between the exposure and sham exposure groups induced by 1.0 and 2.0 W/kg irradiation were not significant in each time points (P > 0.05) ; there were significant difference in both groups at the exposure dose of 3. 0 and 4. 0 W/kg immediately and at the time of 30 minutes after irradiation (P <0. 01) ; if the radiation exposure time was beyond one hour no differences were be able to detected in 3.0 W/kg group (P > 0. 05) compared with control, but the evidence of significant DNA damage still existed in 4. 0 W/kg group at the same time point. Cell proliferation rate had no significant difference when the application of SAR was < or = 3. 0 W/kg (P >0. 05) , however the cell proliferation was decreased significantly at the dose of 4. 0 W/kg irradiation ( P < 0. 01). CONCLUSIONS: No effective DNA damage was induced using comet assay after 2 hours irradiation of 1. 8 GHz microwave on hLECs at the dose SAR < or = 3.0 W/kg. 4.0 W/kg irradiation caused significantly DNA damage and inhibition of hLECs proliferation.

[Effect of acute exposure to microwave from mobile phone on DNA damage and repair of cultured human lens epithelial cells in vitro].

OBJECTIVE: To investigate the DNA damage of human lens epithelial cells (LECs) caused by acute exposure to low-power 217 Hz modulated 1.8 GHz microwave radiation and DNA repair. METHODS: Cultured LECs were exposed to 217 Hz modulated 1.8 GHz microwave radiation at SAR (specific absorption rate) of 0, 1, 2, 3 and 4 W/kg for 2 hours in an sXc-1800 incubator and irradiate system. The DNA single strand breaks were detected with comet assay in sham-irradiated cells and irradiated cells incubated for varying periods: 0, 30, 60, 120 and 240 min after irradiation. Images of comets were digitized and analyzed using an Imagine-pro plus software, and the indexes used in this study were tail length (TL) and tail moment (TM). RESULTS: The difference in DNA-breaks between the exposure and sham exposure groups induced by 1 and 2 W/kg irradiation was not significant at every detect time (P > 0.05). As for the dosage of 3 and 4 W/kg there was difference in both group immediately after irradiation (P < 0.01). At the time of 30 min after irradiation the difference went on at both group (P < 0.01). However, the difference disappeared after one hour's incubation in 3 W/kg group (P > 0.05), and existed in 4 W/kg group. CONCLUSION: No or repairable DNA damage was observed after 2 hour irradiation of 1.8 GHz microwave on LECs when SAR < or = 3 W/kg. The DNA damages caused by 4 W/kg irradiation were irreversible.

Assessment of human DNA repair (NER) capacity with DNA repair rate (DRR) by comet assay.

OBJECTIVE: Alkaline comet assay was used to evaluate DNA repair (nucleotide excision repair, NER) capacity of human fresh lymphocytes from 12 young healthy non-smokers (6 males and 6 females). METHODS: Lymphocytes were exposed to UV-C (254 nm) at the dose rate of 1.5 J/m2/sec. Novobiocin (NOV) and aphidicolin (APC), DNA repair inhibitors, were utilized to imitate the deficiency of DNA repair capacity at the incision and ligation steps of NER. Lymphocytes from each donor were divided into three grougs: UVC group, UVC plus NOV group, and UVC plus APC group. DNA single strand breaks were detected in UVC irradiated cells incubated for 0, 30, 60, 90, 120, 180, and 240 min after UVC irradiation. DNA repair rate (DRR) served as an indicator of DNA repair capacity. RESULTS: The results indicated that the maximum DNA damage (i.e. maximum tail length) in the UVC group mainly appeared at 90 min. The ranges of DRRs in the UVC group were 62.84%-98.71%. Average DRR value was 81.84%. The DRR difference between males and females was not significant (P < 0.05). However, the average DRR value in the UVC plus NOV group and the UVC plus APC group was 52.98% and 39.57% respectively, which were significantly lower than that in the UVC group (P < 0.01). CONCLUSION: The comet assay is a rapid, simple and sensitive screening test to assess individual DNA repair (NER) capacity. It is suggested that the time to detect DNA single strand breaks in comet assay should include 0 (before UV irradiation), 90 and 240 min after exposure to 1.5 J x m(-2) UVC at least. The DRR, as an indicator, can represent the individual DNA repair capacity in comet assay.

[Investigating genetic damage of workers occupationally exposed to methotrexate].

OBJECTIVE: To study genetic damage of workers alone occupationally exposed to methotrexate (MTX) with three end-points. METHODS: The blood samples from 21 workers exposed to MTX and 21 controls were detected with micronucleus test, comet assay, hprt gene mutation test and TCR gene mutation test. RESULTS: The mean micronuclei rate (MNR) and mean micronucleated cells rate (MCR) in 21 workers were 10.10 per thousand +/- 0.95 per thousand and 8.05 per thousand +/- 0.75 per thousand, respectively, which were significantly higher than those (5.48 per thousand +/- 0.82 per thousand and 4.38 per thousand +/- 0.58 per thousand) in control (P < 0.01). The mean tail length (MTL) of 21 workers and 21 controls were (1.30 +/- 0.06) microm and (0.07 +/- 0.01) microm, respectively, there was significant difference between workers and controls (P < 0.01). But the difference between workers and controls for mean tail moment (MTM) was not significant (P > 0.05). The average mutation frequency (Mf-hprt) of hprt and (Mf-TCR) of TCR in workers were 1.00 per thousand +/- 0.02 per thousand and (6.87 +/- 0.52) x 10(-4), respectively, which were significantly higher than those [0.86 per thousand +/- 0.01 per thousand and (1.67 +/- 0.14) x 10(-4)] in control (P < 0.01). CONCLUSION: The genetic damage to some extent appeared in workers occupationally exposed to methotrexate.

[Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens].

OBJECTIVE: To observe the influence of 1.8 GHz microwave (MW) specific absorption rate (SAR, 3 W/kg) on human lymphocytes DNA damage induced by 4 chemical mutagens [mitomycin C (MMC), bleomycin (BLM), methyl methanesulfonate (MMS), and 4-nitroquinoline 1-oxide (4NQO)]. METHODS: Comet assay in vitro was used to detect human lymphocyte DNA damage induced by 1.8 GHz MW, 4 chemical mutagens, and MW plus 4 chemicals 0 h and 21 h respectively after exposure. The time exposed to MW or mutagens was 2 h or 3 h respectively. The results were showed by tail length (TL) and tail moment (TM). RESULTS: The difference of DNA damage between MW group and control group was not statistically significant (P > 0.05). DNA damages in MW plus MMC groups and MW plus 4NQO groups were significantly greater than those in the corresponding concentrations of MMC groups and 4NQO groups (P < 0.01 or P < 0.05). However, MW did not enhance DNA damage induced by MMS and BLM (P > 0.05). CONCLUSION: Exposure to 1.8 GHz (SAR, 3 W/kg) microwave may not induce human lymphocyte DNA damage, but could enhance DNA damage induced by MMC and 4NQO.

Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of mitomycin C using micronucleus test and comet assay in vitro.

OBJECTIVE: To determine the interaction between 2450-MHz microwaves (MW) radiation and mitomycin C (MMC). METHODS: The synergistic genotoxic effects of low-intensity 2450-MHz microwave and MMC on human lymphocytes were studied using single cell gel electrophoresis (SCGE) assay (comet assay) and cytokinesis-blocked micronucleus (CBMN) test in vitro. The whole blood cells from a male donor and a female donor were either only exposed to 2450-MHz microwaves (5.0 mW/cm2) for 2 h or only exposed to MMC (0.0125 microgram/mL, 0.025 microgram/mL and 0.1 microgram/mL) for 24 h; and the samples were exposed to MMC for 24 h after exposure to MW for 2 h. RESULTS: In the comet assay, the comet lengths (29.1 microns and 25.9 microns) of MW were not significantly longer than those (26.3 microns and 24.1 microns) of controls (P > 0.05). The comet lengths (57.4 microns, 68.9 microns, 91.4 microns, 150.6 microns, 71.7 microns, 100.1 microns, 145.1 microns) of 4 MMC groups were significantly longer than those of controls (P < 0.01). The comet lengths (59.1 microns, 92.3 microns, 124.5 microns, 182.7 microns and 57.4 microns, 85.5 microns, 137.5 microns, 178.3 microns) of 4 MW plus MMC groups were significantly longer than those of controls too (P < 0.01). The comet lengths of MW plus MMC groups were significantly longer than those of the corresponding MMC doses (P < 0.05 or P < 0.01) when the doses of MMC were > or = 0.025 microgram/mL. In the CBMN, the micronucleated cell (MNC) rates of MW were 5@1000 and 6@1000, which showed no difference compared with those (4@1000 and 4@1000) of controls (P > 0.05). The MNC rates of 4 MMC groups were 8@1000, 9@1000, 14@1000, 23@1000 and 8@1000, 8@1000, 16@1000, 30@1000 respectively. When the doses of MMC were > or = 0.05 microgram/mL, MNC rates of MMC were higher than those of controls (P < 0.05). MNC rates of 4 MW plus MMC groups were 12@1000, 13@1000, 20@1000, 32@1000 and 8@1000, 9@1000, 23@1000, 40@1000. When the doses of MMC were > or = 0.05 microgram/mL, MNC rates of MW plus MMC groups were much higher than those of controls (P < 0.01). MNC rates of 4 MW plus MMC groups were not significantly higher than those of the corresponding MMC doses. CONCLUSION: The low-intensity 2450-MHz microwave radiation can not induce DNA and chromosome damage, but can increase DNA damage effect induced by MMC in comet assay.