MTHFR and MTRR gene polymorphisms in patients with chronic hepatitis B virus infections in Zigong, Sichuan Province.

BACKGROUND: Chronic hepatitis B virus (HBV) infection is a severe disease affecting the physical and economic well-being of patients. The relationship between polymorphisms in the MTHFR gene and disease progression following HBV infection remains a controversial topic. AIM: To study MTHFR and MTRR gene polymorphisms in patients with chronic HBV infections in Zigong, Sichuan Province. SUBJECTS AND METHODS: One hundred and ninety-one patients with chronic HBV infections were divided into three groups: the chronic hepatitis B (CHB) group (n = 71), the hepatitis B-induced liver cirrhosis (LC) group (n = 56), and the hepatitis B-related primary liver cancer (PLC) group (n = 64). The gene polymorphisms were detected using the PCR-melt curve method and analysed. RESULTS: The distributions of MTHFR C677T (CC: 41.2% vs. 41.8%; CT: 50% vs. 45.5%; TT: 8.8% vs. 12.7%; p = 0.714), MTHFR A1298C (AA: 70.6% vs. 72.7%; AC: 26.5% vs. 25.5%; CC: 2.9% vs. 1.8%; p = 1.000), and MTRR A66G (AA: 58.1% vs. 65.5%; AG: 39.0% vs. 29.1%; 2.9% vs. 5.5%; p = 0.353) genetic polymorphisms did not vary between male and female patients from Zigong. In addition, there were no differences in the distributions of MTHFR C677T (CC: 43.4% vs. 38.8%; CT: 49.1% vs. 48.2%; TT: 7.5% vs. 12.9%; p = 0.444), MTHFR A1298C (AA: 76.4% vs. 64.7%; AC: 20.8% vs. 32.9%; CC: 2.8% vs. 2.4%; p = 0.155), and MTRR A66G (AA: 62.3% vs. 57.6%; AG: 34.0% vs. 38.8%; 3.8% vs. 3.5%; p = 0.353) genetic polymorphisms between the patients <60 and >60 years of age. The distributions of MTHFR C677T (CHB vs. LC, p = 0.888; CHB vs. PLC, p = 0.661; PLC vs. LC, p = 0.926), MTHFR A1298C (CHB vs. LC, p = 0.12; CHB vs. PLC, p = 0.263; PLC vs. LC, p = 0.550), and MTRR A66G (CHB vs. LC, p = 0.955; CHB vs. PLC, p = 0.645; PLC vs. LC, p = 0.355) gene polymorphisms were comparable between the CHB, LC, and PLC groups. CONCLUSION: The distributions of MTHFR and MRRR genetic polymorphisms in the population with HBV infections in Zigong, Sichuan Province did not differ in age and sex. The MTHFR and MRRR genetic polymorphisms were comparable between the CHB, LC, and PLC groups.

Clinical application value of hepatitis B virus basal core promoter 1762/1764 and GGTII and GGT in patients with HBV-DNA-positive primary liver cancer.

BACKGROUND: Hepatitis B virus (HBV) is closely related to the occurrence and development of primary liver cancer (PLC). The early diagnosis of PLC is difficult. The study explored the clinical application value of the HBV gene basal core promoter (BCP) region 1762/1764 combined with gamma-glutamyl transpeptidase (GGT) and its isozyme II (GGTII) in PLC. METHODS: From June 2017 to June 2021, 145 hepatitis B surface antigen-positive and HBV DNA-positive patients were enrolled in the Third People Hospital of Zigong. Of them, 67 were chronic hepatitis B (CHB) patients, 30 were liver cirrhosis patients, and 48 were patients with hepatitis B-associated PLC. The HBV BCP 1762/1764 mutation was detected through the amplification refractory mutation system fluorescence PCR method, and GGTII was detected using the double-antibody sandwich method. RESULTS: The results showed that the serum GGT activity, GGTII level, aspartate aminotransferase (AST) activity, AST/alanine aminotransferase (ALT) ratio, GGT/ALT ratio, and GGT/AST ratio were significantly different between the PLC and CHB groups. Statistically significant differences in serum GGT activity, AST activity, and GGT/ALT ratio were observed between the PLC and LC groups. The BCP 1762/1764 mutation rate between the PLC and CHB groups was statistically significant. The GGTII level in the early PLC (stage I + II) group and the advanced PLC (stage III + IV) group was higher than that in the N-PLC group. Serum GGT activity in the early PLC and advanced PLC groups was higher than that in the N-PLC group. The area under the curve of the receiver operator characteristic curve of GGT and GGTII for diagnosing PLC was 0.775 (95% confidence interval [CI] [0.697, 0.854]) and 0.608 (95% CI [0.512, 0.704]), respectively. The area under curve of GGT and GGTII for diagnosing early PLC was 0.732 (95% CI [0.620, 0.845]) and 0.579 (95% CI [0.452, 0.706]), respectively. CONCLUSION: HBV gene BCP 1762/1764 mutation, GGT, and GGTII may be related to PLC occurrence. The HBV gene BCP region 1762/1764 combined with GGT has certain clinical diagnostic values for PLC and early PLC. However, GGTII is not a good indicator of early PLC and is more relevant to advanced PLC.

Frailty is associated with 90-day unplanned readmissions and death in patients with heart failure: A longitudinal study in China.

BACKGROUND: Frailty has been reported to be significantly associated with adverse health outcomes in people with heart failure (HF). OBJECTIVES: To explore the potential effects of frailty on unplanned readmissions and death in people with HF patients aged 18 years or older. METHODS: 342 HF patients aged 18 years or older from the heart centers of two different tertiary care hospitals located in northwest of China were enrolled between July and December 2020. Frailty was assessed by the Tilburg Frailty Indicator. The patients were followed for unplanned readmissions, and all-cause mortality at 30, 60, as well as 90 days after discharge. Multivariate cox regression models were used to analyze the effects of frailty on 90-day unplanned readmission and death in the patients with HF. RESULTS: Frailty prevalence was 54.7% among 342 HF patients, with a mean age of 64.65 ± 11.90 years. It was found that compared to non-frailty HF patients, the frailty HF patients were older and displayed higher systolic blood pressure, longer duration of HF, more severe cognitive function, and more comorbidities (P < 0.05). On the contrary, the patients in the frail group had a higher incidence of unplanned readmission (73.1% vs. 26.9%, χ2 = 18.87, P < 0.01) and death (100% vs. 0%, χ2 = 6.94, P < 0.01) than those in the non-frail group. Multivariate cox regression analysis showed that frailty could serve as an independent risk factor for 90-day unplanned readmission (HR = 1.469, 95% CI 1.318-1.637, P < 0.01) and 90-day death (HR=2.270, 95% CI 1.091-4.726, P < 0.01) in the patients with HF. CONCLUSION: Frailty can act as an independent predictor of unplanned readmission and death 90-day after discharge in HF patients aged 18 years or older.

The comparative efficacy of supervised- versus home-based exercise programs in patients with ankylosing spondylitis: A meta-analysis.

OBJECTIVES: The aim of this meta-analysis is to investigate the comparative efficacy between supervised- and home-based programs in patients with ankylosing spondylitis (AS). METHOD: A systematic search in PubMed, Web of Science, EMBASE, and the Cochrane Library was electronically performed by 2 independent investigators in order to capture all potential studies comparing supervised- with home-based in patients with AS from inception to April 2018. After extracted essential information, apprised risk of bias, statistical analysis was performed with Review Manager (RevMan) software (version 5.3.0). The protocol was registered at PROSPERO platform with an identifier of CRD42018097046. RESULTS: A total of 7 studies comprising 271 patients were included finally. Meta-analyses showed that, compared to home-based program, supervised-based program was associated with reduced bath ankylosing spondylitis metrology index (BASMI) scores (mean difference [MD], -0.45; 95% confidence interval [CI], -0.73, -0.17), bath ankylosing spondylitis disease activity index (BASDAI) scores (MD, -0.48; 95% CI, -0.88, -0.08), and bath ankylosing spondylitis functional index (BASFI) scores (MD, -0.78; 95% CI, -1.19, -0.37). However, depression scores (standard mean difference, -0.22; 95% CI, -0.58, 0.14) between the 2 groups showed no significant defference. CONCLUSIONS: Both supervised- and home-based programs can benefit to reduce BASMI, BASDAI, and BASFI scores in AS patients. However, short-term, supervised exercise program may be more effective than home-based exercises at decreasing disease activity with AS.

The comparative efficacy of group- versus home-based exercise programs in patients with ankylosing spondylitis: Protocol for a meta-analysis.

BACKGROUND: Ankylosing spondylitis (AS) is an important factor to not only cause employment obstacle, but also result in serious social economic load. Several randomized controlled trials investigated the efficacy of group- versus home-based exercise programs in patients with AS. This systematic review will collect and summarize the available evidence to realize the effectiveness of group- and home-based programs in patients with AS. METHODS: A search in PubMed, Web of Science, EMBASE, and the Cochrane Library will be electronically performed by 2 independent investigators to capture all potential studies comparing group- and home-based in patients with AS. The time limit of search will be from their inception to April 2018. Two independent investigators provide their agreement in presencial meeting for a final selection, and at a later stage, the articles will be reviewed in full-text by the all authors. Quantitative analysis will be performed with Review Manager (RevMan) software (version 5.3.0). RESULTS: This meta-analysis will provide a high-quality synthesis of current evidence of group- versus home-based exercise programs in patients with AS. CONCLUSION: The conclusion of our meta-analysis will provide the evidence which program is an effective intervention for patient with AS.

Chronic occupational exposure to hexavalent chromium causes DNA damage in electroplating workers.

BACKGROUND: Occupational exposure to chromium compounds may result in adverse health effects. This study aims to investigate whether low-level hexavalent chromium (Cr(VI)) exposure can cause DNA damage in electroplating workers. METHODS: 157 electroplating workers and 93 control subjects with no history of occupational exposure to chromium were recruited in Hangzhou, China. Chromium levels in erythrocytes were determined by graphite furnace atomic absorption spectrophotometer. DNA damage in peripheral lymphocytes was evaluated with the alkaline comet assay by three parameters: Olive tail moment, tail length and percent of DNA in the comet tail (tail DNA%). Urinary 8-OHdG levels were measured by ELISA. RESULTS: Chromium concentration in erythrocytes was about two times higher in electroplating workers (median: 4.41 µg/L) than that in control subjects (1.54 µg/L, P < 0.001). The medians (range) of Olive tail moment, tail length and tail DNA% in exposed workers were 1.13 (0.14-6.77), 11.17 (3.46-52.19) and 3.69 (0.65-16.20), and were significantly higher than those in control subjects (0.14 (0.01-0.39), 3.26 (3.00-4.00) and 0.69 (0.04-2.74), P < 0.001). Urinary 8-OHdG concentration was 13.65 (3.08-66.30) µg/g creatinine in exposed workers and 8.31 (2.94-30.83) µg/g creatinine in control subjects (P < 0.001). The differences of urinary 8-OHdG levels, Olive tail moment, tail length and tail DNA% between these two groups remained significant (P < 0.001) even after stratification by potential confounding factors such as age, gender, and smoking status. Chromium exposure was found to be positively associated with chromium levels in erythrocytes, urinary 8-OHdG levels, Olive tail moment, tail length and tail DNA%. Positive dose-response associations were also found between chromium levels in erythrocytes and Olive tail moment, tail length and tail DNA%. CONCLUSION: The findings in this study indicated that there was detectable chromium exposure in electroplating workers. Low-level occupational chromium exposure induced DNA damage.

Studying the genotoxicity of vincristine on human lymphocytes using comet assay, micronucleus assay and TCR gene mutation test in vitro.

The results of our previous investigation for workers occupationally exposed to vincristine (VCR) indicated that the genetic damage was detectable with comet assay, cytokinesis-block micronucleus (CBMN) assay and housekeeping gene mutation tests. In order to determine the results of above investigation and to inquire further the characteristics of genotoxicity of VCR, the cytogenetic effects of VCR on human lymphocytes were assessed with comet assay, CBMN assay and T-cell receptor (TCR) gene mutation test in vitro. The lymphocytes from two healthy donors were incubated for 24h at doses of 0.00, 0.01, 0.02, 0.04, and 0.08microgml(-1) VCR. The results of the present experiment showed that VCR not only could induce DNA damage, increase significantly micronucleus frequencies and the apoptotic cell ratios and decrease the nuclear division index (NDI) with dose-response relationship, but also could produce nucleoplasmic bridges (NPBs), a biomarker of DNA misrepair and/or telomere end-fusions and nuclear buds (NBUDs), a biomarker of elimination of amplified DNA and/or DNA repair complexes. Moreover, VCR could enhance TCR gene mutation frequency (Mf-TCR) of human lymphocytes. There was good correlation between the parameters (mean tail length, mean tail moment, micronucleus frequency, micronucleated frequency and Mf-TCR). The results of present study supported the results of our previous investigation for workers occupationally exposed to VCR, and the genotoxicity of VCR was determined at the different genetic end-points in vitro.

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.

Investigating the genetic instability in the peripheral lymphocytes of 36 untreated lung cancer patients with comet assay and micronucleus assay.

The aim of present investigation was to study the genetic instability in peripheral lymphocytes of lung cancer patients. The micronucleus (MN) assay and comet assay were simultaneously used to detect the spontaneous genetic change and ionizing irradiation (IR) induced genetic damage in peripheral lymphocytes from 36 lung cancer patients and 30 controls. In MN assay, the results of both two indicators, micronucleated cell frequency (MCF) and micronucleus frequency (MNF), indicated that the average values of MCF, MNF and IR-induced MCF, MNF of lung cancer patients were 9.25+/-0.58, 10.17+/-0.72, 66.14+/-2.07 and 75.64+/-2.34 per thousand, respectively, which were significantly higher than those (6.10+/-0.65, 6.60+/-0.74, 60.50+/-1.71 and 67.60+/-2.13 per thousand) of controls (P<0.05 or 0.01). In comet assay, the results of mean tail moment (MTM) and IR-MTM showed 0.84+/-0.07 and 1.09+/-0.11, respectively, which were significantly higher than those (0.60+/-0.05 and 0.70+/-0.10) of controls (P<0.05). However, the difference between lung cancer group and control group for the mean tail length (MTL) and IR-MTL was not significant (P>0.05). The results of present investigation indicated that the genetic instability in peripheral lymphocytes of 36 lung cancer patients was significantly higher than that of controls.

Evaluating the genotoxic effects of workers exposed to lead using micronucleus assay, comet assay and TCR gene mutation test.

To evaluate the genotoxic effects of lead (Pb) exposure, 25 workers in a workplace producing storage battery were monitored for three genetic end-points using micronucleus (MN) assay, comet assay and TCR gene mutation test. Twenty-five controls were matched with workers according to age, gender and smoking. The air Pb concentration in the workplace was 1.26 mg/m(3). All subjects were measured for Pb concentration of blood by atom absorption spectrophotometry. The mean Pb concentration of blood in workers (0.32 mg/l) was significantly higher than that in controls (0.02 mg/l). The results of MN test showed that the mean micronuclei rate (MNR) and mean micronucleated cells rate (MCR) in workers were 9.04+/-1.51 per thousand and 7.76+/-1.23 per thousand, respectively, which were significantly higher than those (2.36+/-0.42 per thousand and 1.92+/-0.31 per thousand) in controls (P<0.01). It was found in the comet assay that the mean tail length (MTL) of 25 workers and 25 controls were 2.42+/-0.09 and 1.02+/-0.08 microm, respectively, there was significant difference between workers and controls for MTL (P<0.01), also the difference of the mean tail moment (MTM) between workers (0.85+/-0.05) and controls (0.30+/-0.09) was very significant (P<0.01). However, in TCR gene mutation assay Mfs-TCR of workers and controls were 1.69+/-0.15 x 10(-4) and 1.74+/-0.17 x 10(-4), respectively, there was no significant difference between workers and controls (P>0.05). The results of our study indicated that the genetic damage was detectable in 25 workers occupationally exposed to lead.

[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.

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 in workers occupationally exposed to methotrexate using three genetic end-points.

Genetic damage in workers occupationally exposed to an antineoplastic drug was studied using the micronucleus (MN) test, the comet assay, the hprt gene mutation assay and the TCR gene mutation assay. The subjects were divided into two groups: (i) 21 workers from a plant producing methotrexate (MTX); (ii) 21 controls were matched according to age, gender and smoking. Fresh blood samples were collected from the workers and controls. The results of the MN test showed that the mean micronuclei rate (MNR) and mean micronucleated cell rate (MCR) in workers were 10.10 +/- 0.95 per thousand and 8.05 +/- 0.75 per thousand, respectively, which were significantly higher than those (5.48 +/- 0.82 per thousand and 4.38 +/- 0.58 per thousand) in controls (P < 0.01). It was found in the comet assay that the mean tail length (MTL) of workers and controls were 1.30 +/- 0.06 microm and 0.07 +/- 0.01 microm, respectively. There was a significant difference between workers and controls for MTL (P < 0.01), but the difference between the mean tail moment (MTM, 0.23 +/- 0.03) of workers and MTM (0.17 +/- 0.04) of controls was not significant (P > 0.05). The results of hprt gene mutation assay showed that the average mutation frequency (Mf-hprt) of hprt in workers was 1.00 +/- 0.02 per thousand, which was significantly higher than that (0.86 +/- 0.01 per thousand) in controls (P < 0.01). Meanwhile, the results of TCR gene mutation assay indicated that Mfs-TCR gene mutation frequencies of workers and controls were 6.87 +/- 0.52 x 10(-4) and 1.67 +/- 0.14 x 10(-4), respectively, which were significantly different (P < 0.01). The results of our experiment suggest that genetic damage is detectable in the 21 workers occupationally exposed to methotrexate.

[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.

[Detecting DNA repair capacity of human lymphocytes exposed to ultraviolet C with comet assay].

OBJECTIVE: To assess DNA repair capacity of human lymphocytes with comet assay. METHODS: Fresh lymphocytes form twelve 26-year old donors (6 males, 6 females) were exposed to ultraviolet C (UVC, 254 nm) at the dose rate of 1.5 J/m(2). The lymphocytes of each donor were divided into three parts: UVC group, UVC + aphidicolin (APC) group, UVC + novobiocin (NOV) group. DNA single strand breaks were detected with comet assay in UVC-irradiated cells and unirradiated cells incubated for 30, 60, 90, 120, 180 and 240 min. DNA repair rate (DRR) was calculated and served as an indicator of DNA repair capacity. RESULTS: The maximum average comet tail length (MTL) in three groups appeared 90 min after UVC exposure. The DRR range of UVC group was 81.84% (62.84% - 98.71%); There was no significant difference in DRR between males and females (P > 0.05). However, the average DRRs of UVC + NOV group and UVC + APC group (52.98% and 39.57% respectively) were significantly lower than that of UVC group (P < 0.01). CONCLUSION: Comet assay is a rapid and simple screening test to assess DNA repair capacity. DRR, as an indicator, may express the individual DNA repair capacity.

[Effects of 2,450 MHz microwave on DNA damage induced by three chemical mutagens in vitro].

OBJECTIVE: To study the combined damage-effects of low-intensity 2,450 MHz microwave (MW) with three chemical mutagens on human lymphocyte DNA. METHODS: DNA damage of lymphocytes exposed to microwave and(or) with chemical mutagens were observed at different incubation time (0 h or 21 h) with comet assay in vitro. Three combination-exposure ways of MW with chemicals were used: MW irradiation before chemical exposures, simultaneously exposed to MW and chemicals and MW irradiation after chemical exposures. The three chemical mutagens were mitomycin C (MMC, DNA crosslinker), bleomycin (BLM, radiometric agent), methyl methanesulfonate (MMS, alkylating agent). The exposure time of MW and chemical mutagens were 2 h and 3 h respectively. RESULTS: The differences of comet tail length between MW group and control group were not significant when lymphocytes were incubated for 0 h or 21 h (P > 0.05). However, when lymphocytes were incubated for 21 h with 30.00 micro mol/L of MMC, the comet tail lengths of MW + MMC group, MW-MMC group and MMC + MW group were (18.00 +/- 5.96), (21.79 +/- 11.47) and (22.32 +/- 8.10) micro m respectively; while with 3.00 micro mol/L of MMC, the comet tail lengths were (8.99 +/- 3.75), (12.40 +/- 5.35) and (14.00 +/- 5.38) micro m respectively, which were significantly higher than those of corresponding MMC groups [(9.42 +/- 3.34) and (6.50 +/- 2.89) micro m, P < 0.01 or P < 0.05]. The DNA damage of MW plus BLM groups and MW plus MMS groups were not significantly different from the corresponding BLM and MMS groups (P < 0.05). CONCLUSION: 2 450 MHz MW (5 mW/cm(2)) did not induce DNA damage directly, but could enhance the DNA damage effects induced by MMC. The synergistic effects of 2 450 MHz MW with BLM and MMS were not obvious.

[Effect of low-intensity microwave of on mitomycin C-induced genotoxicity in vitro].

OBJECTIVE: To study that low-intensity microwave whether or not enhances the genotoxic effects of mitomycin C(MMC) on human lymphocytes. METHODS: Single strand DNA breaks and chromosomal aberrations were measured by comet assay and cytokinesis-blocked micronucleus(CBMN) test in vitro when human lymphocytes were exposed to 2,450-MHz microwave (5.0 mW/cm2) alone and in combination with mitomycin C. RESULTS: In the comet assay, the average comet lengths of microwave group[(29.1 +/- 8.1) micron in male and (25.9 +/- 7.5) micron in female] were not significantly different from those of control groups [(26.3 +/- 6.6) and (24.1 +/- 4.3) micron respectively] (P > 0.05). The average comet lengths of MMC group(0.0125, 0.0250, 0.0500, 0.1000 microgram/ml) were significantly longer than those of control groups (P < 0.01) and were increased with the dose of MMC. The average comet lengths of microwave combined with MMC (MW + MMC) also were increased with the doses of MMC and were significantly longer than those of control groups (P < 0.01). When MMC was > or = 0.0250 microgram/ml, microwave and MMC synergistically increased the single strand DNA breaks. In the micronucleus test, the average micronucleus rates of microwave groups were not higher than those of control groups (P > 0.05). The average micronucleus rates of MMC groups and MW + MMC groups were significantly higher than those of control groups (P < 0.01) when MMC was > or = 0.0500 microgram/ml. The average micronucleus rates of MW + MMC groups seemed higher than those of corresponding MMC groups, however the difference was not significant (P > 0.05). CONCLUSION: Low-intensity(2,450-MHz) microwave did not induce DNA and chromosome damages on human lymphocytes, but enhanced the effects of DNA breaks induced by MMC.

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.