Response of lymphocytes to radiation in untreated breast cancer patients as detected with three different genetic assays / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To detect the response of lymphocytes to radiation in untreated breast cancer patients with three different genetic assays.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Assessment of human DNA repair (NER) capacity with DNA repair rate (DRR) by comet assay / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>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).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Influence of 1.8 GHz microwave on DNA damage induced by 4 chemical mutagens / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>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)].</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Investigating genetic damage of workers occupationally exposed to methotrexate / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study genetic damage of workers alone occupationally exposed to methotrexate (MTX) with three end-points.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>The genetic damage to some extent appeared in workers occupationally exposed to methotrexate.</p>

Detecting DNA repair capacity of human lymphocytes exposed to ultraviolet C with comet assay / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To assess DNA repair capacity of human lymphocytes with comet assay.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Effects of 2,450 MHz microwave on DNA damage induced by three chemical mutagens in vitro / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the combined damage-effects of low-intensity 2,450 MHz microwave (MW) with three chemical mutagens on human lymphocyte DNA.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Study of low-intensity 2450-MHz microwave exposure enhancing the genotoxic effects of mitomycin C using micronucleus test and comet assay in vitro / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To determine the interaction between 2450-MHz microwaves (MW) radiation and mitomycin C (MMC).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>