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Low levels of methylmercury induce DNA damage in rats: protective effects of selenium

机译:低水平的甲基汞诱导大鼠DNA损伤:硒的保护作用

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In this study we examined the possible antigenotoxic effect of selenium (Se) in rats chronically exposed to low levels of methylmercury (MeHg) and the association between glutathione peroxidase (GSH-Px) activity and DNA lesions (via comet assay) in the same exposed animals. Rats were divided into six groups as follows: (Group I) received water; (Group II) received MeHg (100 μg/day); (Group III) received Se (2 mg/L drinking water); (Group IV) received Se (6 mg/L drinking water); (Group V) received MeHg (100 μg/day) and Se (2 mg/L drinking water); (Group VI) received MeHg (100 μg/day) and Se (6 mg/L drinking water). Total treatment time was 100 days. GSH-Px activity was determined spectrophotometrically and DNA damage was determined by comet assay. Mean GSH-Px activity in groups I, II, III, IV, V and VI were, respectively: 40.19 ± 17.21; 23.63 ± 6.04; 42.64 ± 5.70; 38.50 ± 7.15; 34.54 ± 6.18 and 41.39 ± 11.67 nmolNADPH/min/gHb. DNA damage was represented by a mean score from 0 to 300; the results for groups I, II, III, IV, V and VI were, respectively: 6.87 ± 3.27; 124.12 ± 13.74; 10.62 ± 3.81; 13.25 ± 1.76; 86.87 ± 11.95 and 76.25 ± 7.48. There was a significant inhibition of GSH-Px activity in group II compared with group I (P < 0.05). Groups V and VI did not show a difference in enzyme activity compared with groups III and IV, showing the possible protective action of Se. Comet assay presented a significant difference in DNA migration between group II and group I (P < 0.0001). Groups V and VI showed a significant reduction in MeHg-induced genotoxicity (P < 0.001) when compared with group II. A negative correlation (r = −0.559, P < 0.05) was found between GSH-Px activity and DNA lesion, showing that the greater the DNA damage, the lower the GSH-Px activity. Our findings demonstrated the oxidative and genotoxic properties of MeHg, even at low doses. Moreover, Se co-administration reestablished GSH-Px activity and reduced DNA damage.
机译:在这项研究中,我们研究了硒(Se)在长期暴露于低水平甲基汞(MeHg)的大鼠中的可能的抗原毒性作用,以及在相同暴露条件下谷胱甘肽过氧化物酶(GSH-Px)活性与DNA损伤之间的关联(通过彗星试验)动物。将大鼠分为以下六组:(第一组)接受水; (第二组)接受MeHg(100μg/天); (第三组)接受硒(2 mg / L饮用水); (第四组)接受硒(6 mg / L饮用水); (V组)接受MeHg(100μg/天)和Se(2 mg / L饮用水); (第VI组)接受MeHg(100μg/天)和Se(6 mg / L饮用水)。总治疗时间为100天。用分光光度法测定GSH-Px活性,用彗星试验测定DNA损伤。 I,II,III,IV,V和VI组的平均GSH-Px活性分别为:40.19±17.21; 23.63±6.04; 42.64±5.70; 38.50±7.15; 34.54±6.18和41.39±11.67 nmolNADPH / min / gHb。 DNA损伤的平均得分为0到300; I,II,III,IV,V和VI组的结果分别为:6.87±3.27; 124.12±13.74; 10.62±3.81; 13.25±1.76; 86.87±11.95和76.25±7.48。与I组相比,II组对GSH-Px活性有显着抑制作用(P <0.05)。与III和IV组相比,V和VI组没有显示出酶活性的差异,表明了Se的可能的保护作用。彗星试验显示II组和I组之间的​​DNA迁移存在显着差异(P <0.0001)。与第II组相比,第V和VI组显示MeHg诱导的遗传毒性显着降低(P <0.001)。在GSH-Px活性和DNA损伤之间发现负相关(r = -0.559,P <0.05),这表明DNA损伤越大,GSH-Px活性越低。我们的研究结果表明,即使在低剂量下,MeHg的氧化和遗传毒性也是如此。此外,Se共同给药可恢复GSH-Px活性并减少DNA损伤。

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