Evaluation of the genetic damage to workers in a Greek shipyard

Shipyards are industrial areas where workers are likely exposed to environmental pollutants such as welding fumes, fine organic solvent and dye dust, that render the occupational environment a high risk one. Assessing the risk that workers are exposed to is a high critical factor in improving their working conditions. The present study aims to investigate the potential genetic damage to workers exposed to a harsh environment in a Greek shipyard. It is focused on assessing the percentage of induced micronuclei, as well as on changes in the various cell types of shipyard workers’ oral mucosa epithelium by implementing the buccal micronucleus cytome assay. Exposed workers appeared with statistically significant induced micronuclei as compared to office employees. Statistically, significant cell lesions were detected and are related to workers’ exposure to environmental conditions. The workers’ smoking habit contributed as well to the observed buccal epithelial cell alterations. The observed data signify the high-risk workers are exposed; resulting in the shipyard’s management the need to implement measures improving the working environment conditions and to reevaluate the workers’ personal protective equipment requirements.     

放射诊疗工作人员血型糖蛋白A基因突变频率及其相关因素的研究

目的 探讨血型糖蛋白A(GPA)基因突变频率用于辐射危险评价及预测电离辐射诱发肿瘤风险的可行性.方法 采用固定人群分层随机抽样的方法,选取上海市放射诊疗工作人员336例(按工种分为X射线影像诊断组、CT影像诊断组、介人放射学组和放射治疗组),健康对照组 112例;其中,经血型鉴定为MN杂合个体的放射诊疗工作人员为176例,健康对照者为58例.分离、固定、荧光免疫标记外周血红细胞后,应用流式细胞仪,按照BR6-1WI方法,分析GPA基因突变频率;采用胞质分裂阻断微核+3-氨基苯甲酰胺指数实验(CB微核+3AB指数实验),检测DNA损伤修复能力以反映研究对象的个体易感性.结果 放射诊疗工作人员GPA基因突变频率明显高于健康对照组(t=2.29～11.48,P＜0.05),尤其是介入放射学组的GPA NO基因突变频率明显高于X射线影像诊断组(t =2.01,P＜0.05).GPA NO基因突变频率受放射工龄、累积剂量和3AB指数的影响作用明显,而GPA NN基因突变频率仅受放射工龄影响,与累积剂量和3AB指数的相关性不明显.结论 对于职业低剂量电离辐射受照人群,GPA NO基因突变频率可较好地反映电离辐射诱发的DNA损伤效应和个体的辐射易感性,较GPA NN基因突变频率更适宜和敏感.     

Oxidative stress and genotoxicity in Rhinella arenarum (Anura: Bufonidae) tadpoles after acute exposure to Ni-Al nanoceramics

The employ of nanomaterials (NMs) has exponentially grown due to the large number of technological advances in industrial, pharmaceutical and medical areas. That is the case of alumina (Al) nanoparticles which are extensively employed as support in heterogeneous catalysis processes. However, these NMs can cause great toxicity because of their ubiquitous properties, such as extremely small size and high specific surface area. So, it is required to assess the potential deleterious effects of these NMs on living organisms. In the present study, we analyze the oxidative stress and genotoxic potential of a nanoceramic catalyst Ni/<gamma>-Al₂O₃ (NC) and the NMs involved in their synthesis, <gamma>-Al₂O₃ support (SPC) and NiO/<gamma>-Al₂O₃ precursor (PC) on Rhinella arenarum larvae. Biomarkers of oxidative stress and genotoxic damage were measured in tadpoles exposed to 5 and 25 mg/L of each NMs for 96 h. The results indicated an inhibition of catalase activity in tadpoles exposed to both concentrations of PC and to 25 mg/L of SPC and NC. Moreover, both exposure concentrations of PC and NC significantly inhibited superoxide dismutase activity. Exposure to the three NMs caused inhibition of glutathione S-transferase activity, but there were no significant variations in reduced glutathione levels. Oxidative stress damage (lipid peroxidation) was observed in tadpoles treated with 25 mg/L PC, while the other treatments did not produce alterations. The MNs frequency significantly increased in larvae exposed to 25 mg/L PC indicating irreversible genotoxic damage. The results show that these NMs exert genotoxic effects and antioxidant defense system disruption in R. arenarum larvae.     

接触甲醛人群鼻粘膜上皮细胞和淋巴母细胞微核率研究

通过接触甲醛人群鼻粘膜鳞状上皮细胞微核（ＮＭＮ）试验和淋巴母细胞微核（ＬＭＮ）试验发现：ＮＭＮ率阳性的接触甲醛时间平均加权浓度（ＴＷＡ）是０．５０８ｍｇ／ｍ３８周，比呈现ＬＭＮ率阳性的ＴＷＡ０．９８５ｍｇ／ｍ３小１倍，比接触时间３６４周缩短４５倍；连续接触甲醛５年以上工人的ＮＭＮ率反而低于５年以下者（Ｐ＜０．０５）；个体间的２种ＭＮ率未见有任何联系。结果提示：鼻粘膜鳞状上皮细胞是甲醛遗传毒作用的靶细胞；高浓度长时间接触甲醛后的ＮＭＮ率下降可能与甲醛对异粘膜细胞的直接杀伤作用有关。     

无菌豚鼠和无菌兔骨髓嗜多染性红细胞微核研究

对无细菌、病毒感染的无菌豚鼠和无菌兔与普通豚鼠和普通兔之间的骨髓嗜多染性红细胞微核率进行实验分析比较。带菌环境对豚鼠和兔的遗传物质的稳定性均有一定影响,普通豚鼠和普通兔骨髓嗜多染性红细胞微核率分别比无菌豚鼠和无菌兔高11倍和8倍多。在遗传背景、环境理化因子作用相同情况下,微生物可能是引起微核率升高的直接原因。无菌豚鼠和无菌兔自发微核率低,可作为检测环境中致癌、致畸和致突变物的优选实验动物。     

生川乌提取物遗传毒性研究

[目的]选用目前新药遗传毒性评价中推荐使用的3种试验方法(小鼠骨髓微核试验、鼠伤寒沙门氏菌回复突变试验、体外CHL细胞染色体畸变试验)研究生川乌的遗传毒性.[方法]小鼠骨髓微核试验设3个生川鸟提取物给药剂量组(26.0、13.0、6.5 g生药/kg)、阴性对照组和阳性对照组(环磷酰胺40 mg/kg).Ames试验选用两种方法:直接法和代谢活化法.试验菌株为鼠伤寒沙门氏组氨酸缺陷型菌株TA97、TA98、TA100、TA102、TA1535,生川乌提取物在试验中设6个剂量组(5.000、2.500、11250、0.625、0.313、0.156 mg生药/皿),同时设自发回复突变对照组、阳性对照组.体外CHL细胞染色体畸变试验也选用两种方法:直接法和代谢活化法.试验设5个生川乌提取物浓度组(5.000、2.500、1.250、0.625、0.313 mg生药/ml),阴性对照及阳性对照组.[结果]小鼠骨髓微核试验生川乌提取物各剂量组小鼠骨髓多染红细胞微核率与阴性对照组相比,差异无统计学意义(P>0.05).Ames试验生川乌提取物在加或不加肝微粒体酶(S9)时均未见引起TA97、TA98、TA100、TA102、TA1535试验菌株基因突变,即Ames试验阴性,试验重复一次,所得结论相同.体外CHL细胞染色体畸变试验生川乌提取物在加或不加S9时均未引起CHL细胞的染色体畸变,试验结果为阴性,试验重复1次,所得结论相同.[结论]在本实验室条件下,生川乌提取物在小鼠骨髓微核试验、Ames试验及体外CHL细胞染色体畸变试验中均为阴性结果,故认为在本实验条件下,生川乌提取物无遗传毒性.     

环磷酰胺对小鼠遗传和生殖毒性影响的研究(2)--对雄性小鼠生殖细胞的影响

目的探讨环磷酰胺对雄性小鼠生殖细胞毒性的影响。方法雄性小鼠随机分为对照组与实验组,每组10只,实验组腹腔注射环磷酰胺溶液30 mg/(kg.d),对照组腹腔注射生理盐水,连续5 d染毒,染毒后28 d取双侧睾丸和附睾,计数小鼠精子畸形率和生殖细胞微核发生情况,评价环磷酰胺对小鼠的生殖毒性作用。结果腹腔注射环磷酰胺实验组精子畸形率与对照组相比显著升高(P<0.05);实验组生殖细胞微核率与对照组相比亦显著升高(P<0.05)。结论小鼠腹腔注射环磷酰胺对雄性小鼠生殖细胞有损害作用。     

半身照射条件下以微核估计全身等效剂量可能性的探讨

作者探讨了半身照射条件下以微核（ＭＮ）率估计相当于全身一次均匀照射剂量的可能性，并与人体模型以相同条件照射后的剂量计算结果及临床反应相验证，结果显示：以ＭＮ率所估算的剂量与人体模型所计算出的相当于一次全身均匀照射的红骨髓干细胞活存计权剂量及临床反应基本一致，照后无或仅有白细胞、血小板计数的轻微下降，多数有恶心呕吐，可能与全腹照射有关。因此，在以下半身为主的高度不均匀照射条件下，ＭＮ检测所估计的生物剂量可用以表示全身等效剂量及反映全身损伤程度。     

双核淋巴细胞微核试验检测4种重金属的诱变性

用双核淋巴细胞微核实验（简称ＣＢ微核实验）对４种金属化合物进行了遗传毒性检测。结果显示：氯化镍、醋酸铅、硫酸镉和重铬酸钾可导致人双核淋巴细胞微核增加，表明这些金属化合物在一定剂量时可对人的遗传物质产生致突变作用。     

Cinnamic acid induces apoptotic cell death and cytoskeleton disruption in human melanoma cells

Anticancer activities of cinnamic acid derivatives include induction of apoptosis by irreversible DNA damage leading to cell death. The present work aimed to compare the cytotoxic and genotoxic potential of cinnamic acid in human melanoma cell line (HT-144) and human melanocyte cell line derived from blue nevus (NGM). Viability assay showed that the IC₅₀ for HT-144 cells was 2.4 mM, while NGM cells were more resistant to the treatment. The growth inhibition was probably associated with DNA damage leading to DNA synthesis inhibition, as shown by BrdU incorporation assay, induction of nuclear aberrations and then apoptosis. The frequency of cell death caused by cinnamic acid was higher in HT-144 cells. Activated-caspase 3 staining showed apoptosis after 24 hours of treatment with cinnamic acid 3.2 mM in HT-144 cells, but not in NGM. We observed microtubules disorganization after cinnamic acid exposure, but this event and cell death seem to be independent according to M30 and tubulin labeling. The frequency of micronucleated HT-144 cells was higher after treatment with cinnamic acid (0.4 and 3.2 mM) when compared to the controls. Cinnamic acid 3.2 mM also increased the frequency of micronucleated NGM cells indicating genotoxic activity of the compound, but the effects were milder. Binucleation and multinucleation counting showed similar results. We conclude that cinnamic acid has effective antiproliferative activity against melanoma cells. However, the increased frequency of micronucleation in NGM cells warrants the possibility of genotoxicity and needs further investigation.