底泥重金属镉对鳙鱼血细胞微核率的影响

目的 研究河流底泥重金属镉污染对鳙鱼血细胞微核率的影响。方法 在含不同浓度Cd^2 底泥环境下饲养鳙鱼，并分别于实验的15、25、35、45、55、65、75和85d，每次每组随机取4尾鱼，取其血细胞涂片、染色．测定其微核细胞率。结果 底泥Cd^2 含量与水体中Cd^2 浓度正相关；随水体中Cd^2 浓度升高，鳙鱼血细胞的微核细胞率也升高，表现出明显的量效关系。结论 河流底泥重金属镉污染对细胞遗传物质有损伤作用。     

SO2吸入对小鼠骨髓细胞微核的诱发效应

目的 探讨空气中SO2污染物遗传毒理效应。方法 采用SO2吸入染毒法，对SO2吸入诱发小鼠骨髓嗜多染红细胞（PCE）形成微核（MN）的效应进行研究。结果 （1）SO2吸入可引起小鼠骨髓PCE微核率和微核细胞率显著升高；（2）随着吸入的SO2浓度的增高，单微核细胞率、双微核细胞率均显著升高。结论 随SO2浓度增加，细胞遗传物质损伤加重，且有明确的剂量-效应关系，表明SO2空气污染物是染色体断裂剂和基因毒性因子。     

硒和锗拮抗苯致小鼠骨髓细胞微核的实验观察

采用小鼠骨髓嗜多染红细胞微核试验方法观察微量元素硒和锗的抗苯诱变活性。结果：苯吸入染毒（１５ｍｇ／Ｌ×５天，每天２小时）后，小鼠微核率明显增高。在苯处理前３０分钟经口给予不同浓度的亚硒酸钠（００５～２５０ｍｇ／ｋｇ）或锗－１３２（５０～５００ｍｇ／ｋｇ），微核细胞率显著降低，微核抑制率随硒或锗剂量的增加而升高。提示，硒和锗对苯诱导的遗传物质损伤具有保护作用     

用彗星实验和微核实验检测地面水污染的遗传毒性效应

目的探索应用彗星实验(单细胞凝胶电泳技术,SCGE)测定鲤鱼红细胞DNA损伤以评价地面水污染遗传毒性效应的可行性。方法应用单细胞凝胶电泳和微核实验对污染指数(PI)不同的5种河流中采集的鲤鱼的红细胞DNA损伤和微核率进行测定。结果5种地面水水源中的鲤鱼红细胞DNA损伤情况不全相同,与阴性对照组比较差异有显著性(P<0.05),与污染严重程度呈正相关,趋势与微核实验一致。结论SCGE测定鲤鱼红细胞DNA损伤,可以检测地面水的污染状况。     

气态甲醛对小鼠外周血淋巴细胞和肝细胞微核率的影响

目的研究气态甲醛对细胞遗传物质的毒性。方法选用SPF级昆明种纯系雄性小鼠作为研究对象，用浓度为0．5、1．0和3．0mg／m3的气态甲醛对小鼠进行连续动态染毒72h，染毒结束后观察外周血淋巴细胞和肝细胞微核形成率。结果气态甲醛能诱导外周血淋巴细胞微核率和肝细胞微核率增加，染毒组与对照组比均有显著性差异。结论甲醛对小鼠外周血淋巴细胞和肝细胞的染色体有明显的损伤作用。     

吸烟者淋巴细胞染色体畸变和微核形成的观察

采用染色体畸变和微核分析两个具有相关性的遗传物质损伤观察指标，同时观察了男性健康吸烟者遗传物质的损伤情况。结果表明，吸烟组超倍体细胞单、染色单体型细胞畸变率、染色体型畸变率、细胞总畸变率、微核率、微核细胞率均显著高于非吸烟组。表明吸烟是诱发人体遗传物质损伤的重要诱变因素之一。     

培养温度对人血淋巴细胞微核率的影响

目的探讨细胞培养法检测微核过程中培养温度对人血淋巴细胞微核率检测结果的影响。方法将每份血液标本同时接种于四瓶淋巴细胞培养液中,一支放置（37±0．5）℃培养箱培养作为对照组;其余三支分别放置（33～39）℃的不同温度进行培养作为实验组。培养72h后同时收获细胞,制片染色,分析细胞微核率、微核细胞率、转化率,结果进行统计学分析。结果经统计学分析,实验组的细胞微核率和微率细胞率明显高于对照组,差异有统计学意义（P〈0．01和P〈0．05）,实验组的细胞微核率和微率细胞率各组间比较差异无统计学意义（P〉0．05）;B组和C组的淋巴细胞转化率明显低于对照组,差异有统计学意义（P〈0．01）。结论体外细胞培养过程中温度的升高或降低可引起淋巴细胞微核率升高,提示细胞增殖期培养温度的变化对人血淋巴细胞遗传物质有损伤作用。     

气态甲醛致小鼠微核作用的实验研究

目的：探讨气态甲醛对细胞遗传物质可能产生的损伤作用。方法：选用SPF级昆明种纯系雄性小鼠作为研究对象，用不同剂量气态甲醛对小鼠进行连续动态染毒处理72h，于染毒结束后24h观察骨髓嗜多染红细胞微核形成率，于首次染毒后第15d观察睾丸细胞的微核率。结果：气态甲醛能诱导小鼠骨髓嗜多染红细胞微核率和早期精细胞微核率增加，均呈现一定的剂量—反应关系。表现出显著的遗传毒性（P〈0．01）和生殖毒性（P〈0．05；P〈0．01）。结论：气态甲醛对小鼠体细胞和生殖细胞的染色体具有明显的损伤作用。     

饮水微囊藻毒素在实验性肝癌形成中对遗传物质的损伤作用

[目的]探讨饮水摄入微囊藻毒素在大鼠实验性肝癌形成模型中对遗传物质的损伤作用。[方法]建立微囊藻毒素促大鼠肝癌前病变的短期实验模型，检测饮水摄入低剂量微囊藻毒素在促肝癌作用的同时诱导骨髓嗜多染红细胞微核的作用。[结果]染毒组大鼹 骨髓嗜多染红细胞微核率明显升高。分别为：饮藻水 二乙基亚硝胺（DEN）启动组11.67‰，腹腔内注射微囊藻纯毒素 DEN启动组14.57‰，与DEN启动组6.80‰比较，有显著性差异。[结论]饮用受微囊藻毒素污染的水，可增强DEN对遗传物质的损伤。     

接触低浓度苯系混合物作业工人细胞微核率及染色体断裂率…

目的：探讨混合苯对作业工人遗传物质是否有损害。方法；采用微核技术对混合苯作业工人４１人进行微核及染色体断裂率观察，结果：工人的微核率，微核细胞率及染色体断裂三项指标分别为１４．４９‰，１２．９７‰，１．７５％均明显高对照组（Ｐ〈０．０１）。在岗年限６年以上组三项指标均高于在岗年限５年以下组（Ｐ〈０．０１）。结论：混合苯对作业工人遗传物质具有损害作用。其损害程度随着接触时间呈递增趋势。     

铜离子诱发■鲦鱼红细胞微核及核异常的研究

目的通过■鲦鱼红细胞研究铜离子的遗传毒性,寻找对诱变物敏感的鱼类。方法选择120尾■鲦鱼,随机分为8组,每组15尾,分别用Cu2+浓度为0.01、0.02、0.04、0.08、0.16、0.32、0.64、1.28mg/L的CuSO4溶液染毒,染毒在同一规格的塑料箱内进行。对照组以纯净水饲养。每一浓度组在6、12、24、48h时随机取鱼3尾(0.64mg/L组每次处理2尾),用纱布将鱼体表水分擦干。断尾取血,涂片,观察不同浓度、不同染毒时间铜离子对■鲦鱼红细胞微核及核异常的影响。结果各染毒组■鲦鱼红细胞微核率及核异常率均低于对照组,差异有统计学意义(P<0.05或P<0.01)。在12、24h时,在一定浓度(0.01～0.16mg/L)范围内■鲦鱼红细胞微核率与铜离子浓度成正相关,但当浓度过高(0.32、0.64mg/L)时,微核率反而降低。当铜离子浓度较低(0.01～0.08mg/L)时,微核率随染毒时间的延长而升高。结论■鲦鱼对诱变物敏感,可以作为微核实验的良好材料来检测诱变物的遗传毒性。     

Hematological findings in neotropical fish Hoplias malabaricus exposed to subchronic and dietary doses of methylmercury, inorganic lead, and tributyltin chloride

Hematological indices are gaining general acceptance as valuable tools in monitoring various aspects the health of fish exposed to contaminants. In this work some effects of methyl mercury (MeHg), inorganic lead (Pb2+), and tributyltin (TBT) in a tropical fish species were evaluated by hematological methods after a trophic exposition at a subchronic level. Forty-two mature individuals of the freshwater top predator fish Hoplias malabaricus were exposed to trophic doses (each 5 days) of MeHg (0.075 microg g(-1)), Pb2+ (21 microg g(-1)), and TBT (0.3 microg g(-1)) using young fish Astyanax sp. as prey vehicle. After 14 successive doses over 70 days, blood was sampled from exposed and control groups to evaluate hematological effects of metals on erythrocytes, total leukocytes and differential leukocytes counts, hematocrit, hemoglobin concentration, and red blood cell indices mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC). Transmission electron microscopy and image analysis of erythrocytes were also used to investigate some morphometric parameters. Results show no significant effects in MCH and MCHC for all tested metals, but differences were found in erythrocytes, hemoglobin, hematocrit, MCV, and white blood cells counts. The number of leukocytes was increased in the presence of MeHg, suggesting effects on the immune system. Also the MCV increased in individuals exposed to MeHg. No ultrastructural damages were observed in red blood cells but the image analysis using light microscopy revealed differences in area, elongation, and roundness of erythrocytes from individuals exposed to Pb2+ and TBT but not in the group exposed to MeHg. The present work shows that changes in hematological and blood indices could highlight some barely detectable metal effects in fish after laboratory exposure to contaminated food, but their application in field biomonitoring using H. malabaricus will need more detailed studies and a careful consideration of environmental parameters.     

Comparison of in vivo effect of inorganic lead and cadmium on glutathione reductase system and delta-aminolevulinate dehydratase in human erythrocytes.

The activity of delta-aminolevulinate dehydratase (ALAD) of erythrocytes, the lead (Pb-B) and cadmium (Cd-B) concentration in whole blood, the content of reduced glutathion (GSH) in erythrocytes, and the regeneration rate of GSH by intact erythrocytes were measured during an epidemiological survey of 84 men employed in a Belgian cadmium and lead producing plant. A control group of 26 persons (students and laboratory staff) was also examined. The logarithm of the ALAD activity is highly inversely correlated with log Pb-B (r = -0.760) but no correlation was found with log Cd-B. There exists a significant negative correlation between GSH and log Pb-B (r = -0.423) but not between GSH AND LOG Cd-B. The apparently good relationship between log ALAD and GSH disappeared completely by holding log Pb-B constant, but log ALAD remained highly inversely correlated with log Pb-B when standardized for GSH concentration (r = -0.748). In vivo investigation of the GSH regeneration rate of intact erythrocytes demonstrated clearly that the overall activity of the glutathione oxidation-reduction pathways is not impaired in Pb and Cd-exposed workers with significantly increased Pb-B and Cd-B, since their initial GSH regeneration rate (first 15 minutes) was identical with that of the control group. Results of similar in vitro experiments in which control whole blood was incubated before-hand with Pb2+ or Cd2+, or both, reinforce this conclusion. Since increased Cd-B and Pb-B do not influence the glutathione reductase system of erythrocytes, and since endogenous erythrocyte GSH is not correlated with Cd-B, the moderate decrease in endogenous erythrocyte Gsh found in Pb-exposed workers might result from a Pb-induced impairment for the erythrocyte mechanism for glutathione synthesis.     

Comparison of in vivo effect of inorganic lead and cadmium on glutathione reductase system and delta-aminolevulinate dehydratase in human erythrocytes.

The activity of delta-aminolevulinate dehydratase (ALAD) of erythrocytes, the lead (Pb-B) and cadmium (Cd-B) concentration in whole blood, the content of reduced glutathion (GSH) in erythrocytes, and the regeneration rate of GSH by intact erythrocytes were measured during an epidemiological survey of 84 men employed in a Belgian cadmium and lead producing plant. A control group of 26 persons (students and laboratory staff) was also examined. The logarithm of the ALAD activity is highly inversely correlated with log Pb-B (r = -0.760) but no correlation was found with log Cd-B. There exists a significant negative correlation between GSH and log Pb-B (r = -0.423) but not between GSH AND LOG Cd-B. The apparently good relationship between log ALAD and GSH disappeared completely by holding log Pb-B constant, but log ALAD remained highly inversely correlated with log Pb-B when standardized for GSH concentration (r = -0.748). In vivo investigation of the GSH regeneration rate of intact erythrocytes demonstrated clearly that the overall activity of the glutathione oxidation-reduction pathways is not impaired in Pb and Cd-exposed workers with significantly increased Pb-B and Cd-B, since their initial GSH regeneration rate (first 15 minutes) was identical with that of the control group. Results of similar in vitro experiments in which control whole blood was incubated before-hand with Pb2+ or Cd2+, or both, reinforce this conclusion. Since increased Cd-B and Pb-B do not influence the glutathione reductase system of erythrocytes, and since endogenous erythrocyte GSH is not correlated with Cd-B, the moderate decrease in endogenous erythrocyte Gsh found in Pb-exposed workers might result from a Pb-induced impairment for the erythrocyte mechanism for glutathione synthesis.     

土壤中萘降解菌的耐铅性能及机制初步研究

目的探讨土壤中萘降解菌对萘和重金属双重污染的耐受性。方法对油田石油污染土壤中分离到的一株高效萘降解菌——伯克霍尔德菌(Burkholderia sp.)TN的重金属耐受性、铅富集机制及在土壤生物修复中的应用进行研究,以分光光度法测定不同Pb~(2+)浓度(100~500 mg/L)对菌悬液吸光度的影响,以电感耦合等离子体发射光谱仪(ICP-OES)测定培养基中重金属(50 mg/L,Pb~(2+),Zn~(2+),Cu~(2+)和Cd~(3+))在菌体培养液、细胞壁、细胞内富集物中的分布,以扫描电镜(SEM)、能谱仪(EDS)和傅里叶变换红外光谱(FTIR)观察100 mg/L Pb~(2+)对菌体形态、元素及官能团分布的影响。结果菌株TN对Pb~(2+)的最高耐受浓度为500 mg/L并可耐受一定浓度的Zn~(2+)、Cu~(2+)和Cd~(3+),TN对Pb~(2+)富集程度最高,细胞壁及胞内富集率达到98.33%;菌体蓄积Pb~(2+)后细胞壁表面有沉淀物附着并有铅元素检出,对Pb~(2+)的蓄积主要依靠细胞壁上的羧基、羟基、酰胺基及磷酸基团;将TN菌株接种到含有2.5 mg/g萘及200 mg/L Pb~(2+)的灭菌土壤中,经过13 d室温培养之后,萘的去除率为94.29%。结论 TN菌株对Pb~(2+)、Zn~(2+)、Cu~(2+)和Cd~(3+)均具有一定的耐受性,对Pb~(2+)的富集能力强。该菌株能够依靠细胞壁上的活性基团富集Pb~(2+),适用于萘和Pb~(2+)双重胁迫的土壤修复。     

Induction of micronuclei in eel (Anguilla anguilla L.) by heavy metals

Micronucleus test was performed in situ on eels (Anguilla anguilla) from river sites with different levels of heavy metal pollution (cadmium and mercury). Cadmium content in eel liver but not micronuclei averages in kidney were associated with cadmium content in sediments. Mercury content in liver was not significantly associated with mercury content in sediments. Both cadmium and mercury induced micronuclei expression in eels when injected, the concentration tested being 1.7 mg metal/kg body weight and the micronuclei induction being 2.64 and 2.35 micronuclei per 1000 cells for cadmium and mercury respectively. It was concluded that these heavy metals are genotoxic for European eel, that eel liver metal content is a sensitive indicator for environmental monitoring of cadmium pollution, and that the micronuclei scores in eels are not a sensitive method to detect heavy metals pollution in freshwater ecosytems.     

Distribution of lead-203 in human peripheral blood in vitro.

In-vitro experiments using 203Pb were performed to identify the lead binding components in human peripheral blood. The distribution of lead in plasma, in the red cell membrane, and within the red cell was also investigated. Studies of the distribution of 203Pb in whole blood showed that at a lead concentration of 2.45 mumol/l (50 micrograms/100 ml) about 94% of lead had been incorporated by the erythrocytes and 6% remained in the plasma. After extraction of lipid by a methanol/chloroform mixture, about 75% of the lead was found to be associated with the protein fraction. The lipid contained about 21% of the 203Pb, the remainder being in the aqueous plasma. SDS polyacrylamide gel electrophoresis of blood plasma showed that almost 90% of the 203Pb was present in the albumin fraction; the remainder was likely to be associated with high molecular weight globulins. Several binding sites were identified on the erythrocyte membrane. The high molecular weight component, about 130 000-230 000, was the most important 203Pb binding site. Chemical modification of membrane proteins suggested that the carboxyl groups are the major ligand responsible for most of the lead binding. SH groups of the membrane may have a minor role, but amino groups did not appear to affect the lead binding. The binding of lead to erythrocytes was not confined to membranes, over 80% of lead in blood penetrates into erythrocytes and binds to intracellular components. Gel chromatography of the haemolysate showed that over 90% of the 203Pb was attached to the haemoglobin molecule.     

Pyruvate Kinase Activity and δ-Aminolevulinic Acid Dehydratase Activity as Biomarkers of Toxicity in Workers Exposed to Lead

Lead (Pb(2+)) is a heavy metal that has long been used by humans for a wide range of technological purposes, which is the main reason for its current widespread distribution. Pb(2+) is thought to enter erythrocytes through anion exchange and to remain in the cell by binding to thiol groups. Pyruvate kinase (PK) is a thiol-containing enzyme that plays a key role in erythrocyte cellular energy homeostasis. δ-aminolevulinic acid dehydratase (δ-ALAD) is the second enzyme in the heme biosynthetic pathway and plays a role in the pathogenesis of Pb poisoning. Our primary objective was to investigate the effect of Pb(2+) on the activity of the thiolenzymes δ-ALAD and PK and on the concentration of glutathione (GSH), a nonenzymatic antioxidant defense, in erythrocytes from Pb-exposed workers. The study sample comprised 22 male Pb workers and 21 normal volunteers (15 men and 6 women). The Pb-exposed workers were employed in manufacturing and recycling of automotive batteries. Basic red-cell parameters were assayed and total white blood cell counts performed. PK and δ-ALAD activity and blood Pb (BPb) concentrations were determined in all subjects. Pb-exposed individuals had significantly greater BPb levels than controls. Both PK and δ-ALAD activity levels were significantly lower in Pb-exposed individuals than in controls. Pb significantly inhibited PK and δ-ALAD activity in a dose-dependent manner. We found that erythrocyte GSH levels were lower in Pb-exposed individuals than normal volunteers. Pb-exposed individuals had lower values than controls for several red cell parameters (hemoglobin, hematocrit, red blood cell count, mean corpuscular volume). These results suggest that Pb inhibits δ-ALAD and PK activity by interacting with their thiol groups. It is therefore possible that Pb disrupts energy homeostasis and may be linked with decreased glucose metabolism because it affects the heme synthesis pathway in erythrocytes, contributing to the cell dysfunction observed in these in Pb-exposed individuals. These results indicate an apparent dose-effect relationship between PK activity and BPb. PK activity in human erythrocytes can be used for biological monitoring of Pb exposure. Study of the mechanisms by which Pb acts may contribute to greater understanding of the symptoms caused by Pb.     

Water pollution by Cu and Pb can adversely affect mallard embryonic development

The effects of heavy metal pollutants on aquatic birds have been widely studied in ecotoxicological investigations; however, the predominant focus has been on the postnatal period of life. Limited information on the adverse effects of metals to bird eggs is available. The possible toxic effects of lead and copper were studied in mallard eggs. After the accidental severe heavy metal pollution of the Tisa river (Hungary) in March 2000, these metals were detected in the highest concentration in both the water and the sediment, reaching far beyond acceptable concentrations. Pb treatment (2.9 mg/L) significantly increased the rate of mortality after a single immersion of the eggs into polluted water for 30 min. The rate of dead embryos significantly increased after the combined exposure to Cu and Pb (0.86 and 2.9 mg/L, respectively) both in the single- (once for 30 min) and in the multiple- (10s daily during first trimester of incubation) immersion groups. It was concluded that elevated metal concentrations similar to those found in the Tisa river after the tailing dam failure may cause toxic effects (mortality and teratogenicity) upon exposure of mallard eggs.