底泥重金属铅对鲤鱼红细胞遗传物质的损伤

目的 研究河流底泥重金属污染对水生生物遗传物质的损伤。方法 在含不同浓度Pb^2 的底泥环境下饲养鲤鱼，取其红细胞涂片、染色，测定其微核细胞率。结果 底泥Pb^2 含量在196．23—2519．60mg/kg范围内时，随Pb^2 浓度升高，鲤鱼红细胞的微核细胞率也升高(P＜0．01)，表现出明显的量效关系。同时观察到，随高浓度的Pb^2 作用时间延长，红细胞的微核细胞率有升高的趋势。结论 河流底泥重金属铅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。     

人造板材释放的甲醛对小鼠骨髓细胞微核率影响

目的 探讨不同浓度气态甲醛对暴露小鼠的骨髓嗜多染红细胞微核的诱发效应。方法用不同剂量气态甲醛对小鼠进行连续动态染毒处理72h，取小鼠骨髓细胞制片，观察小鼠骨髓嗜多染红细胞微核形成率，从而判断气态甲醛对小鼠骨髓嗜多染红细胞微核的诱发效应。结果经甲醛染毒处理后，小鼠骨髓嗜多染红细胞微核率逐渐升高，与对照组相比有极显著性意义。结论甲醛可不同程度地影响小鼠骨髓嗜多染红细胞的微核形成率，并呈良好的剂量一效应关系。     

甲醛与苯对动物细胞的遗传学效应及联合毒性研究

目的探讨不同浓度的甲醛与苯对小鼠外周血红细胞、骨髓细胞微核的诱发效应。方法甲醛、苯及两者联合作用分高、中、低三个剂量组，采用静吸式染毒方法，每天2h，连续染毒15d，考查微核率的变化。结果染毒后小鼠外周血红细胞、骨髓PCE细胞微核率均明显升高，与对照组相比差异显著。结论甲醛和苯均可不同程度的影响小鼠外周血红细胞和骨髓细胞的微核细胞率，并呈现剂量效应关系，联合作用时效应最强。     

三种不同蚕豆的根尖细胞微核检测技术比较

目的利用3种不同来源的蚕豆根尖细胞进行微核试验,进行重铬酸钾、硝酸铅和环磷酰胺对蚕豆的遗传毒理学研究。方法以蒸馏水为对照组,以不同浓度的重铬酸钾(30、50、100、150 mg/L)、硝酸铅(50、100、150、200 mg/L)和环磷酰胺(1、2 mg/ml)为实验组,观察并比较不同来源的蚕豆根尖细胞微核率。结果随着环磷酰胺浓度的增加,3种蚕豆的根尖细胞微核率升高,其浓度为1 mg/ml时,松滋青皮蚕豆、农学院普通蚕豆及市售蚕豆的根尖细胞微核率分别为(29.33±7.64)‰,(21.33±8.96)‰和(16.33±5.03)‰。重铬酸钾在30~100 mg/L范围时,3种不同来源的蚕豆根尖细胞微核率均随其浓度的增加而升高(rMCN分别为0.931,0.943,0.879,P0.01),在100 mg/L浓度时蚕豆初生根细胞的微核率达最高值。随着硝酸铅浓度的增加,3种蚕豆的根尖细胞微核率均呈先增加后减小的趋势,其浓度为100 mg/L时,3种蚕豆的初生根细胞微核率达最高值,分别为(32.00±4.36)‰,(22.67±2.81)‰和(19.67±3.21)‰,其浓度为150、200 mg/L时,3种蚕豆根尖细胞微核率降低,根尖变黑、变细、变硬。结论重铬酸钾、环磷酰胺和硝酸铅均能诱发微核,但松滋青皮蚕豆最敏感,其次为天津农学院普通蚕豆,最不敏感的是市售蚕豆,提示蚕豆个体和生长环境的不同会对试验结果有影响。     

大蒜提取物对阿昔洛韦诱发的大蒜根尖细胞遗传损伤的修复作用

目的 探讨大蒜提取物对阿昔洛韦诱发的大蒜根尖细胞遗传损伤的修复作用。方法 通过微核实验,观察阿昔洛韦对大蒜根尖细胞微核的影响,研究大蒜提取物对诱变后的大蒜根尖细胞微核的修复作用。结果 低浓度阿昔洛韦（10 mg/mL）诱发的微核率与对照组差异无显著性;中、高浓度的阿昔洛韦（50～100 mg/mL）能诱发大蒜根尖细胞微核的形成,大蒜根尖细胞产生的微核率随浓度增加而升高,呈明显的剂量 效应关系。在一定的作用时间内,中、高浓度阿昔洛韦诱发的微核率随着作用时间的延长而升高,呈明显的时间-效应关系。将100 mg/mL阿昔洛韦诱变后的大蒜根尖放置于大蒜提取物中,以不同的时间进行修复培养,微核率都显著降低。但仍显著高于对照组。结论 50～100 mg/mL阿昔洛韦能诱发根尖细胞微核的产生,且微核的产生随着阿昔洛韦诱变浓度的增加或诱变时间的延长而升高。大蒜提取物对阿昔洛韦诱发的大蒜根尖细胞微核有一定修复作用。     

阿特拉津增强苯并[a]芘对Hep G2细胞的遗传毒性

目的探讨除草剂阿特拉津预处理HepG2细胞后对苯并[a]芘(B[a]p)所诱发的遗传毒性的影响。方法运用体外HepG2细胞微核试验检测不同浓度阿特拉津(62.5、125、250和500μmol/L)预处理HepG2细胞24h后对50μmol/LB[a]p诱导的微核率的影响。结果B[a]P诱发的微核率随着预处理阿特拉津的浓度增大而显著地升高,62.5、125、250和500μmol/L的阿特拉津预处理HepG2细胞后B[a]P所诱导的微核率比未预处理组分别增加了45.5%、51.6%、115.2%和145.5%。当阿特拉津预处理浓度为250和500μmol/L时,B[a]P所诱导的微核率与未预处理组的微核率相比有统计学意义的升高(P<0.01)。结论阿特拉津可显著地增强B[a]P在HepG2细胞中诱导的遗传毒性,这种遗传毒性的增强可能与阿特拉津对细胞色素P450(CYP)1A1的诱导有关。     

串场河水诱发蝌蚪血红细胞微核的研究

本文通过测定蝌蚪血红细胞微核率进行串场河河水致变效应的研究。实验中用蝌蚪作实验动物，在串场河不同地段采来的水样中染毒一周，测定其血红细胞微核率。实验结果表明，串场河水能诱发蝌蚪血红细胞微核率升高，与饮用水相比差异极显著。     

滇池水的蚕豆根尖细胞微核率及其诱变因素

本文就滇池水体对蚕豆根尖细胞微核率的影响进行了研究,结果显示放鸭区水体中含有使蚕豆根尖细胞微核率增高的诱变物。对水体中诱变物的来源作了初探,提示与Cd、Cr、Pb、As、F等诱变物无联系,可能来自养鸭场鸭粪的污染。     

硝酸铕对蚕豆根尖细胞遗传毒性的研究

目的探讨硝酸铕对蚕豆根尖细胞的遗传毒性。方法将蚕豆初生根浸入铕系列溶液(64、32、16、8、4、2、1μg/ml)中,25℃恒温培养6h,之后双蒸水中修复培养24h。切取根尖,固定、染色、镜检,统计微核率、有丝分裂指数和染色体畸变率。结果在1～32μg/ml浓度范围内,微核率随硝酸铕处理剂量的增加而升高,呈剂量-效应关系(r=0.949)。在2～64μg/ml浓度范围内,有丝分裂指数随硝酸铕处理剂量的增加而下降,呈剂量-效应关系(r=-0.852)。在1～64μg/ml浓度范围内,染色体断片和总畸变率随Eu(NO3)3处理剂量的升高而上升,且具有明显的剂量-效应关系(r剂量-断片=0.915,r剂量-总畸变率=0.872)。结论硝酸铕对蚕豆根尖细胞具有一定的遗传毒性,染色体断片可能是形成微核的原因之一。     

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.     

Phytochelatin induction, cadmium accumulation, and algal sensitivity to free cadmium ion in Scenedesmus vacuolatus

Phytochelatins are small, intracellular, metal-binding polypeptides produced by algae on exposure to increased metal concentration in their environment. The aim of the present study was to examine the relationship between phytochelatin concentration, bioaccumulated metal, and sensitivity of algal growth on cadmium exposure. For that purpose, intracellular cadmium concentration and thiol (glutathione, gamma-glutamylcysteine [gammaGluCys], and phytochelatins [PCn]) content were determined in the freshwater green alga Scenedesmus vacuolatus exposed to growth-inhibitory and noninhibitory concentrations of free Cd2+ in the range from 10(-14) to 10(-7) M. The algal growth rate was optimal up to a free Cd2+ concentration of 10(-9) M and then decreased by 40% at higher concentrations. The intracellular cadmium content increased sharply from 0.22 to 746 amol/cell over this free Cd2+ range. At the lowest Cd2+ concentration (control), glutathione was the only detectable thiol (127 amol/cell). With increasing Cd2+, formation of gammaGluCys and phytochelatins from PC2 to PC6 were observed. The predominant oligomer was PC3, with 42 amol/cell at the highest Cd2+ concentration (10(-7) M). The ratio of the concentration of total thiol groups to intracellular cadmium was important for maintaining optimal growth. In contrast, thiol groups from phytochelatins were never measured in excess to intracellular cadmium content.     

Toxicity of metal mixtures to a tropical freshwater alga (Chlorella sp): the effect of interactions between copper,cadmium, and zinc on metal cell binding and uptake

The individual and combined effects of copper, cadmium, and zinc on the cell division rate of the tropical freshwater alga Chlorella sp. were determined over 48 to 72 h. Metal mixtures were prepared based on multiples of their single-metal median effective concentration (EC50) values, i.e., toxic units (TU) using a triangular mixture design with five toxicant levels (0, 0.75, 1.0, 1.25, and 1.5 TU). Single-metal EC50 values after a 72-h exposure were 0.11, 0.85, and 1.4 microM for copper, cadmium, and zinc, respectively. Significant interactions were observed for all metal combinations after 48 and 72 h. An equitoxic mixture of Cu + Cd was more than concentration additive (synergistic) to the growth of Chlorella sp., while combinations of Cu + Zn, Cd + Zn, and Cu + Cd + Zn were all less than concentration additive or were antagonistic. To determine the effect of each metal on the uptake of the other, extracellular (membrane-bound) and intracellular metal concentrations, both alone and in mixtures, were compared. The increased growth inhibition observed for mixtures of Cu + Cd was due to higher concentrations of cell-bound and intracellular copper in the presence of cadmium compared with copper alone (i.e., cadmium-enhanced copper uptake). In contrast, both extra- and intracellular cadmium concentrations were reduced in the presence of copper. In mixtures of Cu + Zn, copper also inhibited the binding and cellular uptake of zinc, which resulted in decreased toxicity. Zinc had no appreciable effect on the uptake of copper by Chlorella sp. Our results suggest that all three metals share some common uptake and transport sites on Chlorella cells and that copper out competes both cadmium and zinc for cell binding. Determination of metal cell distribution coefficients (K(d)) confirmed that K(d) values for cadmium and zinc in single-metal exposures decreased in the presence of copper.     

Effect of pH on cadmium toxicity,speciation, and accumulation during naphthalene biodegradation

Lowering pH of a microbiological medium from 7 to 4 decreased cadmium toxicity during naphthalene biodegradation by a Burkholderia sp. Cadmium speciation and cadmium accumulation in the system were studied to explain this effect. Cadmium speciation was determined by direct measurement and by geochemical modeling. Previous studies have implicated the monovalent hydroxylated cadmium (CdOH+) species in the effect of pH on cadmium toxicity. Modeling analysis predicted CdOH+ formation only at very low concentrations (< or = 0.0128 microM), while the measured concentration of divalent ionic cadmium (Cd2+) was at least three orders of magnitude greater, suggesting that Cd2+ is the more significant metal form. With respect to cadmium accumulation, cells contained in media adjusted to pH 4 accumulated only 2.76 +/- 0.76 mg Cd/g cells, whereas cells in media adjusted to pH 7 accumulated 8.52 +/- 0.71 mg Cd/g cells. These data suggest that cadmium toxicity is correlated with increased cadmium accumulation rather than the formation of CdOH as pH is increased. At low pH, the decrease in cadmium accumulation may be caused by increased competition between hydrogen and cadmium ions for binding sites on the cell surface or by an increase in metal efflux pump activity due to an increase in the proton gradient that drives the efflux pump.     

Mechanisms of cadmium toxicity in terrestrial pulmonates: programmed cell death and metallothionein overload

A sublethal dose of cadmium (Cd2+) administered via the diet during short-term exposure over 10 d induced programmed cell death in the hepatopancreas of the terrestrial pulmonate snail Helix pomatia. Condensed cell residues were predominantly phagocytosed by calcium cells, suggesting a specific function of these epithelial cells in metal detoxification or in clearing the organ of cellular debris from cell death. The considerable cell loss recorded by histological analysis was accompanied by enhanced cell proliferation. Intoxication with Cd was further associated with the pronounced abundance of residual bodies, predominantly recorded in excretory cells, and with pathological changes in the endoplasmic reticulum. During long-term Cd exposure, mortality increased with increasing Cd concentrations in the diet, as demonstrated by feeding experiments in the laboratory. Lethal effects of Cd appeared to be correlated with Cd overloading of the Cd-specific metallothionein isoform (Cd-MT), isolated and characterized previously from the animal's hepatopancreas. Stoichiometric analysis shows that the capacity of Cd-MT to bind six molar equivalents of Cd corresponds to a tissue Cd concentration of approximately 4 micromol/g dry weight. At this tissue concentration, all high-affinity metal-binding sites of Cd-MT are occupied by Cd2+. Cadmium exposure beyond this level gives rise to progressive destabilization of Cd-MT cluster structure in vitro, resulting in increasing proportions of weakly bound, or even unbound, Cd2+ ions. Our results suggest that in vivo, the observed overburdening of Cd-MT with Cd2+ reduces the viability of affected animals.     

Biomonitoring results and cytogenetic markers among harbour workers with potential exposure to river silt aerosols

Background: Workers on dredgers and lighters on rivers are potentially exposed to a variety of substances.

Aims: To determine the internal load of heavy metals and arsenic as well as levels of cytogenetic markers in workers exposed to river silt aerosols.

Methods: One hundred exposed workers were examined up to eight times within three years. Additionally, 100 control workers were studied once. Blood samples were analysed for lead, mercury, and cadmium. Additionally, micronuclei frequency and sister chromatid exchange (SCE) rates were determined. Urinary samples were analysed for cadmium, mercury, nickel, chromium, and arsenic. Information on potential confounders, such as smoking habits and consumption of fish were assessed.

Results: Apart from some increased concentrations of mercury in blood (maximum 14.6 µg/l) and arsenic in urine (maximum 356.5 µg/l) all measurements were within reference values. None of the exposure and effect markers were found to be significantly increased in exposed workers compared to non-exposed controls. In multiple linear regression models, mercury levels in blood as well as the concentration of arsenic in urine were strongly related to fish consumption. Cadmium levels in blood as well as urinary cadmium concentrations were strongly related to smoking habits. After adjusting for smoking habits, SCE rates were associated with cadmium levels in blood.

Conclusion: Increased exposure levels or enhanced levels of cytogenetic markers were not found in workers exposed to river silt aerosols. However, cadmium exposure in blood was related to SCE frequency.

     

Cytogenetic effects of cadmium accumulation on water hyacinth (Eichhornia crassipes)

Cadmium was bioassayed to observe cytogenetic effects in the water hyacinth (Eichhornia crassipes). Plants were exposed for 96 hr to freshwater containing 0.01, 0.05, 0.10, 1.5, and 10 mg/liter of cadmium. Metal concentrations in tissues were determined by atomic absorption spectrophotometry. The highest level was found in roots, thus root-tip cells were used for cytogenetic studies; after 24 hr of exposure, micronuclei, c-mitotic effects, and pycnosis were detected and after 48 hr polyploidy was observed. A linear relationship between frequencies of micronuclei and cadmium concentrations was found: at 1.5, and 10 mg/liter micronuclei numbers were always the lowest. The inhibition of cell proliferation. shown by the low mitotic index, was proportional to the concentration and time of exposure. From the results presented in this paper it may be concluded that water hyacinth is a good sensor, due to its fast rate of metal accumulation, which allows an easy way to determine the presence of potential mutagenic compounds in water.     

Low dose exposure to cadmium and its health effects. (3) Toxicity in laboratory animals and cultured cells

We have reviewed studies on cadmium (Cd) toxicity in laboratory animals and cultured cells with special attention to the disruption in cellular signal transduction, involvement in apoptosis of Cd, the cellular transport system for Cd and roles of metallothionein as a protective factor against Cd. Cd affects cellular functions by perturbing signal transductions, such as protein kinase C, mitogen-activated protein kinase and cyclic AMP pathways, but how the disruption of these pathways by Cd leads to the manifestation of toxicity in vivo is largely unknown. Exposure to cadmium at relatively high and low levels causes necrosis and apoptosis, respectively, which suggests that the mode of cell death by cadmium is dependent upon its exposure level. On the other hand, utilization of Ca2+ channels, DMT1 (divalent metal transporter 1) and a novel transport system having high-affinity for Mn2+ and Cd2+ were found to act as Cd transport systems via the cellular membrane. Metallothionein-I/II-null mice are highly susceptible to renal toxicity, hepatotoxicity, bone injury, hematotoxicity and immunotoxicity caused by chronic Cd exposure. Thus, metallothionein plays an important role in detoxification of Cd toxicity.     

Effect of cadmium on transmembrane Na+ and K+ transport systems in human erythrocytes.

The effects of cadmium (Cd2+) on Na+,K(+)-ATPase in disrupted human erythrocyte membranes and on various transmembrane Na+ and K+ transport systems in intact erythrocyte suspensions were studied. Cadmium2+ inhibited the erythrocyte Na+,K(+)-ATPase enzyme with a 50% inhibition at a Cd2+ concentration of 6.25 microM. The Cd2+ inhibition in the human erythrocyte was non-competitive with respect to Na+,K+, and ATP. Cadmium2+ exerted no acute effect, however, on the Na+,K(+)-ATPase pump activity as measured by the ouabain sensitive 86Rb uptake or Na+ efflux in intact red blood cells. Cadmium2+ also inhibited the Ca2+ dependent K+ channels in human red blood cells, whereas it had no effect on Na+,K+ cotransport, Na+,Li+ countertransport, anion carrier, and the number of active Na+ pump units. The data indicate that in human erythrocytes under acute conditions Cd2+ exerts an inhibitory effect on Na+,K(+)-ATPase enzyme in disrupted erythrocytes and the Ca2+ stimulated K+ efflux in intact red blood cells without affecting the Na+ pump, Na+,K+ cotransport, and Na+,Li+ countertransport activity.