The use of the embryo‐culture techniques in the research on the Teratogenic and Mutagenic properties of metals†

Actually, embryos can be cultured from the one‐cell stage up to the blastocyst stage, and their development can be easily monitored at any time: severe effects caused by toxic compounds are traduced by rapid embryonic death, less pronounced effects can be expressed by a lowered cleavage activity or by an arrest of the development from a particular stage. The system can be improved by transferring the embryos at the blastocyst stage in another more complete medium where they can “implant”; and form an inner cell mass with differentiated ectoderm and endoderm. Since last years, it has also become possible to culture postimplantation rodent embryos for short periods involving a number of particularly critical stages of organogenesis, such as the formation and closure of the anterior neuropore. Embryo‐culture also represents a useful system to study cytogenetic effects of chemicals which are often linked to lethal or teratogenic effects. These different possibilities are illustrated by examples of studies already performed with metals, and dealing with their teratogenic and/or cytogenetic effects on pre‐ and postimplantation rodents.     

Comments on the Carcinogenicity and Mutagenicity of metals and their compounds†

The carcinogenicity of metals has received extensive study, both epidemiologically and in the laboratory. These have included case reports of occasional human occurrence or clusters of cancer cases as well as extensive epidemiologic studies; in addition, there has been significant laboratory research on the whole animals and in vitro systems. This body of information will be examined selectively.

I will not in this paper attempt a comprehensive review of the mutagenicity and carcinogenicity of metals and their compounds. Rather, I will attempt to set forth some historical perspectives, and to comment on some current gaps and needs.

Other papers in this workshop have presented thorough and very current reviews of most of the topics briefly noted in this presentation and do not require repetition here.

The cancer issue has been studied and reported on far more extensively than that relating to heritable mutations. There has been in recent years increasing interest in the use of short term tests for mutagenicity and cell transformation. These, however, are primarily with respect to their relationship to cancer production rather than to germ cell injury. Interest in cancer from metal compounds goes back a long time; in fact, one of the earliest reports was on the carcinogenicity of arsenic not many decades after the pioneering report of Sir Perceval Pott on cancer in chimney sweeps. Since then cancer has been definitely associated in humans with chromium compounds, nickel, and with less assurance but probably definitely with beryllium and cadmium. The confirmation of these findings in laboratory animals has been uneven. In the case of arsenic, for example, there has been only limited success in the production of cancer in laboratory animals with arsenic.

Many other metals have been found in laboratory studies to produce cancer, although with most of these, evidence of production of cancer in humans is either absent or extremely uncertain.

The extensive body of recent information relating to the testing of metals with a variety of short term tests will be briefly reviewed.     

Occupational exposures,delivered doses and exposure limits for chromium and nickel†

The interaction of HCH (50 mg/kg) and dietary protein levels on microsomal drug metabolizing enzymes system and liver lipids were studied in the rats for 90 days. The results indicated that rats fed a lower protein diet and HCH has a higher rate of mortality, lower rate of growth and an increased liver weight. A significant induction in the hepatic microsomal aminopyrine‐N‐demethylase, p‐nitroanisole‐O‐dealkylase, benzo(a)pyrene hydroxylase and glutathione‐S‐transferase activity was observed in pesticide treated animals as compared to control animals. The pathological changes observed in liver of HCH treated animals consisted mainly of necrosis and fatty degeneration of hepatocytes. HCH also induced the significant accumulation of cholesterol, triglycerides, phospholipid and total lipid in liver in low protein diet animals. Protein accelerates the metabolism of HCH, resulting in a decrease of HCH concentration with the increase of dietary protein level. A close correlation existed between lipid accumulation, induction of drug metabolizing enzyme system and deposition of HCH in liver.     

Enhancement of UV and chromate mutagenesis by nickel ions in the Chinese hamster HGPRT Assay †

1. The HGPRT (Hypoxanthine‐Guanine‐Phospho‐Ribosyl‐Transferase) assay with Chinese Hamster V79 cells was used to measure the mutagenic effects of UV irradiation, potassium dichromate and nickel chloride. The agents were tested separately and in the combinations of UV plus nickel and dichromate plus nickel.

2. UV, Cr(VI) and Ni(II) were confirmed to be mutagenic in the V79 cell assay. The combination of UV(5J/m²) and Ni(II) (0.5 mM) caused a mutation rate 11.2 times above that corresponding to the sum of the individual mutation rates of these agents. The combined action of Cr(VI) (0.1 mM) and Ni(II) (0.5 mM) produced a mutation rate 2.8 fold above that corresponding to the sum of the individual rates of the separate agents.

3. The enhancing effect of nickel chloride on the mutagenicity of UV or Cr(VI) is interpreted by an interference of Ni(II) with the repair of DNA lesions.     

Large plasmids governing multiple resistances to heavy metals: A genetic approach∗

Gram negative bacteria classified as Alcaligenes eutrophus and carrying large resistance plasmids (generally two) were found in various industrial sites highly contaminated by heavy metals (Zn⁺⁺, Cu⁺⁺, Co⁺⁺,...). These strains were detected by DNA hybridization with a probe made with a 9kb fragment (ccz⁺ fragment) encoding for resistances to Cd⁺⁺, Co⁺⁺ and Zn⁺⁺, and cloned from plasmid pMOL30. This plasmid was isolated from the representative strain A. eutrophus CH34 which harbours the plasmids pMOL30 (240 kb) and pMOL28 (165 kb). Phenotypes related to pMOL28 and pMOL30 include the tolerance to Cd⁺⁺, Co⁺⁺, Cr0₄ ⁼, Cu⁺⁺, Hg⁺⁺, Ni⁺⁺, Pb⁺⁺ and Zn⁺⁺. The described genetic properties of these plasmids refer to some cloned or mapped functions and to some plasmid rearrangements. Plasmid pMOL85 (250 kb) which is related to pMOL30 was also described. Its host (A. eutrophus DS185) was isolated from a zinc desert. pMOL85 can efficiently self transfer in plasmidfree derivatives.     

含柠檬酸盐电镀废水的处理

对含柠檬酸盐电镀废水的几种处理方法的比较表明,氯化钡添加法能较好地使柠檬酸盐沉淀,操作简便,处理效果理想,其柠檬酸根离子的去除率达98％以上。     

污泥施肥时重金属镍对农作物的毒害研究

采用盆栽和小区试验,研究了在石灰性土壤中镍污染对小麦和水稻的影响;两种作物对土壤中镍的吸收、迁移和累积规律。建议农田污泥施肥时镍的控制标准为330PPm。     

大气降尘对土壤重金属累积量估算方法探讨——以重庆市綦江县永新冶炼厂为例

中国的有色金属冶炼企业、矿区周围土壤重金属污染日趋严重.本文对可能造成土壤污染的途径进行了简要分析,并以重庆市綦江县永新冶炼厂为例,分析了冶炼厂排放废气中含重金属颗粒物沉降进入土壤的途径,结合厂址周围土壤中镍含量的监测数据,计算分析了冶炼厂投产30年后,受影响区域因大气降尘引起的土壤镍污染分布状况及趋势,估算得出每年大约有250 kg的镍沉降到厂址周围约4 km2范围内的土壤中,自然沉降率约为32%,为区域土壤重金属污染防治提供了科学依据.     

镍渣的重金属浸出特性

在分析镍渣的矿物相组成和重金属元素含量的基础上,鉴定了镍渣样品的浸出毒性,并考察了pH、液固比和浸出时间等条件对镍渣样中铬、铅、铜和锌等重金属浸出特性的影响。结果表明,镍渣中的重金属总量约为渣样的0.9%,且铬、铜和锌的含量较高,需进行安全管理。实验所用镍渣样品为第Ⅰ类一般工业固体废物。在强酸条件下镍渣中重金属浸出浓度较大,pH3后浸出浓度显著降低;液固比40 L/kg时,镍渣中重金属不断溶出,液固比40 L/kg后,浸出达到饱和,浸出浓度趋于平衡;随着浸出时间的增加,重金属离子的浸出浓度先增加后减少,但由于各重金属性质不同,各重金属达到最大浸出浓度的时间不同。