不同类别农药助剂对蚯蚓(Eisenia foetida)的急性毒性

为评价农药助剂对土壤生物的毒性效应,分别采用滤纸接触法和人工土壤法测定了不同类别农药助剂对赤子爱胜蚓(Eisenia foetida)的急性毒性。结果表明：19种非离子表面活性剂中,烷基酚聚氧乙烯醚与脂肪醇聚氧乙烯醚毒性较高,滤纸法48 h-LC₅₀为7.630～39.65 μg·cm^-2,人工土壤法14 d-LC₅₀为876.5～2786.6 mg·kg^-1,其它类型非离子表面活性剂毒性较低。5种阴离子表面活性剂中,十二烷基硫酸钠、十二烷基苯磺酸钙毒性高于木质素磺酸钠、木质素磺酸钙、亚甲基双萘磺酸钠,滤纸法48 h-LC₅₀为6.575～41.89 μg·cm^-2,人工土壤法14 d-LC₅₀为1195.0～1911.7 mg·kg^-1。13种溶剂中,二甲苯、乙苯、甲苯、正丁醇、环己酮表现出较高的毒性,滤纸法48 h-LC₅₀为6.587～57.62 μg·cm^-2,密封人工土壤法48 h-LC₅₀为181.9～781.5 mg·kg^-1。采用两种方法测得的5种填料高岭土、白炭黑、硅藻土、凹凸棒土和轻质碳酸钙的毒性均较低。由此可见,采用两种方法测得的毒性系统偏差接近,重现性均较好,并且滤纸接触法测得的毒力高于人工土壤法。     

全氟辛烷羧酸(PFOA)与全氟辛烷磺酸(PFOS)的细胞毒性效应

新型污染物全氟辛烷羧酸(PFOA)与全氟辛烷磺酸(PFOS)在全球范围内的各种环境介质中被广泛检出,对生态安全和人体健康造成威胁。利用MTT(噻唑蓝)法研究了PFOA/PFOS对人体细胞的毒性效应。结果表明,低剂量PFOA和PFOS对人体正常肝细胞增殖具有显著毒性,其3 d半数抑制浓度(IC50值)分别约为5和0.5μg·L-1。此外,PFOA和PFOS均对MCF-7细胞增殖表现出显著的非单调剂量-毒性效应,并且在环境浓度范围(0.6μg·L-1)内均可促进MCF-7细胞增殖,表现出潜在的类雌激素作用风险。     

4-硝基酚对大鼠肝脏的毒性及氧化损伤

研究环境内分泌干扰物4-硝基酚(4-nitrophenol,PNP)对大鼠肝脏功能的毒性作用及其对核因子相关因子-2(Nrf2)通路的影响.20只SD雄性大鼠随机分成4个组,分别为对照组、1、10和100 mg·kg-1体重PNP处理组,连续皮下注射28d,检测肝脏的结构变化、氧化损伤和Nrf2及其相关基因的表达情况.结果表明,与对照组相比,100 mg·kg-1PNP处理组大鼠的血清肝功能主要指标ALT、AST、AKP活性和TBIL含量显著性升高p＜005);100 mg·kg-1组肝脏GSH-PX、CAT和SOD活性显著性降低p＜005);大鼠肝脏中Nrf2及其下游基因NQOI和HO-1 mRNA表达水平在1mg·kg-1组显著升高(p＜0.05),10、100 mg·kg-1组有升高趋势;100 mg ·kg-1组肝脏显微和超微结构都发现有不同程度的损伤.结果提示,皮下注射1 mg·kg-1 PNP引起了大鼠肝脏氧化损伤,机体可能通过提高Nrf2及其相关基因mRNA的表达水平来抵抗PNP引起的肝脏损伤;皮下注射100 mg·kg-1 PNP改变了肝脏的正常生理功能,造成肝细胞超微结构病理损伤,引起肝脏毒性.     

吡草醚原药对大鼠胚胎及胎仔发育的影响

经口染毒大鼠检测妊娠动物接触吡草醚原药后引起致畸的可能性,初步评价吡草醚原药致畸危害程度。依据《GB15670-1995农药登记毒理学试验方法》,选用的大鼠按雄、雌2:1比例同笼交配,次日清晨阴道涂片检查雌鼠,发现精子即确定为受孕第0天,设低、中、高三个剂量组(18.56、92.80、464.00 mg·(kg·d)-1)、一个阴性对照组和一个阳性对照组。在雌鼠受孕第6~15天灌胃给予受试物,连续共10天,在妊娠第19.5天,处死孕鼠检查胚胎发育情况。高剂量组和阳性对照组大鼠孕期体重增重值降低,差异有显著性(p0.05);中、高剂量组和阳性对照组大鼠吸收胎率与阴性对照组比较差异有显著性(p0.05);中、高剂量组和阳性对照组胎鼠重量与阴性对照组比较,差异有显著性(p0.01);阳性对照组胎鼠外观畸形明显,与阴性对照组比较差异有显著性(p0.01);各剂量组胎鼠外观畸形与阴性对照组比较,差异均无显著性(p0.05);中、高剂量组组和阳性对照组胎鼠骨骼及内脏畸形例数明显增多,差异有显著性(p0.01)。实验结果表明吡草醚原药中、高剂量组可明显影响雌鼠体重增长及其胚胎的发育。     

The polymorphism of the human serum paraoxonase †

The activity of paraoxonase, the enzyme which hydrolyses paraoxon, 0,0‐diethyl‐0–4‐nitrophenylphosphate, in human serum shows a genetically determined polymorphism with strong interethnic differences. The serum paraoxonase genotype has a significant influence on the paraoxon clearance. Individuals with high serum paraoxonase activity may be better protected against the toxic effects of parathion (0,0‐diethyl‐0–4‐nitrophenylthiophosphate).

In Caucasians the polymorphism is governed by two alleles. The first allele has a gene frequency p _low of 0.67 to 0.78, and is manifested in both the form of a first homozygotic group with low activities and a second heterozygotic group with medium activities. About 50% of all Europeans belong to the low activity group. The second allele with a gene frequency q _high of 0.22 to 0.33 is manifested in the second heterozygotic and a third homozygotic group with medium resp. high activities. The Hardy‐Weinberg rule for a two allele model is valid for the distribution.

The percentage of the low activity group decreases as one moves from Europe to Africa and Asia. In most of the Mongoloids and Negroids only 5 to 20% of the population can be included in the low activity group, which is not even demonstrable in Aborigines, Maoris, Tonga and some African and Indian (Central America) tribes. The validity of the Hardy‐Weinberg rule for a two‐ or three‐allele model must be rejected in non‐Caucasians.     

Choice of chelating antidotes for acute cadmium intoxication∗

During acute oral intoxication by cadmium compounds, gastrointestinal epithelial damage contributes to immediate toxicity. However, secondary systemic toxicity may develop due to intestinal uptake of cadmium. This review presents an evaluation of the effects of chelators on the acute toxicity of cadmium after parenteral or oral exposure and on the intestinal uptake of cadmium. This review shows:

1. Chelating agents may affect the acute toxicity of cadmium in a variety of ways depending on the exposure route for cadmium and administration route for the chelator.

2. With regard to survival, systemic toxicity of absorbed cadmium is of major importance, as intraperitoneal administration of chelators could eliminate or reduce mortality due to orally administered cadmium chloride.

3. Lipophilicity of chelators and their cadmium complexes may result in extensively augmented intestinal uptake. However, hydrophilic chelators may efficiently reduce the intestinal cadmium uptake.

4. For hydrophilic chelators, the stability of the cadmium complex is an important determining factor of efficacy.

5. The optimal oral antidote towards orally administered cadmium are the BAL analogs, especially DMSA, while the optimal intraperitoneal antidotes towards orally or intraperitoneally administered cadmium are the higher members of the polyaminopolycarboxylate family, especially TTHA.

6. When administered simultaneously (DMSA orally and TTHA intraperitoneally), these chelators synergistically reduce the whole‐body retention of cadmium.

In conclusion, chelation treatment in acute oral cadmium intoxication should first prevent/reduce intestinal damage and uptake by rapid oral administration of a chelating antidote and then alleviate systemic toxicity due to absorbed cadmium and enhance renal/biliary cadmium excretion by parenteral administration of a chelating antidote.     

Metallothionein induction in mice by CCL4: Hepatic Zn‐status and distribution of administered Cd∗

Induction of metallothionein (MT), Zn status and the subcellular distribution of administered Cd were studied in liver after single administration of CC1₄ to mice. Hepatic MT was increased up to 153±16 μMT/g liver 18 h after injection of 2ml CCl₄/kg body weight. The observed decrease in Zn bound to cytosolic high molecular weight proteins from 25.5 ± 0.6 to 19.8±1.1 resp. 19.0 ± 1.7 μgZn/g and the increase in MT bound Zn from 4.0±0.5 to 9.5 ± 1.1 resp. 10.9±1.1 μgZn/g compensate each other.

Zn content of whole liver and hepatic cytosol remained unchanged. Hepatic subcellular distribution of 4 mg Cd/kg body weight, administered 2 h prior termination was also influenced by CC1₄. Cd bound to high molecular weight proteins decreased from 10.0±1.0 to 7.2±1.6 resp. 3.7 ± 2.6 μg Cd/g and Cd bound to MT increased from 12.5 ± 1.4 to 18.0 ± 3.8 resp. 23.1± 6.4 μgCd/g. Cd content of both, whole liver and cytosol was not significantly different from control. The induction of MT has been suggested to be beneficial due to its role in the sequestration of toxic metals. The depletion of Zn from cytosolic high molecular weight proteins however might adversively influence essential physiological processes.     

Application of QSARS to predict potential aquatic toxicities of organochlorine pesticides∗

On the basis of physico‐chemical data, such as water solubility and vapour pressure as well as acute toxicity tests we developed an ecotoxicological model for preliminary hazard assessment. By use of the reciprocal product from log H and LC₅₀ we developed a suitable ranking system that allows us to predict potential damage to aquatic organisms through pesticides.     

Nickel toxicity in partially hepatectomized rats: I. accumulation of radioactive nickel in various organs and subcellular fractions of liver

The distribution of radioactive nickel (50 μmol/kg/200μ Ci S.C.) was studied in various organs as well as in the hepatic subcellular fractions of sham operated and partially hepatectomized rats at 16 hr after injection. ⁶³Ni was maximally accumulated in kidney followed by lung, liver, heart and spleen. The incorporation of ⁶³Ni was lowered in partially hepatectomized rats compared to sham operated ones. Subcellular binding of ⁶³Ni showed significantly high affinity of nickel to cytosol followed by nuclear, mitochondria and microsomes in both the groups.     

pH值和硬度对两种氯酚类化合物对大型溞急性毒性的影响

以大型溞为研究对象,系统研究了pH值和硬度对2,4,6-三氯酚(2,4,6-TCP)和五氯酚(PCP)对大型溞急性毒性的影响.结果表明,pH值的影响非常显著.在实验pH值范围内(6~10),随pH值升高,两种氯酚对大型溞的急性毒性迅速降低,对不同pH值下两种氯酚在水中的形态分布与其毒性的相关性分析显示,pH值对毒性的影响机制与氯酚在水中的存在形态有密切关系,氯酚类物质的毒性主要由其分子态贡献,而pH值的升高促使分子态向离子态转化从而使其毒性降低.与pH值相比,硬度虽然对两种氯酚对大型溞急性毒性有一定的影响,但影响不显著.因此,在制定该类污染物的基准和标准时水体硬度的影响可以不作为关键因素考虑.