摘要:

The acute pressor effect of intraperitoneally administered cadmium was explored over the dose range 0.015–2 mg/kg in both pentobarbital‐anesthetized and conscious rats. The former first respondent at 0.031 mg/kg, and successive doublings of that dosage increased the highest pressures attained in a stepwise fashion until a dosage of 0.25 mg/kg, the maximally effective quantity, was reached. Arterial pressure did not rise in conscious rats until a dose of 1 mg/kg, which gave the maximum response within the range examined. Heart‐rate changes with Cd were slight, and rarely significant at a given dosage, but pentobarbital invariably caused tachycardia. Anesthetized rats thus gave a graded response, while conscious animals reacted in an all‐or‐none fashion. The increased pressor responsiveness of rats under pentobarbital can not be ascribed to its cardiac parasympatholytic effects, since sensitivity was not conferred upon conscious rats when pretreated with atropine at a dose producing even greater tachycardia than that caused by pentobarbital. Nifedipine, which blocks calcium entry into smooth muscle cells, prevented the pressor response to cadmium when given as pretreatment and terminated an ongoing response when give intercurrently. Possible mechanisms to account for the observed behavior are considered.

ISSN:0098-4108    

DOI:10.1080/15287398209530217

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Teratogenic and antiteratogenic effects of nine nicotinamide analogs in chick embryos were investigated. Further, the teratisms of 6‐aminonicotinamide (6‐AN), nicotinamide analogs, and an organophosphate (diazinon) were compared. White leghorn chick embryos were used. Agents were injected into the yolk of eggs on d 3 of incubation. Morphological observations were made on d 17 of incubation. Chemical names for compounds I to IX are: I, 6‐dimethylaminonicotinamide; II, 6‐diethylaminonico‐tinamide; III, 6‐methylamino‐3‐(N‐methyl)‐nicotinamide; IV, 6‐dimethylamino‐3‐pyrimidine carboximide; V, 6‐(dimethylamino)‐nicotinic acid; VI, 6‐chloro‐3‐[N‐(5‐diethylamino)‐2‐pentyl]‐nicotinamide; VII, 6‐mercaptonicotinamide; VIII, [N‐acetyl‐N'‐(3‐pyridyl)‐carbonyl]‐hydrazine; IX, nicotinamide 1‐N‐oxide. The LD50 values in μmol per egg were as follows: 6‐AN, 0.073; compound II, 0.23; compound III, 1.11; compound I, 1.32; compound VI, about 3. Compounds IV, V, VII, VIII, and IX showed no toxicity or lethality at the highest doses tested (10 μmol/egg). Among the nine nicotinamide analogs, compounds I, II, and III, which have an amino group at the 6‐position of the pyridine ring, were teratogenic. Their teratogenic signs were similar to those caused by 6‐AN: they showed growth retardation, anteriorly directed short legs, and coarse, dense feathering. The teratogenic effects of compounds I, II, and III were prevented by pretreatment with nicotinamide, as were the effects of 6‐AN and diazinon. Among the nine analogs, only compound VIII had an antiteratogenic effect against the diazinon‐induced micromelia (in which the cardinal signs were tibiotarsal anguiations and poor feathering). For teratisms produced by 6‐aminonicotinamide analogs and organophosphates, nicotinamide was an effective antiteratogenic agent. However, some differences in the malformations induced by both types of agents were found. We suggest that the addition of a 3‐acetylpyridine type to the nicotinamide‐related teratisms (6‐AN type, 3‐acetylpyridine type, and organophosphate type) will provide a clearer distinction among the types.

ISSN:0098-4108    

DOI:10.1080/15287398209530218

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Using bacterial bioassays, we have screened for the presence of mutagens and toxins in extracts from groundwater, and in tar from product gas, at the sites of two Lawrence Livermore National Laboratory (LLNL) in situ experiments: Hoe Creek II and Hoe Creek III. The sites exhibited different potential biological hazards, suggesting that different gasification processes may represent different human health concerns. We found that mutagens are present in groundwater, persist for at least 2 yr after gasification has been terminated, and show a change in activity with time‐possibly in parallel with changes in chemical composition. Preliminary evidence suggests that the mutagens in groundwater are quinoline and aniline derivatives, while the toxins in groundwater may be phenolic compounds. In tar from the product gas, the organic bases and neutrals were found to be genotoxic in both bacterial and mammalian cells; the neutral compounds appear to be the major mutagenic health hazards. Neutral compounds constitute most of the tar (85–97 wt%) and were mutagenic in both the bacterial and mammalian cell assays. Tar in the gas stream may be a problem for the aboveground environment if gas escapes through fractures in the overburden. Because it is mutagenic and induces chromosomal damage to mammalian cells, the tar may represent a disposal problem as well. However, it is difficult to assess tar quantitatively as a health hazard because its mutagenic activity is low, possibly due to contaminants in the neutral fraction that act to suppress mutagenicity.

ISSN:0098-4108    

DOI:10.1080/15287398209530219

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Cytotoxicity of ammonium metavanadate to cultured bovine pulmonary alveolar macrophages was measured by cell viability, inhibition of phagocytosis, and reduction of superoxide‐dependent chemiluminescence. The degree of toxicity was dependent on the levels of vanadium, the temperature, and the time of exposure. Thus macrophages exposed to vanadium at 0.01 and 0.1 μg/ml did not exhibit cytotoxic effects even with up to 24 h of exposure, as measured by cell viability and phagocytic index. Vanadium at 0.5 μg/ml, however, reduced cell viability to 24% and the phagocytic index to 2% of the control within 8 h of exposure. Exposure to NH4VO3(up to 1 μg vanadium/ml) for short periods of time stimulated phagocytic activity. Vanadium toxicity was also demonstrated in suspension culture at 37°C by chemiluminescence assay. This assay seems to be more sensitive than the conventional viability and phagocytic index tests. Thus, the peak light production by macrophages during zymosan phagocytosis was reduced to 93, 59, and 63% by vanadium at 0.1 μg/ml exposing for 2, 4, and 8 h, respectively, and to 71, 27, and 24% by vanadium at 1.0 μg/ml for the same time periods. The phagocytic activity of macrophages as measured by chemiluminescence response was not significantly altered by exposure to either 0.1 or 1.0 μg vanadium/ml measured during the first 24 h of culture at 4°C.

ISSN:0098-4108    

DOI:10.1080/15287398209530220

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Female Wistar rats were injected intravenously with tracer levels of210Pb, alone or combined with carrier Pb(NO3)2at 5 or 25 mg/kg body weight at 9 or 15 days of gestation (dg). Tissue210Pb distribution and retention, and lead excretion, were measured several times during the first 30 h and at 20 dg. Toxic effects following the administration of 25 mg/kg (a teratogenic dose) included an early decrease in hematocrit, hematuria, gastrointestinal hemorrhage, and diarrhea, as well as an eventual loss of body weight and an increase in spleen and kidney weights. The stage of pregnancy at injection did not affect the retention and distribution of lead in major organs other than the reproductive system. Following injection of the 25‐mg/kg dose, deposition of lead in the liver, kidney, spleen, and lung was elevated. Disproportionately high plasma lead levels were also observed at early times after the injection of the 25‐mg/kg dose, and may act as a significant factor in placental lead transfer and subsequent malformations or fetal mortality.

ISSN:0098-4108    

DOI:10.1080/15287398209530221

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Lead metabolism was studied in the fetoplacental unit (FPU) of Wistar rats during the genesis of developmental abnormalities and embryonic death. Female rats were injected iv with tracer210Pb(NO3)2, alone or in combination with 5 or 25 mg Pb(NO3)2/kg, at 9 or 15 days of gestation (dg). The distribution of lead and its effects were determined in the FPUs during the ensuing 30‐h period and at 20 dg.

ISSN:0098-4108    

DOI:10.1080/15287398209530222

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

摘要:

Serum glucose, serum protein, serum glutamic oxalacetic transminase (SGOT), serum glutamic pyruvic transaminase (SGPT), and hepatic and renal gluconeogenic enzymes [pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK), fructose‐1,6‐diphosphatase (F‐1, 6‐DPase), and glucose‐6‐phosphatose (G‐6‐Pase)] were determined in rats treated daily with cadmium alone (0.25 mg/kg·d, injected ip) and in rats pretreated with spironolactone (50 mg/kg·d and 100 mg/kg·d, injected sc) prior to cadmium administration. Rats receiving no treatment, propylene glycol, or spironolactone (100 mg/kg·d, injected sc) were used as controls. The daily treatments were continued for an extended period of 90 d, and the rats were sacrificed at 30‐, 60‐, and 90‐d intervals during the continuous daily treatment schedule. Cadmium treatment significantly increased the amount of serum protein, glucose, serum enzymes, and all the four key gluconeogenic enzymes as compared to controls. Pretreatment of rats with spironolactone 6 h prior to cadmium injection daily antagonized the cadmium effect of the above parameters. It appears from these results that spironolactone reduces the effects of cadmium on the key gluconeogenic enzymes in rat kidney and liver.

ISSN:0098-4108    

DOI:10.1080/15287398209530223

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor

ISSN:0098-4108    

DOI:10.1080/15287398209530196

出版商:Taylor & Francis Group    

年代:1982

数据来源: Taylor