Search PubMedSearch

SEARCH · Search PubMed

Results for “Mixture toxicity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Toxicity of low concentration long-term exposure to an airborne mixture of nitrous oxide and halothane.

To evaluate experimentally the questions of reproductive, teratological, cytogenetic, and tumorigenic sequelae of long-term exposures to escape levels of halothane plus nitrous oxide (N2O), male and female rats were exposed either to air, to 1 ppm halothane plus 50 ppm N2O, or to 10 ppm halothane plus 500 ppm N2O for 7 hr/day, 5 days/wk for appropriate periods of time. In one experiment, young adult female rats were exposed for 60 days, then mated and reexposed either staring with Day 1 or Day 6 of gestation until Day 15. The former were permitted to deliver naturally while the latter were delivered by C-section on Day 20. The young adult males used in breeding were also exposed for 60 days prior to mating and then for a total of 52 weeks thereafter. At termination, bone marrow cell and spermatogonial metaphase preparations were made and assessed for cytogenetic abnormalities. The mated females were evaluated for ovulation, pre- and post-implantation loss, fetal growth, fetal abnormalities, and early post-natal development, as appropriate. In a parallel experiment, 50 male and 50 female weanling rats in each group were exposed for 104 weeks to the same levels and then evaluated for tumor development with emphasis on the reticuloendothelial system. The results indicated a significant reduction in ovulation and implantation efficiency from exposure to the higher levels and slightly retarded fetal development at both levels. No teratological or abortifacient effects were noted. No tumorogenic effects were observed. However, cytogenetic damage to both bone marrow and spermatogonial cells was seen at both levels.

Air Pollutants

Differential toxicities of mercury to bacteria and bacteriophages in sea and in lake water.

Mixtures of anionic HgCl3-/HgCl4(2)-complexes were less toxic to terrestrial bacteria (Erwinia herbicola, Agrobacterium tumefaciens), to marine bacteria (Acinetobacter sp., Aeromonas sp.), and to bacteriophages (phi 11 M 15 of Staphylococcus aureus and P1 of Escherichia coli) than were equivalent concentrations of Hg as cationic Hg2+. The toxicity of 1 ppm Hg to A. tumefaciens. Aeromonas sp., and phi 11 M 15 was less in seawater than in lake water. Inasmuch as the Hg-Cl species are formed in environments of high chloride concentration, it was postulated that the lower toxicity of Hg in seawater was a result of the formation of HgCl3-/HgCl4(2)-complexes.

Acinetobacter

Ascorbate anion potentiates cytotoxicity of nitro-aromatic compounds under hypoxic and anoxic conditions.

The nitro-aromatic radiosensitizing drugs are selectively toxic to hypoxic mammalian cells, and this toxicity can be greatly increased by the addition of ascorbate. The ascorbate itself is not toxic to either hypoxic or aerobic cells (as long as catalase is present to prevent the formation of significant concentrations of hydrogen peroxide) and the mixture of ascorbate plus radiosensitizer is not more toxic to aerobic cells. Sulphydryl reducing agents and dithionite have an effect opposite to ascorbate and decrease the toxicity of nitro-aromatic drugs under hypoxic conditions. Sulphydryl reducing agents are also reported to nullify the radiosensitizing properties of nitro-aromatic drugs, in contrast to ascorbate which has no effect on the radiosensitizing properties. The toxicity of nitro-aromatic drugs decreases rapidly with increasing O2 concentration. This decrease is much less rapid when ascorbate is present. The role of ascorbate in this case may be primarily as an O2 scavenger, although it is also possible that the toxic species produced by radiosensitizer-ascorbate mixtures is less easily removed or detoxified by O2.

Animals

[Effect of polychlorinated biphenyls in the rat: II.--Preliminary report on metabolic alterations (author's transl)].

Rats were fed with a diet containing 10 and 100 ppm (wet weight) of Phenoclor DPR for 4 weeks in order to evaluate the toxicity of a French PCB mixture. The influence of PCB was studied by determining the liver weights, the hepatic and muscular proteins, glycogen and humidity content as well as hematocrite, glucose, proteins and lipids in the plasma, and the lipidic contents of the liver and the carcass. There was a significant increase in both liver to body weight ratios and liver lipid and protein content. A large increase in plasma proteins and lipids was observed at 100 ppm. Liver glycogen content and blood glucose were slightly modified by the PCB intoxication. Muscular parameters remain-ded stable. A consistent effect on liver microsomal proteins was noted for all doses studied. At the same diet levels, Phenoclor DP6 determines more métabolic alterations than Aroclor 1260 or 1268.

Animals

Comparison of the toxicities of patulin and patulin adducts formed with cysteine.

The toxicities of patulin and of the patulin adducts formed with cysteine were compared using the mutation-sensitive strain Escherichia coli W3110 thy polA1 and its polA1+ revertant. The acute toxicities of patulin and of the adduct mixture were also compared using NMRI mice. The adduct mixture was shown by thin-layer chromatography to consist of one ninhydrin-positive, one ninhydrin- and MBTH (3-methyl-2-benzothiazolinone hydrazone)-positive, three MBTH-positive, and two ninhydrin- and MBTH-negative components. The results showed that patulin was over 100 times more toxic to E. coli than the adduct complex. Neither patulin nor the adduct mixture was found to induce the repair effect in E. coli. In the mouse feeding tests, the oral 50% lethal dose for patulin was 29 mg/kg, while that of the adduct mixture was greater than 2,370 mg/kg.

Animals

[Peripheral arteriographies under intraarterial analgesia (author's transl)].

45% contrast medium, to which lignocaine had been added in a concentration of 0.1%, was injected for 44 translumbar aortograms, 26 femoral arteriograms and 4 brachial arteriograms under premedication with pethidine-promethazine. Few patients described their sensations spontaneously; most patients graded their pain as minimal and described only the sensation of heat. When the contrast medium was injected, first without and then with lignocaine, the pain was markedly reduced by lignocaine. No patient showed signs of CNS-toxicity. After the injection of the mixture of contrast medium and lignocaine, the heart rate rose slightly, the arterial blood pressure fell slightly, both not more than after injection of the contrast medium only. The ECG showed no anomalies. The addition of lignocaine to a contrast medium in low concentration represents a simple and, for the patient, acceptable method of analgesia as well as a safe alternative to general, spinal or epidural anesthesia.

Anesthesia, Local

Evaluation of a proteolytic enzyme mixture isolated from crude trypsins in tissue disaggregation.

Trypsin, chymotrypsin and elastase are the pancreatic enzymes required for neonatal rat heart tissue disaggregation. We have previously developed a procedure for the isolation of a mixture of these three enzymes from commercial crude-trypsin samples. Toxic materials present in certain crude-trypsin samples are removed during purification. An evaluation of this mixture was conducted for its ability to disaggregate neonatal rat heart tissue for cell culture. Large numbers of cells were released with minimal cellular damage as determined by their ability to survive and function in culture. Rat lung and kidney tissue also were disaggregated successfully and cultured with this preparation. It is apparent that this enzyme preparation has a potential for disaggregating a wide variety of tissues.

Animals

In vitro and in vivo indications of the carcinogenicity and toxicity of food dyes.

Eight food dyes or commercial color mixtures certified for use in the United States were tested for their ability to transform in vitro a serial line of Fischer rat embryo cells previously reported to be a sensitive indicator of chemicals having carcinogenic potential. Malignant cell transformation was induced by a commercial mixture (G2024) of two of these dyes (Blue 1 and Yellow 5) and by Blue 2, Green 3 (one of two experiments) and Red 4. Food dyes Blue 1, Red 3, Yellow 5 and Yellow 6 did not induce cell transformation. One to 1.5 mg of each dye was injected into suckling LVG or Graffi hamsters which were monitored for tumor induction and/or death over a 330-day period. None of the non-transforming dyes (Blue 1, Red 3, Yellow 5, Yellow 6) or Green 3 induced a significant increase in tumor (mostly lymphoma) incidence or animal mortality. Three of the transforming dyes (Blue 2, Green 2024, Red 4) did increase tumor incidence and/or mortality in at least one strain of hamster. We conclude the the in vitro assay suggested that certain food dyes were carcinogens and that in vivo studies in hamsters supported this interpretation.

Animals

A protective effect of caffeine on drosophila larvae treated with methyl methanesulfonate.

Lethality induced in larval populations of Drosophila melanogaster was recorded after treatment with (1) caffeine, (2) MMS or (3) caffeine plus MMS. The mixture of caffeine plus MMS was less toxic than expected from the effects observed after treatment with either substance individually. It is postulated that in the combined treatment the caffeine, by inhibiting semiconservative DNA replication, allows for some additional time for repair of alkylated DNA by a repair pathway which is not sensitive to caffeine, possibly excision repair.

Animals

Inhibiting effect of vitamins C and B12 on the mitotic activity of ascites tumors.

The mitotic activity of the transplantable mouse tumors, Sarcoma 37, Krebs-2, and Ehrlich carcinomas, in the ascites form, were inhibited after treatment with a mixture of vitamins C and B12 with no apparent toxic side effects. These vitamins when administered alone, at the same dosage, did not seem to have any apparent effect on mitosis or the morphology of the cells studied. Microscopic examination of the stained ascites fluid taken from the mice treated with the vitamin mixture showed few tumor cells, and these in various stages of disintegration. Also, an increase in lymphocytes, monocytes and neutrophils were noticed; however, later in the experiment, no tumor cells could be found and monocytes and macrophages were abundant.

Animals

Chimeric toxins: toxic, disulfide-linked conjugate of concanavalin A with fragment A from diphtheria toxin.

A disulfide-linked conjugate of concanavalin A (Con A) and fragment A from diphtheria toxin has been synthesized and shown to be toxic for HeLa (human), Chinese hamster ovary (CHO), and SV3T3 (murine) cells. The conjugate was constructed by first coupling cystamine to Con A with a carbodiimide reagent and then reacting the modified Con A with reduced fragment A under conditions promoting disulfide interchange. The desired conjugate, obtained in nearly 50% yield relative to input of fragment A, was purified by affinity chromatography on Sephacryl S-200 and NAD-Sepharose; on analysis, it gave an average of 1.4 molecules of fragment A per tetrameric Con A molecule. The conjugate proved to be about equally active in inhibiting protein synthesis in HeLa, CHO, or SV3T3 cells in culture but was inactive relative to controls in a toxin-resistant strain of CHO cells containing altered elongation factor 2, the target protein of fragment A. With toxin-sensitive strains the conjugate was 100- to 1000-fold more active than controls, including fragment A, cystaminyl-Con A, and mixtures thereof, but was 1/50th to 1/500th as toxic as diphtheria toxin itself. Similar activity relative to controls was observed after intradermal inoculations in rabbits, and intravenous injections of the conjugate were lethal for mice. The activity of the conjugate in tissue culture was inhibited by Con A or alpha-methylmannoside but not by galactose. This and similar conjugates should be useful in studying mechanisms of entry of biologically active proteins into cells.

Cell Line

[Nucleic acids in the tissues of white rats with toxic liver damage following protein starvation and parenteral nitrogen nutrition].

The authors studied the content of nucleic acids in the tissues (the skeletal muscle and myocardium, the liver) in albino rats with toxic affection of the liver caused by ccl4, in protein deficiency and parental administration of amino acid mixture of moriamin S-2 and "improved" caseine hydrolysate. Protein deficiency in albino rats with toxic hepatitis was accompanied by a considerable increase of RNA and DNA in the skeletal muscle and the myocardium with a simultaneous reduction of their level in the liver. The RNA/DNA ratio changed. The RNA content in the hepatocytes diminished on account of reduction of the nuclear RNA fraction closely bound with chromatin. Parenteral administration of nitrogen preparations led to normalization of the nucleic acid content in all the tissues under study.

Amino Acids

Bromodeoxyuridine resistance induced in mouse lymphoma cells by microsomal activation of dimethylnitrosamine.

Many chemicals are not mutagenic per se, but when metabolized by mammalian tissues yield mutagenic products. Dimethylnitrosamine (DMN) is such a promutagen. It has no effect on cell growth or mutant frequency when incubated alone with L5178Y mouse lymphoma cells, but exerts both mutagenic and toxic effects when incubated in a microsome reaction mixture. Microsomes were prepared from C3H/f We 16-wk-old male mice by the calcium preciptation technique. L5178Y continuously cultured mouse lymphoma cells heterozygous for thymidine kinase (TK+/-) were incubated for 15 min with calcium-precipitated microsomes and various concentrations of DMN in appropriate reaction mixtures. After a 48-hr expression time, treated cells were cloned in soft agar with and without bromodeoxyuridine (BUdR) (50 mug/ml); 10 days later colonies grown to greater than about 200 mum diameter were counted. The frequency of BUdR-resistant (mutant) colonies increased linearly with the DMN concentration. A reconstruction experiment showed that the assay conditions did not significantly alter the relationship between parent and BUdR-resistant cells in growth and cloning efficiency. The smallest dose of DMN used in these experiments was 100mumol/liter, the one-sided (100 mumol greater than control frequency) -p value is 0.036. The locus is extremely sensitive to mutagenesis by DMN compared with other known mutagens at similar levels of cell survival.

Animals

[Mutagenic action of nitroso compounds on Escherichia coli cells].

An attempt to induce some forward and back mutations in two Escherichia coli strains (his- and HfrH requiring thiamine) under the action of the carcinogenic nitrosamines--dimethylnitrosamine (DMN) and diethylnitrosamine (DEN)--is described. For this purpose the cells of E. coli were treated with 5% DMN or 1% DEN for 1 hour at 37 degrees C in 0.14 M NaCl. It was shown that the sensitivity of both strains to both nitrose compounds was not the same. DEN was 5-fold as toxic as DMN for the E. coli cells. DMN and DEN induced neither mutations of resistance to 10(-3) M valine, nor reversions in histidine-dependent strain. These mutations were obtained after the cells were treated with 0.1 M NaNO2. Lethal effects of DMN increased more than in 5 times and the toxicity of DEN did not change in hydroxylating mixture, in which nitrosamines derived to active compounds. Under these conditions both carcinogenes showed a mutagenic activity. DEN proved to be about twice as strong mutagenically as DMN. Thus, in our experiments we could see that DMN and DEN could induce both forward and back mutations in E. coli.

Culture Media

Influence of some factors on cadmium pharmacokinetics and toxicity.

Cadmium metabolism in the young and in conditions of dietary contamination with ash from coal gasification were investigated. The experiments were performed in adult rats which received ash in the diet (5%) and/or cadmium in drinking water (100 ppm) over a period of five weeks and in sucklings whose mothers were given the same treatment throughout pregnancy and lactation. In pharmacokinetic studies, (115m)Cd was administered orally or intraperitoneally to determine the intestinal absorption, retention, and distribution. Cadmium toxicity (LD(50)) was determined in different age groups of animals treated with ash for five weeks before a single oral or intraperitoneal administration of cadmium chloride. After intraperitoneal administration, (115m)Cd body retention decreased with age and was independent of the dietary treatment. Sucklings had a higher retention in the blood, carcass, and gut than adults. After oral administration, sucklings had a much higher body retention than adults regardless of the dietary treatment of their mothers. Cadmium toxicity was also independent of the dietary treatment. Most striking was a very high oral toxicity of cadmium in sucklings. It is concluded that the young might be at a special risk at the same level of environmental cadmium exposure because of the high oral cadmium toxicity at this age which is most probably due to a high cadmium retention in the gut. It is also concluded that the mixture of elements contained in ash is not likely to influence cadmium metabolism and toxicity in conditions of dietary exposure.

Age Factors

[Preservation of food wastes by a mixture of quinosol and salicyclic acid].

A 90-day experiment has shown that a number of toxic gaseous contaminants are released into the atmosphere as a result of storage of mixed food wastes. The microorganisms dwelling upon decaving food wastes include different microbial species from the environment and food products. A preserving agent consisting of a mixture of quinosole and salicylic acid (1:1) has been used. The agent inhibited microbial activity and terminated processes of decay. This was indicated by a decline in the concentration of ammonia and amine compounds. In the presence of the agent fermentation processes, on the contrary, continued and increased.

Air Pollution

Oleander poisoning.

The two common oleanders, Thevetia peruviana and Nerium oleander, contain a mixture of poisons including cardiac glycosides, and are extremely toxic. They are cultivated universally throughout Australia, and rank equally with mushrooms as the major cause of children's admission to hospital after accidental plant ingestions. A seven-year total population survey from south-east Queensland has revealed that, in practice, the rate of clinical poisoning due to oleander is inconsequential, and mortality is negligible. The annual age-specific admission rate for children (aged from birth to 12 years of age), for all plant ingestions is 2.33 per 100 000, and 0.62 per 100 000 specifically for oleander. Oleander ingestion causes a syndrome of combine cardiac and gastrointestinal symptoms and signs. A case series of 13 children is described, and the clinical features summarized. After accidental oleander ingestion, current experience indicates that the prognosis is excellent.

Antidotes

Cytotoxic effect of fatty acids in vitro on Ehrlich exudative carcinoma cells and normal exudative cells (leukocytes).

A mixture of pure fatty acids isolated hydrolytically from linseed oil in the form of water-soluble salts with ethanolamine were examined for cytotoxicity for Ehrlich carcinoma and normal exudative cells. Cytotoxicity of the mixture was similar to that of salts of oleic and linolenic acids. On the other hand, the mixture of fatty acids and oleic acids was more toxic for normal exudative cells than linolenic acid.

Animals