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Biomedical subjects

H W Taylor

Publications and source records attributed to H W Taylor.

At least 91 records · Page 5Linked to original sources
PubMed1977

Carcinogenicity of nitrosoazetidine and tetradeuteronitrosoazetidine in Sprague-Dawley Rats.

Nitrosoazetidine was fed to rats in drinking water at three different concentrations. At 2 mmol (10 mmol total dose) all of the rats died with hepatocellular carcinomas by the 62nd week. This was a greater response than to an equivalent dose of nitrosopyrrolidine. At 0.67 mmol, 6 of 21 rats developed liver tumors, and at 0.17 millimolar 2 of 30 animals had liver tumors. The comparable responses to feeding of nitrosoazetidine-2,2,4,4-d4 were 3 of 21 rats with liver tumors at 0.69 millimolar and 3 of 30 rats with liver tumors at 0.17 mmol. These results show only a small deuterium isotope effect in liver carcinogenesis with nitrosoazetidine.

Animals↗
PubMed1977

Carcinogenesis tests of nitroso-N-methylpiperazine, 2,3,5,6-tetramethyldinitrosopiperazine, nitrosoisonipecotic acid and nitrosomethoxymethylamine in rats.

Four nitrosamines; nitroso-N-methylpiperazine, 2,3,5,6-tetramethyldinitrosopiperazine, nitrosoisonipecotic acid and nitrosomethoxymethylamine, closely related in structure to potent carcinogens, were fed chronically to rats in drinking water for one year. No toxic effects leading to life shortening were observed. There was no significant incidence of any malignant tumor other than the endocrine tumors normally found in untreated animals of our colony. This indicated that the small changes in structure represented by these compounds were sufficient to reduce greatly, or eliminate, the carcinogenic action.

Adrenal Gland Neoplasms↗
PubMed1977

Liposolubility as an aspect of nitrosamine carcinogenicity: quantitative correlations and qualitative observations.

Carcinogenicity data for a number of nitrosamines have been examined for possible structure-activity correlations with liposolubility by the method of Hansch. Correlations were found in two cases which support a previous mechanistic suggestion and which also suggest a possible difference between the action of nitrosopiperidines and dinitrosopiperazines in inducing olfactory carcinomas. No correlations were found for non-cyclic nitrosamines.

Alcohols↗
PubMed1977

Ischemic myelopathy caused by fibrocartilaginous emboli in a horse.

A horse that suddenly became recumbent had a focal ischemic infarct of the spinal cord between C6 and C7. The infarct was attributed to multiple fibrocartilaginous emboli. Adherence of fibrocartilaginous debris to the outer surface of the dura was interpreted as evidence that intervertebral disc degeneration and displacement of the nucleus pulposus had occurred and that the emboli arose from the disc.

Animals↗
PubMed1976

Epithelial lesions induced by N-nitrosoheptamethyleneimine in host and transplanted rat tracheas.

N-Nitrosoheptamethyleneimine (NHMI) was given by gastric intubation, at a dosage of 10 mg/kg body weight twice weekly for 5-20 weeks, to F344 rats bearing subcutaneous tracheal transplants. Groups of 5 rats were killed at 5, 10, 15, and 20 weeks, and 1 group was killed at week 33 of the experiment (13 weeks after the last NHMI dose). Sequential changes in host tracheas consisted of hyperplasia with complete loss of mucociliary epithelium, squamous metaplasia, intense mononuclear infiltration, reestablishment of mucocillary epithelium (during the course of NHMI administration) except for focal areas of hyperkeratotic squamous metaplasia or marked dystrophic changes, and finally, papillomas, polyps, and invasive squamous cell carcinomas. Lesions in tracheal transplants consisted mostly of atrophic and dystrophic changes, with only a few small foci of squamous metaplasia and no neoplastic changes.

Animals↗
PubMed1976

Carcinogenicity of N'-nitrosonornicotine in Sprague-Dawley rats.

N'-Nitrosonornicotine was added to the drinking water of outbred Sprague-Dawley rats. Adenocarcinomas of the olfactory epithelium occurred in all 15 rats, squamous papillomas o- the esophagus in 1, squamous papillomas of the nonglandular stomach in 1, and a hepatacellular tumor in 1. The possible ingestion and subsequent in vivo nitrosation of nicotine and/or nornicotine could create a serious carcinogenic hazard to cigarette smokers.

Adenocarcinoma↗
PubMed1976

Reduction of rat liver carcinogenicity of 4-nitrosomorpholine by alpha-deuterium substitution.

Groups of 30 males Sprague-Dawley rats were given 4-nitrosomorpholine-3,3,5,5-d in their drinking water at concentrations of 0.35 and 0.07 X 10(-3) M for 30 weeks. Two similar groups of rats were simultaneously given unlabeled 4-nitrosomorpholine (NM) at the same malar concentrations; all animals were observed throughout their lives. Those receiving the alpha-deuterium-labeled compound had significantly fewer liver tumors than did the corresponding animals receiving the unlabeled compound. The difference in potency appeared to be at least fivefold, a magnitude consistent with a primary kinetic isotope effect on the carcinogenic action of NM. Thus breakage of a bond linking a hydrogen (deuterium) atom with carbon adjacent to the nitrosamino function may be involved in a rate-limiting step of carcinogenesis by NM.

Animals↗
PubMed1976

Carcinogenicity test of two unstaurated derivatives of N-nitrosopiperdine in Sprague-Dawley rats.

Two unsaturated derivatives of N-nitrosopiperidine (NP), N-nitroso-1,2,3,6-tetrahydropyridine (NTP) and N-nitrosoguvacoline (NGC), were administered to Sprague-Dawley rats as solutions in drinking water at concentrations equimolar (0.88X10(-3) M) with those used to test NP. NTP gave rise to hepatocellular tumors in contrast to the esophageal or olfactory tumors that were induced by NP. NGS did not induce tumors under these test conditions.

Animals↗
PubMed1976

The effect of substituents on the carcinogenicity of n-nitrosopyrrolidine in Sprague-Dawley rats.

N-Nitrosopyrrolidine and two of its derivatives were prepared and fed in drinking water to Sprague-Dawley rats to compare the effects of substituents on the carcinogenicity of the N-nitrosopyrrolidine molecule. 3,4-Dichloro-N-nitrosopyrrolidine induced esophageal tumors in 13 of 14 animals, olfactory carcinomas in 4, and a hepatocellular tumor in 1. All animals that received this compound were dead at 55 weeks after the start of the experiments. N-Nitrosopyrrolidine induced hepatocellular tumors in 26 of 29 animals and induced 1 olfactory carcinoma. Not all animals in this group were dead until 104 weeks of the experiment. 2,5-Dimethyl-N-nitrosopyrrolidine induced only 2 hepatocellular tumors in 29 animals. The alpha-methyl substitution diminished the liver carcinogenicity, while the beta chlorine substitution affected a different target organ, the esophagus, and greatly reduced the time to death with tumors.

Animals↗
PubMed1976

Carcinogenesis in Sprague-Dawley rats of N-nitroso-N-alkylcarbamate esters.

Nitrosocarbaryl, nitroso-N-methylurethane and nitroso-N-ethylurethane were administered by gavage in olive oil solution to groups of 12 female Sprague-Dawley rats. The dose was 0.2 ml of 0.11 M solution once a week for 10 weeks, a total dose of 0.22 mmol. The rats given nitrosocarbaryl survived longer, but had as high an incidence of tumors (75%) as did rats given nitrosomethylurethane. Most of the tumors induced were invasive squamous carcinomas of the stomach. Nitrosoethylurethane appeared to be a little more potent than nitrosomethylurethane; all 12 animals in this group had squamous stomach tumors at death. A higher total dose of nitrosocarbaryl, 1.3 mmol, given to male rats twice weekly for 20 weeks did not produce a higher incidence of stomach tumors than did thelower dose in females, although the males died earlier with tumors.

Administration, Oral↗
PubMed1975

Tumor induction in rats by feeding aminopyrine or oxytetracycline with nitrite.

Sprague-Dawley rats were given combinations of aminopyrine or oxytetracycline and sodium nitrite in drinking water. Of 30 animals receiving 0.1% (1,000 ppm) of aminopyrine and sodium nitrite for 30 weeks, 29 died with hemangioendothelial sarcomas of the liver. The same tumor caused death in 26 of 30 animals that received 0.025% (250 ppm) of both aminopyrine and sodium nitrite for 50 weeks. No animals in a control group of the same size that received 0.1% aminopyrine for 30 weeks developed this tumor, although one-half of them were still alive 2 years after the experiment was begun. After feeding a comparable dose (0.1%) of oxytetracycline and sodium nitrite for 60 weeks, liver tumors were present in 4 of 30 rats (3 hepatocellular tumors and 1 cholangioma). Since aminopyrine has been widely used for medicinal purposes in the human population, it is possible that many people have been exposed to a potent carcinogen (dimethylnitrosamine) by its formation in vivo. It is not certain whether the result of feeding oxytetracycline and sodium nitrite indicates significant carcinogenicity of this combination.

Adenoma, Bile Duct↗
PubMed1975

Carcinogenicity of methylated nitrosopiperidines.

The carcinogenicity of nitrosopiperidine and five methylated derivatives was compared by feeding them to rats at equimolar concentrations in drinking water, at the rate of 20 ml per day, 5 days a week. The maximum treatment time was 50 weeks. Nitrosopiperidine, 2-methyl-, 3-methyl- and 4-methyl-nitrosopiperidine induced tumors of the nasal turbinates or upper gastrointestinal tract in almost 100% of the animals. There was a significantly longer time to death from these tumors in the group treated with 2-methylnitrosopiperidine and a number of hepatocellular carcinomas appeared in this longer lived group. Very few tumors of these sites were seen in rats treated with 2,6-dimethyl- or 2,2,6,6-tetramethyl-nitrosopiperidine. It was concluded that blockage by methyl groups of one or more carbon atoms alpha to the nitroso function in nitrosopiperidine significantly reduces carcinogenic activity of the molecule.

Animals↗
PubMed1975

Induction of neurogenic tumors by nitrosotrialkylureas in rats.

Four nitrosotrialkylureas were each fed to groups of 15 male and 15 female Sprague-Dawley rats for 50 weeks in drinking water at the same molar concentration. Tumors of nervous origin arose after treatment with nitrosotrimethylurea (3/30), notrosotriethylurea (7/30), nitrosomethyldiethylurea (23/30), and nitrosoethyldimethylurea (8/30). A comparison of the relative stabilities of the four nitrosoureas in aqueous solution at various pH's showed no correlation with the tumorigenicities of the compounds.

Animals↗
PubMed1975

Influence of administration route and dosage schedule on tumor response to nitrosoheptamethyleneimine in rats.

Nitrosoheptamethyleneimine (NHMI) was tested for carcinogenicity in Fischer-344 and Sprague-Dawley rats by intragastric administration and subcutaneous injection. Cumulative doses ranged from 5.5 to 1,200 mg/kg, and dosage schedules ranged from 40 serial administrations to one single injection. No difference in response was seen between sexes or strains of rats. Following the highest carcinogen doses by intragasritc administration, a high incidence of squamous-cell tumors occurred in the lung. The highest incidence of squamous-cell tumors occurred in the nasal cavity, trachea and esophagus. Following subcutaneous injection, tumors induced in the lungs were all alveologenic adenocarcinomas. The upper respiratory and gastrointestinal tracts were again the most commonly affected sites, with tumors similar to those of the first group. Intragastric administration was more effective in producing tumors than was subcutaneous injection, and administration of multiple small doses was more efficient than single large doses. The results demonstrated that the route and schedule of administration markedly influenced the tumor response to NHMI, both quantitatively and qualitatively.

Adenocarcinoma↗
PubMed1975

Tumorigenesis by oxygenated nitrosopiperidines in rats.

Three oxygenated N-nitrosopiperidines--nitroso-3-piperidinol, nitroso-4-piperidinol, and nitroso-4-piperidone--were prepared and given in drinking water at equivalent molar doses to Sprague-Dawley rats. All were potent carcinogens, 100% of the rats developed tumors in all treatment groups. Nitroso-3-piperidinol resembled nitrosopiperidine in inducing a high incidence of tumors of the nasal cavity and upper alimentary tract, and a few liver tumors. Nitroso-4-piperidinol and nitroso-4-piperidone caused a high incidence of tumors of the nasal cavity but very few tumors of the upper alimentary tract. After treatment with the 4-substituted compounds, a high incidence of liver tumors was observed in females but not in males.

Animals↗