Biomedical subjects

C C Irving

Publications and source records attributed to C C Irving.

At least 37 records · Page 2Linked to original sources

PubMed1977

Polyamine-stimulated growth of cultured rat urinary bladder epithelial cells.

A technique for isolating and establishing long-term cultures of rat urinary bladder epithelium has been devised. Cells isolated and cultured by this method have been grown for 12 weeks without subculturing. Rat bladder epithelial cells require the addition of putrescine, spermine, and spermidine to attain maximum growth and long-term survival. Monolayer cultures have been subcultured and carried through five passages.

Animals↗

PubMed1977

Influence of the aryl group on the reaction of glucuronides of N-arylacethydroxamic acids with polynucleotides.

The reactions of the glucuronide conjugates of the carcinogens N-hydroxy-2-acetylaminofluorene (N-hydroxy-AAF), N-hydroxy-4-acetylaminostilbene (N-hydroxy-AAS), N-hydroxy-4-acetylaminobiphenyl (N-hydroxy-AABP), and N-hydroxy-2-acetylaminophenanthrene (N-hydroxy-AAP) with transfer RNA, ribosomal RNA, DNA, polyadenylate, polyguanylate, polyuridylate, polycytidylate, poly(adenylate, guanylate), and poly(guanylate, uridylate) were studied. The relative order of reactivity of these glucuronides with nucleic acids, measured by the covalent binding of the aryl group labeled with 3H or 14C, was glucuronide of N-hydroxy-AAF greater than glucuronide of N-hydroxy-AAS greater than glucuronide of N-hydroxy-AABP greater than glucuronide of N-hydroxy-AAP. The glucuronide of N-hydroxy-AAP showed only marginal or negligible reactivity. The glucuronide of N-hydroxy-AAF showed greater reactivity with polyguanylate than with polyadenylate, but the reverse was true for the glucuronide of N-hydroxy-AAS. Both of these glucuronides had much lower extents of reaction with polyuridylate and polycytidylate. Except for the reaction of the glucuronide of N-hydroxy-AABP with polyadenylate, there was no detectable reaction of this glucuronide or the glucuronide of N-hydroxy-AAP with the homopolynucleotides. Under comparable conditions the glucuronide conjugates of N-hydroxy-AAF, N-hydroxy-AAS, and N-hydroxy-AABP demonstrated greater reactivity with poly(adenylate, guanylate) and poly(guanylate, uridylate) than with the homopolynucleotides. Furthermore, the synthesis of two new glucuronide conjugates, those of N-hydroxy-AAS and N-hydroxy-AAP, is described.

Animals↗

PubMed1977

Biochemically detectable tumor markers in urine of bladder cancer patients.

Potential biochemical markers excreted in the urine of bladder cancer patients have been considered, with the conclusion that none alone has yet proven to be useful as a screening procedure for the detection of urothelial cancer. Quantitative fluctuations in urinary levels of several of these markers in combination, such as pseudouridine, beta-amino-isobutyric acid, and fibrinogen degradation products, appear to be valuable in the assessment of the treatment of bladder cancer patients and in helping to predict recurrences in these patients.

Aminoisobutyric Acids↗

PubMed1976

Effect of N-methyl-N-nitrosourea on the DNA of rat bladder epithelium.

Bladder cancer can be induced in the rat by the intravesicular administration of N-methyl-N-nitrosourea. DNA damage in rat bladder epithelial cells after administration of methylnitrosourea has been examined by measuring the change in sedimentation of the DNA in alkaline sucrose gradients. A dose response of DNA damage in the urothelium was observed with single intravesicular doses of 0.1, 0.3, and 0.5 mg of methylnitrosourea. Larger doses of methylnitrosourea damaged the epithelium so extensively, that biochemical studies were not feasible. DNA repair, measured by the return to a normal sedimentation pattern of DNA on alkaline sucrose gradients, was followed over a period of 9 days with the use of 0.5 mg of methylnitrosourea to initiate the damage. Bladder epithelial cells were able to repair the DNA damage induced by methylnitrosourea. However, the possibility of persistent damage not detectable by sedimentation of DNA on alkaline sucrose gradients cannot be ruled out.

Animals↗

PubMed1975

Damage and repair of DNA in various tissues of the rat induced 4-nitroquinoline 1-oxide.

4-Nitroquinoline 1-oxide induces pulmonary tumors when given by a s.c. route or skin cancer by repeated local applications. This carcinogen is absorbed by the lung more readily than other tissues. Therefore, we have compared the ability of 4-nitroquinoline 1-oxide to damage DNA of the liver, lung, and kidney in the intact animal. A differential effect of DNA damage was detected in all three organs, with the lung showing the greatest amount of damage. All three tissues were able to repair the damaged DNA. The preferential damage of rat lung DNA by 4-nitroquinoline 1-oxide correlates with the specificity of this carcinogen to induce pulmonary tumors.

Animals↗

PubMed1975

Comparative toxicity of N-hydroxy-2-acetylaminofluorene in several strains of rats.

Male Spraque-Dawley rats were 6 or 7 times more susceptible than females to the acute toxic effects of a single i.p. injection of N-hydroxy-2-acetylaminofluorene. The N-hydroxy compound were equally toxic in male and female Fischer rats and about twice as toxic to male as to female Wistar rats. A negative correlation between the 50% lethal dose of N-hydroxy-2-acetylaminofluorene and hepatic N-hydroxy-2-acetylaminofluorene sulfotransferase activity was found. These data substantiate earlier indications that the level of the liver sulfotransferase is an important factor in determining the degree of toxicity of N-hydroxy-2-acetylaminofluorene. It is suggested that the reported sex difference in the hepatocarcinogenicity of N-hydroxy-2-acetylaminofluorene might be peculiar to the Sprague-Dawley rat.

Animals↗

PubMed1974