Disease relevance of Cresidine

• Tumors were examined first for loss of the wild-type p53 allele. p-cresidine induced p53 LOH in three of 13 bladder tumors, whereas hepatocellular tumors showed p53 LOH in carcinomas (2/2), but not in adenomas (0/3) [1].
• Benzene-induced sarcomas, p-cresidine-induced bladder carcinomas and phenolphthalein-induced thymic lymphomas were allelotyped at the Trp53 locus and chromosome 11 simple sequence length polymorphic (SSLP) loci [2].
• Mice given p-cresidine exhibited a moderate reduction in body weight gain over the course of the study [3].
• Administration of p-cresidine also resulted in a regenerative anemia, splenic and hepatic hemosiderosis, renal findings, and ovarian and uterine atrophy [4].
• Toxicity and carcinogenicity studies of chlorpromazine hydrochloride and p-cresidine in the p53 heterozygous mouse model [4].

High impact information on Cresidine

• Heterozygous p53-deficient mice received a bladder carcinogen, p-cresidine, to induce preneoplasia [5].
• These results indicate that the transcriptional regulation of these three transgenes is a major determinant in the response to p-cresidine and reserpine [6].
• Evaluation of cytotoxicity, cell proliferation, and genotoxicity induced by p-cresidine in hetero- and nullizygous transgenic p53 mice [7].
• Increased tumor susceptibility associated with a reduction in p53 dosage may be dependent on neoplastic progression rather than initiation and promotional events elicited by p-cresidine [7].
• We used a modification of the alkaline single-cell gel electrophoresis (SCG) (Comet) assay to evaluate the in vivo genotoxicity of two potent rodent bladder carcinogens, o-anisidine and p-cresidine, in mouse liver, lung, kidney, brain, and bone marrow, and in the mucosa of stomach, colon, and bladder [8].

Biological context of Cresidine

• Analysis of the p-cresidine-induced bladder tumors by cold single-strand conformation polymorphism (SSCP) analysis of exon 4-9 amplicons failed to demonstrate polymorphisms associated with mutations in tumors that retained the p53 wild-type allele. p-cresidine induced a dose-related increase in lacI mutations in bladder DNA [1].
• Also, no point mutations were observed in codon 12 of the c-Ha-ras gene from urinary bladder DNA from p-cresidine treated p53 mice [7].

Anatomical context of Cresidine

• Morphology of nasal cavity neoplasms in F344 rats after chronic feeding of p-cresidine, and intermediate of dyes and pigments [9].

Associations of Cresidine with other chemical compounds

• During a 26-wk study to assess the potential carcinogenicity of oxymetholone using p-cresidine as a positive control, glass/polypropylene microchips (radio transponder identification devices) were subcutaneously implanted into male and female p53+/- mice [10].
• Clofibrate produced non-neoplastic findings in the adrenals, pancreas, and prostate, whereas p-cresidine affected the kidney, liver, pancreas, and spleen [11].

Gene context of Cresidine

• The high doses of both PTI G-2535 and BBIC were limited by viscosity. p-Cresidine (400 mg/kg/day) served as a positive-control article in both studies [12].

References