Galactosamine induces a dose-dependent hepatic injury in rats and many other animals. The toxicity of Dgalactosamine appears to be a consequence of the loss of hepatic UTP. It has previously been reported that regenerating liver cytosol is able to prevent, at least in part, the lethal effect of this
Enhancement of hepatic and renal tumorigenesis in thyroidectomized NZR/Gd rats treated with dimethylnitrosamine
✍ Scribed by R. F. X. Noronha; C. M. Goodall
- Publisher
- John Wiley and Sons
- Year
- 1976
- Tongue
- English
- Weight
- 762 KB
- Volume
- 8
- Category
- Article
- ISSN
- 0022-4790
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✦ Synopsis
Abstract
Endocrine modulation of DMN carcinogenesis was studied in NZR/Gd rats preconditioned by starving 48 hr and then injected i.p. once with 20 mg DMN/kg. Intact rats developed kidney tumors (44% TBA), most of tubular epithelial type resembling human tumors rather than mesenchymal. Thyroidectomy (Tx) 45 days before DMN significantly enhanced DMN carcinogenesis, renal carcinoma incidence increasing to 69%. Renal carcinomas showed more signs of malignancy in Tx rats. Other neoplastic responses useful for further studies included tumors in nasal epithelium (13%), liver (18%, increased to 59% in Tx rats), and lung (40%): these tumors were rare or not previously reported in single‐dose experiments in other rat strains. A sex difference in lung tumor incidence (male 70%, female 16%) was statistically significant and thyroidectomy reduced the sex‐differential (to 54% and 39% respectively). The increased incidence of kidney and liver tumors could be due to altered metabolism of DMN in tissues of Tx rats.
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