Oesophageal neoplasia in male wistar rats due to parenteral di(2‐hydroxypropyl)nitrosamine (DHPN): A combined histopathological, histochemical and electron microscopic study

Levison, David A.; Hopwood, David A.; Morgan, R. G. H.; Coghill, G.; Milne, G.; Wormsley, K. G.

doi:10.1002/path.1711290106

Cited by 14 publications

(1 citation statement)

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“…The concentration of carcinogen in drinking water was the same as that used in other experimental models; 36 , 42 , 51 , 52 the aim was to reduce the mortality caused by the hepatotoxic action of DEN. Ingestion of the drug in drinking water, rather than by administration by gastric intubation, 53 intraperitoneal injection 31 , 54 or subcutaneous injection, 55 , 56 required little manipulation of the rat and its efficiency has been proven 36 . 42 , 51 , 57 …”

Section: Discussionmentioning

confidence: 99%

Influence of surgically induced gastric and gastroduodenal content reflux on esophageal carcinogenesis – experimental model in Wistar female rats *

Ll.

et al. 1999

Diseases of the Esophagus

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Studies in human beings and animals have shown that esophageal exposure to duodenal and gastric contents may be important for the development of Barrett's esophagus and its complications, including adenocarcinoma and epidermoid carcinoma. Diethylnitrosamine (DEN) is a carcinogen that stimulates the development of epidermoid carcinoma in the esophagus of mice. The aim of this study was to evaluate the effect of gastroduodenal and gastric content reflux on induction of esophageal carcinogenesis. Gastroesophageal reflux (GER) and gastroduodenoesophageal reflux (GDER) were produced by cardioplasty and esophagoduodenostomy. The chosen carcinogen was DEN, diluted in drinking water, given 3 days a week for 20 consecutive weeks. One hundred Wistar female rats were divided into six groups, as follows: group 1 (18 rats), cardioplasty without DEN; group 2 (18 rats), cardioplasty with DEN; group 3 (10 rats), only water; group 4 (17 rats), cardioplasty with DEN; group 5 (17 rats), esophagoduodenostomy with DEN; group 6 (20 rats), only DEN. GER in isolation induced papillomatosis or ulceration in 22.2% of rats and, when associated with DEN, induced papillomatosis in 61.1% of rats. GDER in isolation induced marked esophagitis in 61.1% of rats, Barrett's esophagus in 16.7% and esophageal adenocarcinoma in 16.7%; when associated with DEN, 23.5% of rats presented marked esophagitis, papillomatosis or ulceration, whereas 76.5% had esophageal carcinoma, with 70.6% epidermoid carcinoma and 5.9% adenocarcinoma. Rats treated with water alone did not show histologic abnormalities of the esophageal mucosa. Rats treated with DEN alone developed papillomas in 50.0% of the cases and remained histologically unchanged in 50.0%. There was no development of low- or high-grade dysplasia in any group. The conclusions are that (1) GDER is significantly more deleterious to esophageal mucosa than GER; (2) in this study, GER did not present carcinogenic potential in relation to the esophagus; (3) GDER in isolation is an esophageal carcinogen, producing Barrett's esophagus and esophageal adenocarcinoma; (4) esophageal oncogenesis caused by GDER is potentiated by DEN, inducing esophageal epidermoid carcinoma; (5) in this study, DEN in isolation did not generate tumors in the esophagus of rats.

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