Morphine does no promote esophageal carcinogenesis in rats exposed to diethylnitrosamine.

BACKGROUND: The high incidence of esophageal cancer in the north of Iran has been associated to the consumption of opium and exposure to nitrosamines. Diethylnitrosamine has an established potential of producing experimental cancer in the esophagus and liver. AIM: To evaluate by histopathology the effect of oral administration of morphine and diethylnitrosamine during 23 weeks on the hepatic and esophageal carcinogenesis on 176 rats. METHODS: We divided the rats into the following groups: Morph: morphine; Den: diethylnitrosamine; Den+morph: Den and morphine in the same solution; Den/morph: Den and morphine in different solutions and days. RESULTS: Morphine did not promote neoplasias. The highest neoplastic incidents were found: a) in the esophagus, Den in relation to Den/morph and Den+morph (71.1%, 55.8%, and 50.0%); b) in the liver, Den and Den/morph in relation to Den+morph (73.8%, 81.4%, and 40.9%); c) higher incident of hepatic neoplasia than esophageal in Den/morph (81.4% and 55.8%). Different doses of diethylnitrosamine were ingested among the groups Den, Den/morph, and Den+morph, respectively 2.9, 2.8, and 2.3 mg/kg/day. CONCLUSIONS: These results show that the morphine did not promote esophageal carcinogenesis and may have stimulated the hepatic metabolism of the first pass of the carcinogen.

Morphine does no promote esophageal carcinogenesis in rats exposed to diethylnitrosamine

BACKGROUND: The high incidence of esophageal cancer in the north of Iran has been associated to the consumption of opium and exposure to nitrosamines. Diethylnitrosamine has an established potential of producing experimental cancer in the esophagus and liver. AIM: To evaluate by histopathology the effect of oral administration of morphine and diethylnitrosamine during 23 weeks on the hepatic and esophageal carcinogenesis on 176 rats. METHODS: We divided the rats into the following groups: Morph: morphine; Den: diethylnitrosamine; Den+morph: Den and morphine in the same solution; Den/morph: Den and morphine in different solutions and days. RESULTS: Morphine did not promote neoplasias. The highest neoplastic incidents were found: a) in the esophagus, Den in relation to Den/morph and Den+morph (71.1 percent, 55.8 percent, and 50.0 percent); b) in the liver, Den and Den/morph in relation to Den+morph (73.8 percent, 81.4 percent, and 40.9 percent); c) higher incident of hepatic neoplasia than esophageal in Den/morph (81.4 percent and 55.8 percent). Different doses of diethylnitrosamine were ingested among the groups Den, Den/morph, and Den+morph, respectively 2.9, 2.8, and 2.3 mg/kg/day. CONCLUSIONS: These results show that the morphine did not promote esophageal carcinogenesis and may have stimulated the hepatic metabolism of the first pass of the carcinogen.

RACIONAL: A alta incidência de câncer esofagiano no norte do Irã foi associada ao consumo de ópio e exposição às nitrosaminas. A dietilnitrosamina possui potencial estabelecido de produzir câncer experimental em esôfago e fígado. OBJETIVO: Avaliar por histopatologia o efeito da administração oral de morfina e de dietilnitrosamina na carcinogênese esofágica e hepática em ratos. MÉTODOS: Durante 23 semanas, 176 ratos ingeriram diferentes soluções, sendo divididos em grupos: Morf: morfina; Den: dietilnitrosamina; Den+morf: dietilnitrosamina e morfina numa mesma solução; Den/morf: dietilnitrosamina e morfina em diferentes soluções e dias. RESULTADOS: Morf não promoveu neoplasias. Encontraram-se maiores incidências neoplásicas: a) no esôfago, Den em relação à Den/morf e Den+morf (71,1 por cento, 55,8 por cento e 50,0 por cento); b) no fígado, Den e Den/morf em relação à Den+morf (73,8 por cento, 81,4 por cento e 40,9 por cento); c) maior incidência de neoplasia hepática do que esofágica em Den/morf (81,4 por cento e 55,8 por cento). Diferentes doses de dietilnitrosamina foram ingeridas entre os grupos Den, Den/morf e Den+morf, respectivamente 2,9, 2,8 e 2,3 mg/kg/dia. CONCLUSÕES: A morfina não promoveu a carcinogênese esofágica e pode ter estimulado o metabolismo hepático de primeira passagem do carcinógeno.