Effects of high molybdenum intake on 1.2 - dimethylhydrazine-induced intestinal tumors in rats

Wistar male rats, 3 months of age were given ad-libitum a nutritionally adequate diet and demineralized drinking water. The Molybdenum (Mo) and Tungsten (W) were provided in the drinking water at 200 ppm concentration. Intestinal tumors were induced by 1,2-dimethylhydrazine (DMH) given subcutaneously as 16 weekly doses at 20 mg/kg body weight. Mo in the form of (NH4)6 Mo7O24 4H2O or W in the form of (Na2WO4) were provided in the drinking water two months before the first DMH treatment and were continued during 4 months more until the last DMH treatment. Three months after the last carcinogen injection, all animals were sacrificed and examined for intestinal tumors. The number, size and location of the tumors were recorded and the pathology was examined. The addition of Mo to the drinking water induced an increase of hepatic Mo content. At the end of the second month, the hepatic content of Mo was 5.61 ppm, compared with control and W groups (2.18 and 0.96 ppm, respectively). A significantly lower incidence of tumors was observed in the Mo group (47), compared with the control group given DMH alone (105) and W group (113). On the other hand, the Mo group showed a significant decrease in the numbers of multiple tumors per rat.

Effects of high molybdenum intake on 1.2 - dimethylhydrazine-induced intestinal tumors in rats

Wistar male rats, 3 months of age were given ad-libitum a nutritionally adequate diet and demineralized drinking water. The Molybdenum (Mo) and Tungsten (W) were provided in the drinking water at 200 ppm concentration. Intestinal tumors were induced by 1,2-dimethylhydrazine (DMH) given subcutaneously as 16 weekly doses at 20 mg/kg body weight. Mo in the form of (NH4)6 Mo7O24 4H2O or W in the form of (Na2WO4) were provided in the drinking water two months before the first DMH treatment and were continued during 4 months more until the last DMH treatment. Three months after the last carcinogen injection, all animals were sacrificed and examined for intestinal tumors. The number, size and location of the tumors were recorded and the pathology was examined. The addition of Mo to the drinking water induced an increase of hepatic Mo content. At the end of the second month, the hepatic content of Mo was 5.61 ppm, compared with control and W groups (2.18 and 0.96 ppm, respectively). A significantly lower incidence of tumors was observed in the Mo group (47), compared with the control group given DMH alone (105) and W group (113). On the other hand, the Mo group showed a significant decrease in the numbers of multiple tumors per rat. (AU)

Failure to induce tumors in the large intestine of Capuchin mokeys (Cebus apella) by using 1,2-dimethylhydrazine.

The purpose of this study was to produce tumors in the large intestine of Capuchin Monkeys (Cebus apella) by the administration of the colonotropic carcinogen 1,2-dimethylhydrazine (DMH). The subjects were 12 monkeys, all males, age 30 months, with a mean weight of 2.858 kg. The DMH was administered subcutaneously to six of the monkeys at a dosage of 25 mg/kg of body weight once a week for 16 weeks; control monkeys received an equivalent volume of the stock solution without DMH. Twenty months after administration of the first dose, the animals were sacrificed. None of the monkeys showed intestinal tumors. Samples of the gastrointestinal tract were removed, fixed, and stained according to standard histological techniques. Histological changes were seen in all of the DMH-treated animals; these consisted of glandular hyperplasia and hyperplasia of the epithelium overlying the lymphoid nodules. In addition, foci of dysplasia were found in three of the animals. Our results suggest that the DMH induced pre-neoplastic changes, characterized by hyperplasia and dysplasia, in the mucosa of the large intestine.

Efecto de la sacarina de sodio en el intestino grueso del raton / Sodium saccharin effect in the mice large intestine

Se ha comprobado que la sacarina de sodio es un promotor tumoral del epitelio de la vegija de rata, propiedad no demostrada en el ser humano y actualmente discutida. En este trabajo se describen las alteraciones que produce este edulcorante en el epitelio del colon descendente de ratones cepa C3H, cuando es adicional al alimento en bajas dosis. Se muestra por microscopia electrónica de transmisión, que la sacarina de sodio produce en las células absortivas del epitelio del colon un pleomorfismo microvellositario constituido por microvellosidades de diferente forma, longitud, diámetro y curvatura.

Efecto de la sacarina de sodio en el intestino grueso del raton / Sodium saccharin effect in the mice large intestine

Se ha comprobado que la sacarina de sodio es un promotor tumoral del epitelio de la vegija de rata, propiedad no demostrada en el ser humano y actualmente discutida. En este trabajo se describen las alteraciones que produce este edulcorante en el epitelio del colon descendente de ratones cepa C3H, cuando es adicional al alimento en bajas dosis. Se muestra por microscopia electrónica de transmisión, que la sacarina de sodio produce en las células absortivas del epitelio del colon un pleomorfismo microvellositario constituido por microvellosidades de diferente forma, longitud, diámetro y curvatura. (AU)

[Sodium saccharin effect on the mice large intestine]. / Efecto de la sacarina de sodio en el intestino grueso del ratón.

Sodium saccharin has found to be a tumoral promoter in the rat's bladder epithelium, property not demonstrated in humans. Nevertheless, at present there's no references on the possible alterations produced by sodium saccharin in the epithelium of the mice colon. In this work we describe the alterations produced by low doses of sodium saccharin in the epithelium of the mice colon. The changer produced by sodium saccharin consist in pleomorphic microvill with variations of form, length diameter and curvature and demonstrate by transmission electron microscopy.

Atividade de xantina-oxidase na carcinogênese induzida pela 1.2-dimetil-hidrazina / Xantina-Oxidase activity in carcinogenesis induced by 1,2-dimethylhydrazine

A 1,2-dimetil-hidrazina (DMH) induz a formaçäo de tumores no intestino de ratos após aplicaçöes semanais durante 20 semanas. As atividades de xantina-oxidase (XO) e xantina-desidrogenase (XD) variam de acordo com a distância ao longo do intestino. Nos animais injetados com DMH verifiou-se uma diminuiçäo da atividade enzimática exatamente na porçäo onde ocorre maior incidência tumoral. Anotou-se, também, um aumento da atividade XD em soro sangüíneo de ratos tratados com DMH