ABSTRACT
Yogurt consumption has been associated with decreased risk of colon cancer. The apoptosis induced by yogurt as a mechanism involved in the inhibition of an experimental intestinal tumor induced by 1,2 dimethylhydrazine (DMH) in BALB/c mice, has been studied. An imbalance between apoptosis and mitosis or cell proliferation is believed to underlie colon cancer development and progression. We determined the effect of yogurt feeding in the induction of apoptosis and the relationship between mitosis and apoptosis in mice injected with the carcinogen DMH and in mice injected with DMH and fed with a diet supplemented with yogurt. The percentage of mitotic and apoptotic cells was analyzed every 2 weeks from week 8 to 16. They were analyzed on histological slices from the large intestine by colchicine, or Tunel test for mitosis and apoptosis determination, respectively. An increase in the mitosis during the first 4 weeks of tumor development with apoptosis negative and severe dysphasia, was observed in animals treated with the carcinogen. In those animals that received DMH and were given yogurt, a moderate cell proliferation with a significant increase in the number of apoptotic cells was determined. The increase in the apoptotic activity was also observed in the group of animals that received only a diet supplemented with yogurt. The results suggest that yogurt would influence the balance between mitosis and apoptosis, which was modified during the carcinogenesis process, by increasing cellular apoptosis. Dietary supplementation of yogurt may play a role in modulating cell proliferation or apoptosis during the development of colorectal carcinoma.
ABSTRACT
In order to grow, solid tumors need to develop new blood vessels. Neoplastic cells secrete growth factors that stimulate angiogenesis and tumor growth. Since Carrageenan acts as in vitro blocking agent which interferes with growth factor-receptor binding, we tested its action in vivo in order to analyze its growth inhibition capability in an experimental murine fibrosarcoma model. Indomethacin was used as a non-steroidal anti-inflammatory agent to neutralize the inflammatory action of Carrageenan. A murine fibrosarcoma was induced with methylcholanthrene in Balb/c mice and maintained by serial passage of tumor cells in mice of the same strain. Tumor volume was evaluated measuring two dimensions and applying the formula V = 0.4 x d2 x D. The mice with tumors were separated into groups; one of them was used as control and the other ones were treated with Indomethacin, Carrageenan and Carrageenan-Indomethacin. Tumor volume was compared between groups using the Student t Test. We demonstrated that Carrageenan and Indomethacin inhibit tumor growth. The inhibitory action of Carrageenan is significantly higher than the antitumoral effect of either Indomethacin or Carrageenan-Indomethacin.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/antagonists & inhibitors , Carrageenan/pharmacology , Fibrosarcoma/drug therapy , Indomethacin/antagonists & inhibitors , Receptors, Growth Factor/drug effects , Animals , Carcinogens , Carrageenan/therapeutic use , Female , Fibrosarcoma/chemically induced , Fibrosarcoma/metabolism , Male , Methylcholanthrene , Mice , Mice, Inbred BALB C , Neoplastic ProcessesABSTRACT
In order to grow, solid tumors need to develop new blood vessels. Neoplastic cells secrete growth factors that stimulate angiogenesis and tumor growth. Since Carrageenan acts as in vitro blocking agent which interferes with growth factor-receptor binding, we tested its action in vivo in order to analyze its growth inhibition capability in an experimental murine fibrosarcoma model. Indomethacin was used as a non-steroidal anti-inflammatory agent to neutralize the inflammatory action of Carrageenan. A murine fibrosarcoma was induced with methylcholanthrene in Balb/c mice and maintained by serial passage of tumor cells in mice of the same strain. Tumor volume was evaluated measuring two dimensions and applying the formula V = 0.4 x d2 x D. The mice with tumors were separated into groups; one of them was used as control and the other ones were treated with Indomethacin, Carrageenan and Carrageenan-Indomethacin. Tumor volume was compared between groups using the Student t Test. We demonstrated that Carrageenan and Indomethacin inhibit tumor growth. The inhibitory action of Carrageenan is significantly higher than the antitumoral effect of either Indomethacin or Carrageenan-Indomethacin.
ABSTRACT
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)
Subject(s)
Animals , Male , Female , Mice , Saccharin/adverse effects , Sodium , Sweetening Agents/adverse effects , Intestinal Mucosa/drug effects , Colon/drug effects , Intestinal Mucosa/pathology , Intestinal Mucosa/ultrastructure , Colon/pathology , Microvilli , Intestinal Absorption , Intestinal Neoplasms/chemically induced , Microscopy, ElectronABSTRACT
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.
Subject(s)
Animals , Male , Female , Mice , Colon/drug effects , Intestinal Mucosa/drug effects , Saccharin/adverse effects , Sodium , Sweetening Agents/adverse effects , Colon/pathology , Intestinal Absorption , Intestinal Mucosa/pathology , Intestinal Mucosa/ultrastructure , Intestinal Neoplasms/chemically induced , Microscopy, Electron , MicrovilliABSTRACT
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.
Subject(s)
Colon/drug effects , Intestinal Mucosa/drug effects , Saccharin/adverse effects , Sweetening Agents/adverse effects , Animals , Colon/pathology , Female , Intestinal Absorption/drug effects , Intestinal Mucosa/pathology , Intestinal Mucosa/ultrastructure , Intestinal Neoplasms/chemically induced , Male , Mice , Microscopy, Electron , Microvilli , SodiumABSTRACT
The present study evaluated the effect of sodium saccharin on mouse tracheal epithelium, in relation to its possible structural alterations. Mice of the C3H strain were fed with standard pellets supplemented with sodium saccharin for 180 days. At that time the mice were sacrificed and their trachea were processed for transmission electronic microscopy. We demonstrated that sodium saccharin produces alterations in cellular surface cilia, with cytoplasmic excrescences and ciliary malformations. These results suggest that sodium saccharin is not an innocuous sweetener and that it may cause structural alterations in epithelial tissues.
Subject(s)
Saccharin/pharmacology , Trachea/drug effects , Animals , Epithelium/drug effects , Male , MiceABSTRACT
Saccharin and cyclamates have been proved to cause organic damage. This work attempt to describe drug-induced changes brought about by drugs in 1/1000 saccharin and cyclamate-fed rats for 90 days. The ultrastructural findings show: microvilli hypertrophy; membranous mitochondrial increase in absorptive cells; and secretion changes in calciform cells. Such changes are cell-response phenomena to interference or mutagenic action on nuclear DNA or on cytoplasmatic metabolism.
Subject(s)
Cyclamates/adverse effects , Intestine, Large/drug effects , Intestine, Large/ultrastructure , Saccharin/adverse effects , Animals , Cell Membrane/drug effects , Cell Membrane/ultrastructure , Cyclamates/toxicity , Diet , Female , Male , Mice , Mice, Inbred C3H , Saccharin/toxicityABSTRACT
Saccharin and cyclamates have been proved to cause organic damage. This work attempt to describe drug-induced changes brought about by drugs in 1/1000 saccharin and cyclamate-fed rats for 90 days. The ultrastructural findings show: microvilli hypertrophy; membranous mitochondrial increase in absorptive cells; and secretion changes in calciform cells. Such changes are cell-response phenomena to interference or mutagenic action on nuclear DNA or on cytoplasmatic metabolism.
ABSTRACT
Se realizó un diseño experimental en ratones cepa C3Hs de 45gr de peso, alimentados con dieta standard y agua ad-libitium con acetato de plomo en concentraciones muy bajas (dosis contaminante), por ingreso constante durante períodos determinados. Nuestro objetivo es demostrar el efecto nocivo tóxico y su depósito en la células. Se estudiaron en microscopía óptica y electrónica hígado y bazo por ser órganos con gran cantidad de macrófagos fijos con función fagocitaria, encontrándose lesiones y depósitos que confirman el agente etiológico y su acción tóxica como contaminante
Subject(s)
Animals , Mice , Spleen , Liver , Lead/adverse effects , Spleen/pathology , Liver/pathologyABSTRACT
Se realizó un diseño experimental en ratones cepa C3Hs de 45gr de peso, alimentados con dieta standard y agua ad-libitium con acetato de plomo en concentraciones muy bajas (dosis contaminante), por ingreso constante durante períodos determinados. Nuestro objetivo es demostrar el efecto nocivo tóxico y su depósito en la células. Se estudiaron en microscopía óptica y electrónica hígado y bazo por ser órganos con gran cantidad de macrófagos fijos con función fagocitaria, encontrándose lesiones y depósitos que confirman el agente etiológico y su acción tóxica como contaminante (AU)
Subject(s)
Animals , Mice , Lead/adverse effects , Liver/drug effects , Spleen/drug effects , Liver/pathology , Spleen/pathologyABSTRACT
The aim of the present paper is to show lead toxicity and cell deposition of concentrations lower than those regarded as toxic on an experimental model with rats C3Hs., forty five grams-rats were used. A standard diet was administered together with water ad-libitium, containing very low doses of lead acetate which was constantly administered and at fixed periods. Light and electron microscopy were used to study the liver and the spleen. These organs are considered to harbour a great amount of constant macrophages with phagocytic function. The findings showed lesions and lead deposits which confirmed the causative agent as well as its toxic contaminating action.
Subject(s)
Lead Poisoning/pathology , Liver/pathology , Spleen/pathology , Animals , Mice , Mice, Inbred C3HABSTRACT
The aim of the present paper is to show lead toxicity and cell deposition of concentrations lower than those regarded as toxic on an experimental model with rats C3Hs., forty five grams-rats were used. A standard diet was administered together with water ad-libitium, containing very low doses of lead acetate which was constantly administered and at fixed periods. Light and electron microscopy were used to study the liver and the spleen. These organs are considered to harbour a great amount of constant macrophages with phagocytic function. The findings showed lesions and lead deposits which confirmed the causative agent as well as its toxic contaminating action.
