RESUMO
In magnesium deficient rats with a clinical picture of protein malnutrition, pancreatic changes typical of protein malnutrition were expected. However, in rats fed for four weeks on a low magnesium diet (protein content 25 percent), light and electron microscopic studies revealed that the ascinar cells of the pancreas were packed with zymogen granules, suggesting a disturbance in the discharge (rather than in the production) of the pancreatic enzymes. The mitochondria and the lumina of the RER were swollen. The nuclei had an irregular outline, the chromatin was aggregated into irregular granules and the nucleolemma of the nucleolus was fibrillar. It was suggested that the disturbance in the release of pancreatic enzymes might cause a maldigestion of the dietary protein, which eventually would lead to the condition of protein malnutrition in the magnesium deficient rats. The disturbance of exocytosis in the pancreas of magnesium deficient rats might be due to the preferential use of all the available magnesium for protein (enzymes) synthesis so that there were no magnesium ions left for the energy dependent discharge of the zymogen granules (AU).
Assuntos
21003 , Masculino , Ratos , Deficiência de Magnésio/patologia , Pâncreas/ultraestrutura , Núcleo Celular/ultraestrutura , Grânulos Citoplasmáticos/ultraestrutura , Mitocôndrias/ultraestrutura , Retículo Endoplasmático/ultraestrutura , Complexo de Golgi/ultraestrutura , Junções Intercelulares/ultraestrutura , Microscopia Eletrônica , Ribossomos/ultraestruturaRESUMO
Nine patients had a syndrome characterized by the presence of a sea-blue histiocyte and splenomegaly. Lipid analysis of liver from the most recent patient revealed accumulations of specific glycosphingolipids and phospholipids. Urinary mucopolysaccharide excretion was increased, and there was a suggestion of mucopolysaccharide storage in the hepatic parenchymal cells. Clinically, patients with the disease may have a relatively benign course, with mild purpura secondary to thrombocytopenia, or may have progressive hepatic cirrhosis, hepatic failure and death. The name "syndrome of the sea-blue histiocyte," the striking morphologic feature of the disease, is suggested for these cases (AU)