RESUMEN
A case of black insulinoma is reported. The color was due to a cytoplasmic pigment. Immunostaining for neuron-specific enolase and chromogranin was positive in the tumor cells, and the pigment granules themselves reacted with the chromogranin antibody. Numerous beta cell type dense core granules as well as atypical granules were found by electron microscopy. An important finding was that the dense core granules contribute to the lipofuscin pigment formation.
Asunto(s)
Insulinoma/ultraestructura , Neoplasias Pancreáticas/ultraestructura , Pigmentación , Anciano , Cromograninas/análisis , Gránulos Citoplasmáticos/ultraestructura , Microanálisis por Sonda Electrónica , Retículo Endoplásmico/ultraestructura , Femenino , Aparato de Golgi/ultraestructura , Histocitoquímica , Humanos , Técnicas para Inmunoenzimas , Lipofuscina/análisis , Microscopía Electrónica , Mitocondrias/ultraestructura , Neoplasias Pancreáticas/química , Fosfopiruvato Hidratasa/análisisRESUMEN
The present investigation was undertaken to discover whether in vivo inducers of autophagocytosis such as neutral red (0.40 mg/g body weight), cadmium chloride (0.15 mg/animal), vinblastine sulfate (7.5 mg/kg b.w.), and puromycin dihydrochloride (0.20 mg/g b.w.) are able to produce degranulation of rough surfaced endoplasmic reticulum (ER) of pancreatic acinar cells as we suggested earlier. Using a modified method of Blobel and Potter about 30% of the total ribosomes of untreated control pancreas were recovered in the free form, and 70% in the membrane-bound form. Cycloheximide (0.20 mg/g body weight) had no effect on this distribution of ribosomes, while neutral red, cadmium ions, vinblastine, and puromycin led to the presence of more free ribosomes: thus up to 70% of the total cytoplasmic ribosomes were recovered in the free form 30 to 60 min after treatments with the autophagic inducers. Pretreatments with cycloheximide prevented this shift and the distribution of ribosomes remained normal. On the basis of these and previous results we conclude that in pancreas an initial degranulation of the ER caused by these agents is a precondition of membrane transformation in autophagocytosis which is preventable by cycloheximide. Confirming the ultrastructural data of Longnecker et al. on rat pancreas, puromycin was shown to cause different forms of cellular injury including autophagocytosis. All forms of cellular injury were also prevented by pretreatment with cycloheximide in mouse pancreas.