RESUMO
Ultrastructural features of the cheek oral mucosa of rats (Rattus norvegicus) submitted to experimental chronic alcoholism were studied by transmission electron microscopy. Sixty male rats aged three months and with a mean body weight of 250 g were divided into two experimental groups. The control group received a solid diet (Purina rat chow) and tap water ad libitum. The alcoholic group received the same solid diet but was only allowed to drink sugar cane liquor dissolved in 30 degrees Gay Lussac (v/v). The animals of the two groups were weighed and sacrificed after 60, 120, and 180 days of treatment. Samples of the oral mucosa from the cheek region were dissected and processed for ultrastructural analysis. The results showed cell alterations in the basal and intermediate layer of the mucosal epithelium. The most frequent alterations observed were an increased intercellular space, the presence of lipid droplets in the cytoplasm, and irregular nuclei with a pyknotic aspect.
Assuntos
Alcoolismo/patologia , Mucosa Bucal/efeitos dos fármacos , Mucosa Bucal/ultraestrutura , Animais , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/ultraestrutura , Bochecha/patologia , Citoplasma/efeitos dos fármacos , Citoplasma/ultraestrutura , Desmossomos/efeitos dos fármacos , Desmossomos/ultraestrutura , Modelos Animais de Doenças , Lipídeos , Masculino , Microscopia Eletrônica , RatosRESUMO
We have reported that the local administration of serine protease inhibitors (amyloid precursor protein with the Kunitz insert (APP K+), aprotinin, and leupeptin) to the rat sciatic nerve determines a sprouting response of myelinated axons, proliferation of Schwann cells, and demyelination, 5 to 7 days later. Further study of these nerves with the electron microscope revealed (i) a sprouting response of nonmedullated axons, (ii) the appearance of fine axons with a few turns of compact myclin, (iii) abnormal contracts of axons with basal laminae, with fibroblast-like cells, and between them, (iv) the occurrence of hemidesmosome- and desmosome-like junctions between Schwann cell processes, and between Schwann cells and axons, and (v) the appearance of amorphous and fibrillary extracellular deposits alongside the axolemma. The adjacent proximal and distal segments were normal, i.e., axons remained continuous, and the alterations were confined to the segment exposed to the protease inhibitors. Heated APP Kappa +, APP without the Kunitz insert (APP K-), bovine serum albumin, and saline, did not elicit cytological alterations. Our results suggest that these inhibitors of serine proteases (i) set free a sprouting drive of axons by disrupting an ongoing repressive mechanism: (ii) modify the adhesive properties of axons and Schwann cells, and (iii) alter the natural history of an extracellular material. The imbalance of an extracellular protease system may participate in the pathogenesis of Alzheimer's disease.