Morphological alterations in salivary glands of mice (Mus musculus) submitted to tannin enriched diets: comparison with sialotrophic effects of sympathetic agonists stimulation / Alterações morfológicas das glândulas salivares de camundongos (Mus musculus) submetidos a dietas enriquecidas com taninos: comparação com os efeitos sialotróficos da estimulação com agonistas do sistema nervoso simpático

In order to study the effects of tannins at histomorphological level, mice were either fed with three structurally different types of tannins (tannic acid, chestnut, and quebracho) or treated with isoproterenol, during 10 days. Acini of parotid and submandibular glands increased significantly, being the increase higher for parotid compared to submandibular glands, and higher in the quebracho compared with the other tannin groups. Sublingual acinar size also increased after tannin consumption, by opposition to isoproterenol-treated animals. The results present evidences that the effects produced by tannins are dependent on their structure.

Estudaram-se as alterações morfológicas das glândulas salivares, induzidas por taninos, em camundongos. Os animais foram distribuídos em grupos e tratados com três diferentes tipos estruturais de taninos (ácido tânico, chestnut e quebracho - adicionados à ração) ou isoproterenol via intraperitoneal, durante 10 dias. Os ácinos das glândulas parótida e submandibulares aumentaram significativamente de tamanho, sendo o incremento maior para a parótida que para as submandibulares, e maior com o quebracho comparado com o provocado pelos outros taninos. Os ácinos das glândulas sublinguais também aumentaram após o consumo de taninos em relação aos ácinos dos animais tratados com isoproterenol. Os resultados apresentam evidências de que os efeitos produzidos pelos taninos dependem de sua estrutura.

Expressão da caderina na discondroplasia tibial / Cadherin expression in the tibial dyschondroplasia

By immunohistochemistry the expression of a pan-cadherin antibody that recognizes a wide variety of cadherins in chondrocytes from normal and tibial dyschondroplasia (TD) growth plates was compared. Surprisingly, an upregulated expression that was not expected in TD lesion chondrocytes was observed. The reason for this apparent upregulation is not clear. The increased expression may simply be due to the particular phenotype of lesion chondrocytes, and cadherin may be involved in apoptosis of chondrocytes of TD lesion. Another possibility, is that a low level of calcium in the lesion may be responsible for the observed upregulation. The results of the present study suggest that the formation of the dyschondroplastic lesion is not merely due to the impaired terminal differentiation of lesion chondrocytes and that other mechanisms are probably involved in TD etiology. Further studies will be necessary to provide insight into the precise nature of the condition.