Glandular kallikrein activity in whole saliva was determined in 16 patients with malignant tumors distant from the oral cavity and in an equal number of healthy control subjects of similar age and sex distribution. The level of glandular kallikrein was significantly greater in saliva obtained from the patients with solid tumours as determined with a tripeptide nitro-anilide substrate, D-Val-Leu-ArgpNA. A basis for the higher levels of glandular kallikrein in saliva obtained from the solid tumor patients has not been established, nor is it possible to establish a role for glandular kallikrein in the pathogenesis of malignant disease. The higher level of glandular kallikrein observed in whole saliva obtained from patients with solid tumors suggests the need for further investigation of the role of kallikrein in malignant disease and the usefulness of salivary measurements of this enzyme as a reflection of systemic changes.
Eleven-day-old rat maxillary first molar explants were removed by microdissection and incubated in vitro to determine the direct effects of parathyroid hormone (PTH), calcitonin (CT), 1,25(OH)2D3, 24,25(OH)2D3, and a combination of PTH and vitamin D3 metabolites on calcium uptake in the mineralizing enamel of the explants. None of the agents had a statistically significant effect. These results are in contrast to those observed on explants from six-day-old rats, where PTH + 24,25(OH)2D3 caused a significant increase in net calcium transport. The findings are consistent with the hypothesis that the transcellular transport of calcium through the secretary stage and the maturation stage ameloblasts occurs by different mechanisms.
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