抄録
To clarify the effect of polaprezinc (a chelate compound consisting of zinc ion and L-carnosine) on taste disorder, we investigated the effect of polaprezinc on zinc-deficient (Zn(-)) diet-induced hypogeusia model in rats. After four weeks on the Zn(-) diet feeding, polaprezinc (1, 3 or 10mg/kg) for four weeks or [65Zn] polaprezinc (10mg/kg) for two weeks were administered orally once a day. Zn(-) rats increased the preference rate for quinine hydrochloride solution, while polaprezinc repaired the increased taste preference rate. We also evaluated the proliferation of taste bud cells in the circumvallate papilla using 5-bromo-2'-deoxyuridine (BrdU). The incorporation of BrdU into taste bud cells in Zn(-) rats was reduced as compared with that in zinc-sufficient (Zn(+)) rats and polaprezinc at doses of 3 and 10mg/kg improved the reduced incorporation of BrdU into taste bud cells. The zinc concentration in the lingual epithelium was markedly decreased in Zn(-) rats as compared with Zn(+) rats. After administration of polaprezinc to Zn(-) rats at doses of 1, 3 and 10mg/kg, zinc concentration in the lingual epithelium significantly increased. Moreover, after administration of [65Zn] polaprezinc, the 65Zn radioactivity was mainly detected in the epithelium of the tongue in Zn(-) rats. These findings are indicating that the altered taste preferences by zinc deficiency is induced by the delayed proliferation of taste bud cells, and the restoration of zinc contents by polaprezinc in the lingual epithelium repaired the increased taste preference rate by improving the delay of cell proliferation. The results demonstrate the significance of zinc and the therapeutic efficacy of polaprezinc for taste disorder.
