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Thiocyanate (SCN-) plays a critical part in an oral antimicrobial system by acting as a substrate for peroxidases. Salivary glands concentrate SCN- from blood up to 5 mM in saliva; however, the influence of SCN- on salivary acinar-cell function is unknown. The present study examined the effects of SCN- on the regulation of cytosolic pH (pHi) and free Ca2 concentration ([Ca2 ]i) in rat sublingual mucous acini using the pH- and Ca2 -sensitive fluorescent indicators, 2′,7′-bis-(2-carboxyethyl)-5,6-carboxyfluorescein and fura-2, respectively. SCN- induced a concentration-dependent inhibition of the carbachol-stimulated cytosolic acidification (K1 2, approx. 1.4mM SCN-). Cytosolic pH recovery from an acid load was not changed by substitution of Cl- by SCN-, suggesting that Na /H exchange activity was not affected by SCN-. SCN- did not alter the initial carbachol-stimulated increase in [Ca2 ]i; however, the sustained [Ca2 ]i increase was inhibited by >65%25 (K1 2, approx. 1.0 mM SCN-). Furthermore, SCN- prevented the carbachol-stimulated Mn2 influx, indicating that it inhibits the divalent-cation entry pathway. Consistent with decreased Ca2 mobilization being involved in the blockade of the agonist-induced acidification by SCN-, only total replacement of Cl- with SCN- significantly inhibited the acidification induced by the Ca2 ionophore ionomycin. The permeability to SCN- through the Ca2 -dependent Cl- channels was 5.2-fold higher than the permeability to Cl-. These results suggest that inhibition of the agonist-induced cytosolic acidification by high-concentration SCN- may be mediated by both competitive inhibition of HCO3- efflux and by blockade of Ca2 influx. © 1995.
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Thiocyanate (SCN-) plays a critical part in an oral antimicrobial system by acting as a substrate for peroxidases. Salivary glands concentrate SCN- from blood up to 5 mM in saliva; however, the influence of SCN- on salivary acinar-cell function is unknown. The present study examined the effects of SCN- on the regulation of cytosolic pH (pHi) and free Ca2%2b concentration ([Ca2%2b]i) in rat sublingual mucous acini using the pH- and Ca2%2b-sensitive fluorescent indicators, 2′,7′-bis-(2-carboxyethyl)-5,6-carboxyfluorescein and fura-2, respectively. SCN- induced a concentration-dependent inhibition of the carbachol-stimulated cytosolic acidification (K1 2, approx. 1.4mM SCN-). Cytosolic pH recovery from an acid load was not changed by substitution of Cl- by SCN-, suggesting that Na%2b/H%2b exchange activity was not affected by SCN-. SCN- did not alter the initial carbachol-stimulated increase in [Ca2%2b]i; however, the sustained [Ca2%2b]i increase was inhibited by >65%25 (K1 2, approx. 1.0 mM SCN-). Furthermore, SCN- prevented the carbachol-stimulated Mn2%2b influx, indicating that it inhibits the divalent-cation entry pathway. Consistent with decreased Ca2%2b mobilization being involved in the blockade of the agonist-induced acidification by SCN-, only total replacement of Cl- with SCN- significantly inhibited the acidification induced by the Ca2%2b ionophore ionomycin. The permeability to SCN- through the Ca2%2b-dependent Cl- channels was 5.2-fold higher than the permeability to Cl-. These results suggest that inhibition of the agonist-induced cytosolic acidification by high-concentration SCN- may be mediated by both competitive inhibition of HCO3- efflux and by blockade of Ca2%2b influx. © 1995.
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