Role of calcium ion in Schistosoma mansoni cercarial tail loss induced by unsaturated fatty acids.

Linoleate (C18: 2) and oleate (C18: 1), but not stearate (C18: 0), induced tail removal in cercariae. Linoleate stimulated tail loss more strongly than oleate did. Tail loss induced by linoleate was significantly suppressed by incubating cercariae with ethyleneglycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA). Preincubation of cercariae with EGTA for 5 min caused further inhibition of the tail loss. Calcium ionophore A23187 (A23187) increased the cercarial tail-loss rate. When A23187 was combined with linoleate at 0.03 mM, an additive effect on tail loss appeared, whereas the ionophore in combination with linoleate at 0.3 mM had no such effect. EGTA almost completely abolished cercarial tail loss induced by linoleate at both 0.03 and 0.3 mM in the presence and absence of A23187. Linoleate at 3 mM provoked cercarial tail loss even in the presence of EGTA, although the effect of oleate at 3 mM disappeared. Under these conditions, the effect of linoleate was synergistically enhanced by the combination with A23187. A similar, but not significant, synergism took place in cercariae stimulated by oleate. These findings suggest that unsaturated fatty acids enhance calcium influx into cercariae, resulting in triggering tail loss, and, furthermore, that the fatty acids have other potentiating effects on cercarial tail loss. Protein kinases play an insignificant role in fatty acid-induced cercarial tail loss, because a protein kinase C inhibitor, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), and an inhibitor of various protein kinases, staurosporine, had little or no effect on cercarial tail loss induced by linoleate at 3 mM.