In Ringer solution, gold ions (Au3+) at concentrations more than 50 microM produced a phasic and subsequent tonic contraction spontaneously in single toe muscle fiber of frog. When 1.8 mM Ca2+ in Ringer solution was replaced by 3 mM Mg2+, tonic contraction was no longer provoked in response to Au3+. Only phasic contraction was potentiated by 10 mM perchlorate (an L-type Ca2+ channel activator) irrespective of external Ca2+, and both phasic and tonic contractions were blocked by 10 microM nifedipine (an L-type Ca2+ channel blocker). Upon application of 5 mM dithiothreitol to the contracting fiber, the Au(3+)-induced tension disappeared rapidly. The fiber pretreated with 0.05% H2O2 for 10 min did not respond to Au3+ with visible contraction. Treatment of H2O2-paralyzed fibers with dithiothreitol (to reduce oxidized sulfhydryl groups) fully restored the Au(3+)-induced contraction. These results suggest that the phasic contraction induced by Au3+ probably is mediated through sulfhydryl groups in the L-type Ca2+ channel (dihydropyridine receptor) on the transverse tubular membrane. Sustained contraction was produced by Ca2+ application to Au(3+)-treated fibers in Mg(2+)-Ringer solution, and Au3+ caused membrane depolarization in a dose-dependent manner. These effects of Au3+ may explain tonic contraction development.