Posterior capsule opacification emerges from proliferation of remaining LECs after cataract surgery. Mitogenic cells express T-type calcium (Ca) channels in greater quantities than non-proliferating cells. This study analyses the effect of the T-type Ca channel blocker Mibefradil on proliferative and apoptotic behaviour on LECs. Cell proliferation was determined by cell culture assays. Mibefradil inhibited proliferation (IC50 = 1 ?M), whereas Verapamil in concentrations of 10 ?M. Activation of ERK1/2 and caspase-3 was detected by immunoblot analysis. The activation of MAPK 3 was reduced by both antagonists in the concentration ranges, in which they inhibited proliferation. Mibefradil also induced activation of caspase-3. Patch-clamp recordings were performed to investigate the inhibitory drug effects on Ca-inward currents; they were blocked by Mibefradil (IC50 = 10 nM) and Verapamil (IC50 = 1.5 ?M). Mitogenic HLE-B3 cells reacted more sensitive to a treatment with Mibefradil as to Verapamil possibly caused by higher expression of T-type Ca-channels. Caspase-3 activation and MAPK 3 inhibition are linked to a reduction of intracellular Ca-level, which might be induced by T-type Ca-channel block. It remains unclear, if this is the only mechanism, which induces the observed effects. Supported by DFG No 296/5