Objective:To investigate the effects of 5α - dihydrostestosterone (DHT) on calcium mobilization and growth of prostate cancer cell line LNCaP.Methods: Intracellular calcium concentration (\[Ca2+\]i) was assayed by MiraCal Image System using Fura-2/AM as Ca2+ fluorescence probe. Cell viability was observed by MTT assay and apoptosis by flow cytometry. Results: The calcium levels rapidly increased following addition of DHT, with the latency of response only in seconds. DHT at the concentrations of 1, 10, 100 and 1 000 nmol/L increased \[Ca2+\]i from (28±5), (29±5), (28±4) and (28±9) nmol/L to (31±3) ( P>0.05,65±9) (P<0.01), (193±33) (P<0.001) and (208±42) nmol/L (P<0.001), respectively. The response induced by 1 000 nmol/L DHT was similar to that induced by 100 nmol/L DTH. DHT 1 000 nmol/L did not increase \[Ca2+\]i under extracellular Ca2+ -free condition. Blockers of L-type voltage-gated calcium channels, including verapamil (50 μmol/L), diltiazem (100 μmol/L) or nifedipine (5 mmol/L) at 37℃ for 5 min prior to stimulation with 1 000 nmol/L DHT, completely inhibited DHT-induced \[Ca2+\]i rise. Pre-treatment with inhibitor of phospholipase C such as neomycin sulfate (1 mmol/L) at 37℃ for 3 min or inhibitor of ryanodine receptor such as procaine (50 mmol/L) at 37℃ for 3 min had no influence on \[Ca2+\]i rise induced by 1 000 nmol/L DHT. The optical density (D) values and early apoptosis rates of the cells stimulated with 1 000 nmol/L DHT for 48 h were significantly different from those of cells pre-treated with verapamil prior to stimulation with 1 000 nmol/L DHT (\[0.67±0.10\] % vs \[2.13±0.16\] % and \[14.31±2.29\] % vs \[1.07±0.19\] %,P<0.01).