For this purpose, we evaluated the proliferation inhibition by cytotoxic assay expressed as the concentration of drug inducing a 50%decrease in growth (IC50). The IC50 was reached for testosterone at 100 μM, androstenedione at 375 μM, nandrolone at 9 μM, norandrostenedione at 500 μM. The IC50 value for norandrostenediol was not reached until a concentration of 6000 μM. The apoptotic effect was evaluated by flow cytometry at IC50 for each drug. We observed that testosterone induced 31%of apoptotic cells, norandrostenedione 25%, androstenedione 15%and nandrolone 18%. We have analyzed the effects of these drugs on [Ca2+]i both in the immediate and long-term continuous presence of each compound. Our data show a statistically significant increase of [Ca2+]i in the acute condition and in long-term treated cultures, suggesting that androgen steroids modulate intracellular levels of calcium independent of incubation time or compound identity. As a whole, this study demonstrates that AAS might alter endothelial homeostasis, predisposing to the early endothelial cell activation that is responsible for vascular complications observed frequently in AAS users.