Heme oxygenase (HO) plays a key role in regulating the intracellular heme level by catalyzing the initial and rate-limiting step, of heme degradation, triggering the release of biliverdin, iron and carbon monoxide. Three isoforms of mammalian HO have been identified to date: HO-1, HO-2 and HO-3. HO-1 is the inducible isoform that responds rapidly to diverse stimuli and protects tissues against a wide variety of injuries. Accumulating evidence suggests a vital role for HO-1 in both cell growth and cell death, especially showing the involvement of the enzyme in the regulation of apoptosis. HO-1 plays a protective role in many disease models via its anti-inflammatory, anti-apoptotic, and anti-proliferative actions. Although most evidences corroborate the cytoprotective (anti-apoptotic) effect of HO-1, this is not a universal finding. HO-1 may exert different effects in cell survival, including a pro-apoptotic effect, depending on the level of HO-1 expression and the cell type. The lymphoblastic cell line Jurkat was submitted to serum starvation (0.2%). After 24 hours, cells extracts were prepared and assayed for caspase 3/7 activity using Ac-DEVD-MCA substrate. We observed that extracts of cells under serum starvation hidrolysed 44.307 nmol MCA released/mg protein in 60 minutes, while extracts of cells kept in the presence of 10% serum hidrolysed 38.807 nmol MCA released/mg protein in 60 minutes. The addition of an inhibitor of HO-1, zinc protoporphyrin (ZnPP), in the cells subjected to serum starvation resulted in an upregulation of caspase 3/7 activity (131.65 nmol MCA released/mg protein in 60 minutes). We conclude that the protective role of HO-1 was suppressed by ZnPP, as showed by the increased cell susceptibility to stress stimuli. When the cells growing in 0.2% of serum were subjected to treatment with hemin (20µM), an inducer of HO-1 expression, we observed, after 24 hours, an increase in activation of caspase 3/7 (225.76 nmol MCA released/mg protein in 60 minutes). These findings indicate that a stress stimulus of serum starvation combined with hemin treatment could lead to enhanced HO-1 expression, reaching such high levels that the enzyme now becomes a positive regulator of the apoptosis pathway. Therefore, we propose that HO-1 is an important defense mechanism against cellular stress, possibly exerting a dual role in cell death.