Transforming growth factor- β (TGF- β) is believed to play a central role in fibroblastic wound repair and subsequent scar formation. Fibroblasts undergo apoptosis as granulation tissue evolves into a scar. To determine whether TGF- β influences fibroblast apoptosis, human lung fibroblasts (IMR-90) were treated with TGF- β (2 to 10 ng/mL) and then exposed to H 2 O 2 (50 to 150 μ M), an inducer of fibroblast apoptosis. Apoptosis was evaluated by nuclear staining with Hoechst33342 and terminal deoxynucleotidyl transferase (TdT)-mediated nucleotide nick-end labeling. TGF- β alone did not induce fibroblast apoptosis, but it dose-dependently augmented the apoptosis induced by exposure to H 2 O 2. TGF- β also increased the intracellular level of peroxides measured with carboxydichlorodihydrofluorescein, but it did not affect the protein levels of Bcl-2, Bax, Bad, or p53 proteins. These results suggest that TGF- β promotes lung fibroblast apoptosis induced by H 2 O 2, probably by increasing intracellular peroxides. Thus, TGF- β may promote the elimination of fibroblasts from wounds, particularly under conditions of exposure to enhanced oxidative stress in the lung. apoptosis fibroblast oxidative stress transforming growth factor- β