The murine proapoptotic protein Bax was expressed in Kluyveromyces lactis to 
investigate its effect on cell survival and production of reactive oxygen 
species (ROS). Bax expression decreased the number of cells capable of growing 
and forming colonies, and it increased the number of cells producing ROS, as 
detected by both dihydrorhodamine 123 fluorescence and the intracellular content 
of SH groups. Mutation in the beta-subunit of F(1)-ATPase, or mitochondrial 
deficiency resulting from deletion of mtDNA (rho(0) mutant), increased the 
sensitivity to Bax, indicating that Bax cytotoxicity does not require 
mitochondrial respiratory-chain functions. The antiapoptotic protein Bcl-x(L), 
when co-expressed with Bax, localized to the mitochondria and prevented Bax 
cytotoxicity. However, this co-expression did not prevent the production of ROS. 
These data suggest that in K. lactis cells expressing Bax, ROS are not the sine 
qua non of cell death and that the antiapoptotic function of Bcl-x(L) is not 
limited to its antioxidant property.