The main goal of my research is to understand the molecular mechanism of chemotherapy induced apoptosis, and specially the role of coenzyme Q (CoQ) in this process. A complex aspect of apoptosis regulation is the role of intracellular oxidation and free radicals. It is known that reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) or nitric oxide (NO), induce apoptosis in different cell types, and many apoptotic inducers, such as some chemotherapeutic drugs, which are not proper ROS, cause intracellular oxidation. Antineoplasic agents administrated during cancer chemo therapy induce oxidative stress, increase lipid peroxidation, and reduce blood levels of different antioxidants, such as _- tocopherol, ascorbate, and _-carotene. CoQ or ubiquinone, a lipid-soluble component of virtually all cell membranes, is an isoprenylated benzoquinone. CoQ has an important role in respiratory metabolism, as a mobile electron and proton carrier in the mitochondrial electron transport chain. In eukaryotes, CoQ shuttles electrons from complexes I and II to complex III in the mitochondrial electron transfer system. Recently, it has been demonstrated that CoQ also functions as an antioxidant which protects the cells both directly by preventing lipid peroxidation and indirectly by regenerating other antioxidants such as ascorbate and _-tocopherol. CoQ antioxidant function is also important in vivo as it has been demonstrated in ubiquinone-deficient mutants of S. cerevisiae and S. pombe that are more sensitive to products of oxidized polyunsaturated fatty acids. Products of eight nuclear genes have been described to participate in CoQ biosynthesis in bacteria, yeasts, and nematodes. Different human genes homologous of those described in yeast and nematodes, such as clk-1/coq-7 and coq-8 genes, are thought to participate in CoQ biosynthesis. We are working in analyzing the role of CoQ in chemotherapy-induced apoptosis as part of the antioxidant defense against free radical production under these anticancer treatments.