Dr. Spitz is a well-established investigator studying the role of metabolic oxidative stress in lung cancer biology and therapy as well as radiobiology. His scientific impact on the field includes 1) developing the competitive inhibition superoxide dismutase (SOD) activity assay commonly used today to discriminate between MnSOD and CuZnSOD activity in mammalian tissue homogenates, 2) showing that acute and chronic exposure of mammalian cells in culture to both H2O2 and high levels of O2 induced transient and stable cellular resistance to oxidative stress that was accompanied by profound changes in the expression of many protective proteins and oxidative stress responsive pathways, 3) the discovery that chronic exposure to oxidative stress mediated by H2O2 and high levels of O2 (as well as mutations in mitochondrial electron transport chain proteins) was capable of inducing genomic instability and gene amplification in mammalian cells as well as rendering them cross resistant to agents used to treat cancer, 4) the discovery that glucose deprivation preferentially killed cancer vs. normal cells by metabolic oxidative stress mediated by mitochondrial O2•- and H2O2, 5) the discovery that human tumor cell mitochondria generate greater steady-state levels of O2•-/H2O2, relative to normal cells, that could potentially be exploited for cancer therapy purposes.
Dr. Spitz has been a member of the Human Toxicology program for 20 years and has trained several PhD students from that program as well as regularly publishing in the field of toxicology as it relates to Radiation, Cancer and Free Radical Biology.