Apigenin, a widely distributed plant flavonoid, was previously found to inhibit chemically induced ornithine decarboxylase (ODC) activity and skin tumor promotion. The purpose of the present research was to determine if apigenin is effective in the prevention of ultraviolet-B light (UVB) induced skin carcinogenesis. Further studies ascertained if apigenin would be expected to absorb UVB light in a manner to prevent DNA damage in a cell free system. ODC activity was induced with 0.45 J/cm2 ultraviolet A and B (UVA/B) light. Apigenin (5 mumoles/200 microliters DMSO:acetone, 1:9) treatment from 12 hours before until 1 hour following UVA/B exposure was effective in inhibition (25-45% inhibition) of ODC activity measured at 28 hours following UVA/B exposure. Mouse skin carcinogenesis was induced by exposure to a total dose of 40 J/cm2 UVB over 11 weeks. Treatment with 10 mumoles apigenin in 200 microliters DMSO:acetone (1:9) prior to each UVB exposure resulted in reduction in cancer incidence (52% inhibition) and an increase in tumor free survival in comparison with control mice (P < 0.01). Apigenin (0-100 microM) did not prevent the in vitro production of photoproducts in salmon sperm DNA suggesting that apigenin did not inhibit UVA/B induced ODC activity or UVB induced skin carcinogenesis by simply absorbing ultraviolet light or decreasing DNA damage.