We have previously reported that pyridoxine shows UVA-induced cytotoxicity,
Four other vitamin B6 compounds (pyridoxal, pyridoxamine, pyridoxal phosph
ate, and pyridoxamine phosphate) are metabolically more important in vivo t
han pyridoxine, These compounds were examined for WA phototoxicity to cultu
red human fibroblasts, The cytotoxicity was measured by post-WA irradiation
colony-forming ability. All the B6 compounds except pyridoxal phosphate sh
owed cytotoxicity, Pyridoxamine phosphate, which is the most important form
of vitamin B6 in vivo, had the strongest cytotoxic effect. To examine the
involvement of reactive oxygen species in the phototoxicity, we performed a
n electron spin resonance study using the spin trapping agent, 5,5-dimethyl
-1-pyrroline N-oxide, and diethylenetriaminepentaacetic acid. We failed to
detect radicals derived from vitamin B6, The cytotoxic effect remained in U
VA-irradiated solutions for at least 30 min after the end of UVA irradiatio
n, Hydrogen peroxide was produced in the solution, but the amount was not e
nough to cause cytotoxicity, In addition, the cells from xeroderma pigmento
sum patients who belong to group A or C showed survival curves similar to t
hose of normal fibroblasts. This suggests that cyclobutane pyrimidine dimer
s or 6-4 photo-products of DNA were not involved in this damage. These find
ings suggest that WA-induced vitamin B6 cytotoxicity is caused by toxic pho
toproducts resulting from irradiated vitamin B6.