The presence of molecular oxygen is a determinant in the phototoxicity
of phthalocyanines, and photosensitized oxidation is the accepted che
mical mechanism for photodynamic action. However, it is difficult to e
stablish whether the process is initiated by a type I electron transfe
r, or by a type II energy transfer reaction to form singlet oxygen. Us
ually, the involvement of singlet oxygen in photodamage has been indic
ated by the inhibition of the biological effect by a competitive physi
cal or chemical singlet oxygen quencher, or by a rate increase in D2O,
in which singlet oxygen has a longer lifetime than in H2O. Unfortunat
ely, these techniques are not completely specific for singlet oxygen.
Moreover, thermodynamic considerations suggest that photoinduced elect
ron abstraction from appropriate biomaterials could compete with singl
et oxygen production under in vivo conditions. This likely source of o
ne electron-oxidized primary radicals, which can provide the precursor
s of the oxidative damage in phthalocyanine photosensitization, sugges
ts the possiblity of modulated toxicity by interaction with chemical a
dditives. Examples of such additives recently studied are ascorbate, t
ocopherol and quercetin, all of which are natural antioxidants.