The effect of environmental lighting on porphyrin metabolism in the rat

Abstract

THE direct action of light on the skin in porphyria is well documented. There is a specific spectral response in that light of wavelengths between 400 nm or 500–600 nm causes lesions through photodynamic action of porphyrin in the skin^1–4. Light may however affect abnormal porphyrin metabolism apart from any action on the skin. We noticed that skin lesions were provoked in porphyric rats, whose coats were shaved, by continuous irradiation by white light fluorescent tubes. Some porphyric animals, in which the coat was not shaved off as a control, excreted more porphyrin when under continuous light than other control animals under continuous dark. This implicated light as an environmental factor effecting porphyrin metabolism. Porphyrin excretion as a measure of abnormality, however, gave inconclusive results. Instead we have used the activity of hepatic δ-aminolaevulinic acid synthetase (ALA-S), the rate controlling enzyme in the haem biosynthetic pathway⁵, as an index of porphyrin abnormality. Normally, ALA-S activity is low, but where porphyria is present clinically or has been induced chemically in experimental animals, activity is raised⁶. We used 1, 4-dihydro-2, 4, 6-trimethyl pyridine-3, 5-dicarboxylate (DDC) to induce porphyria; this chemical, like some other porphyrinogenic agents, such as griseofulvin, probably acts through interfering with a negative feedback inducing mechanism involving haem⁷.