protoporphyrin photosensitivity cannot be attenuated by oral nacetylcysteine the photodermatosis in erythropoietic protoporphyria epp is caused by the accumulation of photosensitizing protoporphyrin pp in the skin due to a defect in ferrochelatase the enzyme that inserts ferrous iron into pp to form heme hydroxyl radical oh and singlet oxygen generation with subsequent lipid peroxidation are thought to play a major role in the pathogenesis of the photodermatosis in epp hydrogen peroxide h2o2 can generate oh in the haberweiss as well as the fenton reaction and is thus a potentially harmful intermediate in the photoreduction of o2 the use of oxyradical scavengers such as betacarotene has been reported to be beneficial in the treatment of epp photodermatosis in this study nacetylcysteine nac 1800 mgday was used for 3 reasons i its sh groups directly scavenge h2o2 ii ferrochelatase can be activated by sulfhydryl groups iii nac was reported to upregulate the glutathione redox system which is a major endogenous antioxidant system however in a doubleblind crossover placebo controlled study on 6 epp patients we could neither demonstrate an effect through photosensitivity tests nor on light hypersensitivity as reported by the patients this dosage of nac could not increase reduced glutathione and did not affect the red blood cell pp content nor the excretion of pp in the feces neither were adverse effects observed we conclude that the oral administration of nac in the relatively low dose used here is not effective in the treatment of photodermatosis in epp