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Hemolysatc* of crytbrocyte» from bovine and human subject& having erythropoictic porphyria, and from normal subject*,, have been incubated with PBG*>, Cell* obtained by differential centrifugation or osmotic lysis as well as total cells were hcmolyxcd. The proportion utilised or unaccounted for after incubation was generally much greater with the porphyric than the normal Kemolysates, with the lesser than the greater density fractions, and with the bemolysate» of the osmoticalfy more fragile cells, Larger amount» of PBG in relation to cells left« protection against ambient temperature and longer incubation were associated with greater formation of type J porphyrim by normal a» well as porphyric hcmolysatc*. With more nearly optima) conditions, only or mainly type III was in evidence in the normal while the porphyric hcmolysates formed both T and II). Porphyric hemolysatcs regularly formed larger amounts of protoporphyrin 9 (HI) than the normal. After repeated bleeding of bovine porphyries, the hcmolysates formed larger amount» of porphyrin arid significantly greater proportions of type J isomer than before bleeding. This is interpreted a» an enhanced dcaminasc-isomcrasc imbalance in young cells. Under the same conditions the normal bovine hemo« Jysates formed mainly type III. These observations are considered in respect to the question whether the normobla&t» are unior bimodal in terms of the genetic abnormality, i. e,, the dcaminasc-isomerasc imbalance. The present evidence is in better accord with a unimodal distribution,

clinical chemistry and laboratory medicine

Formation of Porphyrin Isomers from Porphobilinogen by Various Hemolysates of Red Cells from Bovine and Human Subjects with Erythropoietic (Uro-) Porphyria