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1. Aminolevulinate dehydratase (ALA-D) was studied in crude extract from mouse mammary carcinoma, normal mouse liver and tumour bearing mouse liver. 2. A Michaelis-Menten behaviour and Km values between 0.24 and 0.31 mM were obtained for the enzyme in either source. 3. In all three tissues there was a linear relationship between porphobilinogen formation and incubation time, up to 120 min, ALA-D was thermostable and optimum pH was at 6.8. 4. There seems to be no structural alterations in tumoural ALA-D as compared with the enzyme from liver of both normal and tumour bearing mice.

1. Basal levels and allyl-isopropylacetamide (AIA) or veronal induced levels of delta-aminolevulinate synthetase (ALA-S), cytochrome P-450 (cyt P-450) and cytochrome oxidase were determined in tumor (T) and liver of both normal mice (NM) and T bearing mice (TBM). 2. Basal levels of ALA-S were nearly the same in either source. The amount of cyt P-450 was lower in TBM liver than in NM liver, and no detectable in T. While the basal activity of cytochrome oxidase in TBM liver and T were higher than those of NM liver. 3. In AIA intoxicated animals there was a lower induction of ALA-S in liver of TBM than in NM liver. There was no induction in T ALA-S. The loss of cyt P-450 was less in TBM liver when compared with NM liver. 4. The induction level of cyt P-450 after veronal administration was nearly the same in liver of both TBM and NM. 5. We conclude that lower induction of liver ALA-S activity in TBM liver is due to correspondingly lower drug metabolism ability of TBM liver. Otherwise our results suggest that the control mechanism operating in T and probably in its original tissue are different from those described for normal liver.

1. The effect of colchicine, vincristine and griseofulvin (GRIS) on the porphyrinogenic action of 2-allyl-2-isopropylacetamide (AIA) and veronal was studied in vivo and using the in vitro experimental model of tissue explant cultures. 2. Complete prevention by colchicine was found in liver and heart explant from animals treated with AIA and veronal. 3. Vincristine, GRIS and colchicine reversed AIA induction in liver explants, however reversal was partial or nil in skin and heart explants depending on the antimitotic and the tissue. 4. The usefulness of the combination of the in vivo experimental model and the in vitro explant tissue culture model, for this kind of studies is emphasized.

The effect of griseofulvin on porphyrin biosynthesis was studied in vitro and in vivo using liver and skin explants from mice. Neither porphyrin nor precursors accumulation was detected after in vitro treatment of explants with griseofulvin. Culture medium porphyrins formed from added delta-amino-laevulinic acid (ALA) were increased after oral chronic intoxication. Similar results were obtained by cutaneous and oral intoxication. Consequently griseofulvin topical application is proposed as an alternative method to produce experimental erythropoietic protoporphyria. Probable intoxication mechanisms are proposed to explain the porphyrinogenic action of griseofulvin.