6Aminonicotinamide (6AN) can replace the nicotinamide moiety of pyridine nucleotides both in vitro and in vivo in the reaction, catalysed by the enzyme NAD (P) glycohydrolase (EC 3.3. 3.6) or in the course of a de novo synthesis of NAD or NADP; the resulting antimetabolites (6-ANAD or 6-ANADP) may inhibit pyridine nucleotide linked reactions [l-5]. After injection of 6-AN into pregnant experimental animals, embryotoxic effects can be demonstrated [6-81. In adult animals, the application of this antimetabolite leads to typical lesions of the central nervous system, including irreversible paralysis [4, 9]. An increase in the concentration of 6phosphogluconate (6%) in rat brains in vivo following the injection of 6-AN [12, 131 suggests an impairment at the 6-phosphogluconate dehydrogenase level.

Earlier studies have shown an impaired function of the oxidative part of the pentose phosphate pathway (PPP) in embryos of experimental animals treated with 6-AN and an inhibition of the incorporation of carbon atoms from glucose into the ribose moiety of nucleic acids via the NADP dependent steps [8]. We have tried to localize the block in the PPP. In this paper, we present the results of kinetic studies on the effect of 6-aminonicotinamide adenine dinucleotide phosphate (B-ANADP).