Effects of growth, food intake, and dietary zinc on diadenosine tetraphosphate concentrations in rats

The nucleotide diadenosine tetraphosphate has been suggested to function as a signal molecule for the initiation of DNA replication. Previous studies have indicated that diadenosine tetraphosphate is synthesized by certain aminoacyl tRNA synthetases and that diversion of AMP from the amino acid-enzyme complex to ATP to form diadenosine tetraphosphate is facilitated by zinc ions. The growth retardation of zinc-deficient rats is associated with specific reduction in DNA replication and also with a potentially growth-limiting decrease in food intake. The possibility has been investigated that in zinc-deficient rats, lack of Zn(2+) restricts diadenosine tetraphosphate synthesis, resulting in a failure to synthesize DNA and in a reduction in growth. The results indicate that the depressed growth potential caused by the reduction in food intake associated with the deficiency was sufficient to lower diadenosine tetraphosphate concentrations significantly in the liver and spleen. However, there was no indication of a specific effect of zinc deficiency on diadenosine tetraphosphate values.