Abstract
Δ-Aminolevulinic acid (ALA) synthetase catalyses the condensation of succinyl CoA and glycine to yield ALA. This is the first and rate limiting step in the haem biosynthetic pathway and it is now accepted that the rate of haem synthesis in liver is regulated by changes in either the activity or level of ALA synthetase (De Matteis, 1967). This paper is concerned with the factors that determine the level of ALA synthetase in mammalian liver. Study of ALA synthetase control may provide information both on regulation of the expression of a specific gene in liver and on the nature of the genetic defect in the hereditary human diseases, the porphyrias, in which the level of ALA synthetase is abnormally high (Taddeini and Watson, 1968).
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