Abstract This paper describes lead poisoning, focusing on the chemical processes that take place as lead (II) displaces zinc (II) from ALAD and inhibits hemoglobin synthesis. The technical details of the inorganic and biochemical processes at play are explored and discussed, as well as the mechanisms of various lead poisoning therapeutic strategies. This paper also contains several referenced illustrations and figures.
From the Paper "The protein ALAD, also know as porphobilinogen, is crucial in heme biosynthesis (2). ALAD, a ZnII metalloenzyme, consists of A and B subunits each of which contain a zinc atom when functional. The functionality of the A and B sites has been determined experimentally by displacement of zinc. When magnesium displaces zinc at the A site ALAD is marginally active. Furthermore, when magnesium replaces the zinc in the B site no change in the activity of the enzyme is observed (3). Thus the A site is key to the activity of the enzyme. However, when PbII displaces the active ZnII ion present in the A- site, the enzyme is rendered useless."
