An 18-month-old boy was referred to the pediatrics clinic because of persistent anemia and associated failure to thrive. Laboratory analysis confirmed a microcytic anemia and revealed blood lead levels of 50 mg/dL (2 times normal levels) and high levels of coproporphyrinogen III in the urine. The child was put on chelation therapy and recovered uneventfully. The cause of the child's difficulty was most likely due to the effects of the lead. The findings in this patient most closely reflect lead inhibition of which of the following enzymes of heme biosynthesis?a) δ-aminolevulinic acid (ALA) dehydrataseb) ferrochelatasec) porphobilinogen (PBG) deaminased) proporphyrinogen III cosynthasee) uroporphyrinogen decarboxylase

B) Ferrochelatase

Explanation:

The hematological effects of lead poisoning includes the inhibition of the body's ability to produce hemoglobin. This is done by interfering with several enzymatic steps in the heme synthesis pathway.

Lead inhibits or decreases heme synthesis by inhibiting Ferrochelatase enzyme activity.

Ferrochelatase catalyses the insertion of iron into protoporphyrin IX and is very sensitive to lead.

•there must be variation for the particular trait within a population.

•the variation must be inheritable (that is, it must be capable of being passed on from the parents to their offspring).

•individuals with one version of the trait must produce more offspring than those with a different version of the trait.good

explanation: