2. How can you account for the fact that homocysteine, a normal intermediate in methionine metabolism, is not present in the blood control subjects in a loading test?
3. In some patients with deficient cystathionine synthetase activity, a lowering of plasma homocysteine and methionine, as well as a clinical improvement, have benn achieved by treatment with large doses of pyridoxal. Can you explain this finding?
4. Treatment of some homocystinuric patients with parenteral folic acid has affected a "cure" with disappearance of all acute symptoms. How can this be explained?
Orignal From: How could the incorporation of homocysteine into proteins be prevented?
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