1

histidine T

urocanic acid T

4-imidazolone-5-propionic acid T

formiminoglutamic acid T

glutamic acid

Figure 4 Synthesis and catabolism of histidine. Solid lines indicate biosynthetic pathways; broken lines indicate catabolic pathways.

methylation

S-adenosylmethionine —- *-*- S-adenosylhomocysteine reaction for which vitamin B12 is a cofactor, or betaine. Remethylation seems to be quite sensitive to folate status, and plasma homocysteine is becoming accepted as a biomarker of nutritional status with respect to folate.

Homocystinuria is an important inborn error of metabolism that is caused by impaired activity of cystathionine synthetase, the enzyme that catalyzes the condensation of homocysteine with serine. One of the consequences of homocystinuria is premature cardiovascular disease. There is considerable evidence that milder elevations of plasma homocys-teine, caused by poorly active variants of the methylenetetrahydrofolate reductase enzyme (which is required to make the methyl donor methyltetrahy-drofolate) or by low folic acid status, may be an important risk factor for cadiovascular disease throughout the population.

Tyrosine In mammals, including man, tyrosine can only be formed by hydroxylation of the essential amino acid phenylalanine. The inborn error of metabolism phenylketonuria is caused by a failure of the enzyme phenylalanine hydroxylase.

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