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Delta-aminolevulinic acid The health care provider will instruct you, if necessary, to discontinue drugs that may interfere with the test.
Delta-aminolevulinate synthase catalyzes the condensation of glycine with succinyl-CoA to form delta-aminolevulinic acid.
Deficiency of this enzyme leads to the accumulation of the porphyrin precursor delta-aminolevulinic acid, which can potentially result in a variety of symptoms.
Delta-aminolevulinic acid dehydratase is an enzyme that in humans is encoded by the ALAD gene.
It has been reported that animals and patients treated with DCA have elevated levels of delta-aminolevulinic acid (delta-ALA) in the urine.
The neurological symptoms are associated with accumulation of porphyrin precursors, namely delta-aminolevulinic acid (ALA) and porphobilinogen (PBG).
One of the main causes for the pathology of lead is that it interferes with the activity of an essential enzyme called delta-aminolevulinic acid dehydratase, or ALAD, which is important in the biosynthesis of heme, the cofactor found in hemoglobin.