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PubMed1990

Optimized fluorometric determination of urinary delta-aminolevulinic acid by using pre-column derivatization, and identification of the derivative.

We previously reported the usefulness of a fluorometric method to determine urinary delta-aminolevulinic acid (ALA) concentrations by using post-column derivatization to monitor the effect of lead exposure. We have further improved the method by introducing pre-column derivatization by using reaction of ALA with acetylacetone and formaldehyde. Response of the hematopoietic system to lead exposure can now be easily detected at blood lead concentrations as low as 162 micrograms/L. The fluorescent ALA derivative, a new aromatic product, 2-methylideneamino-3,5-diacetyl-4,6-dimethylphenylpropionic acid, is separated on octadecyl silica column by high-performance liquid chromatography and the fluorescence intensity is detected with a fluorophotometer. Sample recoveries for 12 urine samples from workers exposed to lead and unexposed controls were 91.9-110.2%. The results obtained by the pre-column derivatization method agreed with those by the post-column derivatization method. The new method increases the sensitivity to a detection limit to 10 micrograms of delta-aminolevulinic acid per milliliter of urine and is simple enough to be used for routine monitoring of the biological effect of exposure to low concentrations of lead.

Aminolevulinic Acid↗
PubMed1979

Metabolic fate of exogenous delta-aminolevulinic acid in Dubin-Johnson syndrome.

The underlying mechanism of abnormal urinary distribution of CP isomers in DJS is unknown. We administered ALA to DJS patients and carriers as well as to normal controls, and urinary and biliary porphyrins and plasma bilirubin were studied. In sharp contrast to the remarkable increase in urinary CP-III excretion in normal controls (2234 nmol/gm creatinine during the first 2 hr) after ALA, very small increase was observed in DJS patients (19 nmol). In DJS carriers the increase took intermediate values (1122 nmol). The increments in urinary CP-I were smallest in DJS patients, and the peak of its increase was delayed. These data are compatible with the hypothesis that a carrier-mediated mechanism in transporting CP-gen isomers I and III from the liver cells to the plasma may be anomalous in DJS hepatocytes and that the increased urinary CP-I characteristic of DJS may be the result of a disturbance in the uptake process of CP-gen I, derived mainly from the erythropoietic tissues, by DJS liver cells. Although the biliary percent of CP-I in controls decreased after ALA, it remained unchanged in DJS, suggesting the existence of a bile canalicular barrier against CP-gen-III in DJS. The elevated biliary porphyrins and plasma bilirubin after ALA in DJS patients favor an idea that there may be no major enzymatic derangements in the metabolic sequences from ALA to bilirubin. The increased excretion of PP in DJS bile after ALA remained to be explained.

Aminolevulinic Acid↗
PubMed1984

[Binding of delta-aminolevulinic acid by myelin proteins].

Delta-[14C]aminolevulinic acid (ALA) was injected intracranially into experimental animals; the gray and white matter was obtained from the brain 24 hours thereafter. The radioactive label content in the ALA, protoporphyrin, microsomes, mitochondria, cell membranes and myelin was determined; no radioactivity was detected in ALA and protoporphyrin. The radioactive label was localized in the subcellular fractions and myelin, in particular, in the white matter. Analysis of protein myelin fractions demonstrated that ALA was incorporated into practically all basic proteins. The highest capacity to bind ALA was observed in case of Wolfgram proteins; however, almost half of the bound ALA in the myelin fraction was found within the composition of basic proteins. It was assumed that the binding of ALA to proteins occurs via the amide, carboxylic and keto groups of ALA.

Aminolevulinic Acid↗
PubMed1983

[Urinary and fecal excretion of porphyrins and their precursors in leukemia patients].

Delta-aminolevulinic acid (DALA), porphobilinogen (PBG) and porphyrins in urine and feces were determined in 40 healthy controls (20 males and 20 females) and in 60 patients with acute leukosis (27 males and 33 females), with chronic myeloleukosis - 23 (10 males and 13 females), and 25 patients with chronic lympholeukosis (II males and 14 females). Another 15 patients (7 males and 8 females) were studied at the initial stage, recurrence, recidivation of acute leukosis (AL). DALA excreted with the urine, manifested no significant discrepancy as compared with the controls of the three groups examined patients and in all the three stage of AL, whereas PBG was moderately reduced in the AL patients - initial stage and recurrence and was within the normal limits in the patients with chronic myeloleukosis (CML) and chronic lympholeukosis (CLL). The urine excreted coproporhyrin was increased, to various degrees, in the patients with CML and CLL and at the initial stage, recurrence and recidivation of AL, whereas uroporhyrin was within the norm. Coproporphyrin, excreted in the feces, was increased in all three groups of patients with leukosis and in the three stages of AL, whereas the other fractions showed no significant difference as compared with the controls. It could be concluded, from the results obtained, that porphyrins metabolism is disturbed in the patients with leukosis.

Acute Disease↗