Biomedical subjects
Publications and source records attributed to M Stoeppler.
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delta-Aminolevulinic acid dehydratase (ALA-D), respectively porphobilinogen synthase, EC 4.2.1.24) activity can be lowered by toxic, metabolic and hereditary factors. A 30-year-old painter was suffering from lead poisoning with an acute abdominal-neurologic syndrome and anemia. Blood lead was measured at 414 micrograms/l. Urinary ALA and coproporphyrin excretion as well as erythrocyte protoporphyrin had increased extremely, whereas ALA-D activity in erythrocytes had decreased extremely to 8% of controls. Excretion parameters, protoporphyrin, hemoglobin and lead returned to normal after treatment, but four years later ALA-D activity still remained diminished (30% of controls). An inherited enzyme deficiency was assumed and found in the mother, analogous to the subnormal ALA-D activity in heterozygotes of four other families. The inherited enzyme deficiency sensitized the patient to lead exposure and intoxication, which is a toxogenetic disease in this case.
Gel permeation chromatography was used to fractionate zinc-bound constituents in haemolysates of human blood samples. The zinc content of the fractions was determined by electrothermal atomic absorption spectrometry. The zinc-containing enzyme, carbonic anhydrase, was identified by isoelectric focusing. A fraction of more than 0.9 of the zinc eluted from the column was bound to the carbonic anhydrase fraction. The fraction of zinc associated with unbound carbonic anhydrase was 0.786 of the total, and the remainder was found in a carbonic anhydrase-CO-haemoglobin complex.
Analytical chemists are faced with nickel contents in environmental and biological materials ranging from the mg/kg down to the ng/kg level. Sampling and sample treatment have to be performed with great care at lower levels, and this also applies to enrichment and separation procedures. The classical determination methods formerly used have been replaced almost entirely by different forms of atomic absorption spectrometry. Electroanalytical methods are also of increasing importance and at present provide the most sensitive approach. Despite the powerful methods available, achieving reliable results is still a challenge for the analyst requiring proper quality control measures.
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For several years, a 4-12-fold increase of the upper normal limit in erythrocyte protoporphyrin concentrations persisted in two men 34 and 39 years of age who were chronically exposed to lead. We are dealing with a zinc protoporphyrinemia in both cases, without lead intoxication or anemia. The 34-year-old had been a regular blood donor for 10 years and had already been treated for iron deficiency several times. Hemoglobin, red cell counts, hematocrit, and iron were at the lower normal limit. The activity of porphobilinogen synthase (PBG-S), uroporphyrinogen-synthase and -decarboxylase as well as urinary porphyrin precursors and porphyrin excretion were normal. Protoporphyrinemia was said to be due to a prelatent/latent iron deficiency. In the 39-year-old, the activity of PBG-S was lowered to 388 mumol/1 . h, as compared to the mean of controls (1,190 +/- 210, x +/- SD, n = 50), in connection with a slightly elevated excretion of delta-aminolevulinic acid and coproporphyrin in the urine and a high-normal blood lead level. In his family there was no history of either a protoporphyrinemia or a hematological disturbance. Six of eight family members in three generations showed a diminished activity of PBG-S: 600 +/- 160, P less than 0.001 compared to controls. These family members are heterozygous with regard to the PBG-S deficiency; they are clinically unobtrusive in comparison to homozygotes with an acute prophyria syndrome. Activation by zinc and reactivation by dithiothreitol were normal in contrast to PBG-S from patients with lead intoxication. The cause of biochemical symptoms of subclinical lead intoxication developed by the propositus is probably due to the hereditary PBG-S deficiency which sensitizes him to low-level lead exposure. The determination of red cell PBG-S activity can be recommended as a test detecting heterozygotes. The hereditary PBG-S deficiency is recognized as a new molecular basis for the pathogenesis of lead intoxication.
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A new high-performance analytical procedure for the determination of the toxic trace metals cadmium, lead and copper in wines by differential pulse anodic-stripping voltammetry (DPASV) subsequent to UV irradiation of the sample is compared with the hitherto more common application of electrothermal atomic absorption spectrometry (AAS). In this manner also mutually the accuracy attainable with both alternatives has been established. The particularly favourable potentialities of the new voltammetric approach for toxic metal control of wines are demonstrated by the investigation of a typical selection of 36 wines from recent vintages and common vine types of the German and some European wine cultivating regions.
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In an accidental case of exposure to nickel carbonyl with a few persons weak symptoms of illness were observed. Rapid and simple methods of flameless atomic absorption spectroscopy were applied for the determination of nickel in urinary samples and in sections of bundled hairs. The measurements showed in some cases remarkable increased Ni values well above normal levels. The data obtained will be amply discussed and can be used in part for a rough estimation of the biological half life of inhaled Ni.
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Calcium and magnesium levels in the cortex, medulla, and papilla of human kidney from 32 so-called healthy patients and from eleven patients with calcium-oxalate lithiasis were determined by atom-absorption spectralphotometry. A positive calcium gradient with the highest calcium concentration in the papilla was found in all kidneys. Compared to the control group, that calcium concentration in the lithiasic kidneys was reduced by 50% in the papilla, but in the cortex and medulla, the levels were the same. A relative depletion of calcium in the papilla in hypercalciuria goes against the theory that the papilla is the main center of development of calcium-containing stones. The magnesium concentration was practically the same in cortex, medulla, and papilla, and no significant difference was found between lithiasic and healthy kidneys. These findings underline the central role of calcium in the genesis of calcium-containing stones.
Among various procedures for the determination of thallium as a toxic element, micro-techniques by means of flameless AAS play an important role in hair analysis. Referring to two cases of T1-intoxication laboratory procedures, techniques and instrumentation are reported, which prove to be useful, sensitive, and fast. Considerations concerning sample preparation, contamination problems and compensation of spectral background effects by a duochannel spectrophotometer are discussed.
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A method is described for analysis of nickel in urine, which involves dilution of urine with dilute nitric acid and direct quantitation of nickel by electrothermal atomic absorption spectrophotometry with Zeeman background correction. The detection limit for nickel is 0.5 micrograms per L of urine; the coefficient of variation of replicate determinations is 4 to 5 percent (within-run) and 6 percent (run-to-run). Recovery of nickel added to urine (20 micrograms per L) averages 99 +/- 5 percent (mean +/- SD). Analytical results agree closely with measurements by the International Union of Pure and Applied Chemistry (IUPAC) reference procedure (correlation coefficient = 0.99). Nickel concentrations in urine specimens from 34 non-exposed, healthy, adult persons living in Connecticut average 2.0 +/- 1.5 microgram per L (range = 0.5 to 6.0 micrograms per L). Urine nickel concentrations are directly correlated with urine creatinine concentrations and specific gravity measurements. Elevated concentrations of nickel are observed in urine specimens from nickel-exposed workers, including nickel electroplating workers (mean = 27 micrograms per L, range = 3.1 to 82 micrograms per L, N = 19) and nickel battery workers (mean = 32 micrograms per L, range = 2.8 to 103 micrograms per L, N = 7). This method is more rapid and convenient than previous techniques and is suitable for routine use in clinical and industrial laboratories.