Search

Reportedly, serum manganese concentrations increase after myocardial infarction, closely correlated with increased serum aspartate aminotransferase activity. However, these conclusions are apparently based on analyses of contaminated samples. Serum manganese concentrations after myocardial infarction have been re-investigated by neutron activation analysis, and no significant increase could be demonstrated. Because serum copper and zinc could be determined simultaneously, analyses for these trace elements are also reported, which confirm the findings of others. After myocardial infarction a statistically significant (0.02 smaller than P smaller than 0.05) increase in serum copper and a statistically significant (0.001 smaller than P smaller than 0.01) decrease in serum zinc were observed.

In experiments with rabbits is shown weak toxic action of managanese chloride (0,5 and 5 mg/kg intravenously for 2 months) on the organism of animals. The blood managanese level rose only when the element was introduced in a large dose. The ascorbic acid content in the supprarenals diminished. At the site of the preparation administration (muscles) were in evidence manifestations of irritation (necrosis with regeneration), which disappeared 2 weeks after abolishment of the preparation.

An application of X-ray fluorescence spectrometry for the analysis of various toxic metals (lead, cadmium, manganese, chromium, nickel, vanadium) in whole blood was studied, and two techniques for sample preparation (vacuum drying and nitric acid combustion) were compared. The acid combustion method appeared to be superior on the basis of the accuracy and precision of the determinations. The tungsten-target X-ray tube was suitable for determining manganese, nickel, and vanadium, the lowest limits of detection being 0.021 mug/ml, 0.035 mug/ml and 0.017 mug/ml, respectively, and the precisions being between 4.25 and 6.92%. The sensitivity and reproducibility for lead, cadmium, and chromium were unsatisfactory. A comparison between the recoveries of X-ray fluorescence and atomic absorption analyses demonstrated that the X-ray method is suitable for determining manganese, vandium, nickel, cadmium, and lead. The poor sensitivity of the X-ray method, however, restricts its practical use. For vandium the results obtained by X-ray fluorescence were superior to those measured by a colorimetric method. No significant differences were observed between the results of single component and multicomponent analyses at the metal concentrations usual in physiological and toxicological cases.

At physiological pH and concentrations of Mn(++) in excess of 5 x 10(-4)M, study of the Mn(++) ion movement into human red cells is complicated by physicochemical alterations of the ion itself. At concentrations below 5 x 10(x4)M, the rate of uptake bears a linear relationship to the Mn(++) concentration. The permeability constant for inward movement of Mn(++) is 2.87 +/- 0.13 (S.E.) x 10(-9) cm./sec. The rate is not influenced by the addition of metabolic substrates such as glucose or adenosine or the metabolic inhibitors iodoacetate or fluoride. Co(++), Ca(++), and Mg(++) do not appear to compete with Mn(++) for entry, but at high concentrations relative to Mn(++), they reduce the rate of entry. Ca(++) is far more effective than Co(++) or Mg(++) in this regard. The permeability constant for outward Mn(++) movement is 1.38 +/- 0.21 (S.E.) x 10(-9) cm./sec., about half of that for entry. This slower rate of outward movement is consistent with the finding that 40 to 60 per cent of the Mn(++) taken up by the red cells is non-ultrafilterable. Less than 5 to 10 per cent of the Mn(++) appears to be bound to the stroma. It is concluded that entry and exit of Mn(++) is a process of passive diffusion involving no carriers, transport, or metabolic linkage.