The influence of a magnetic field on manganese transport into rat brain.

The aim of this study was to detect the effect of a magnetic field on manganese transport into rat brains. An experimental group of Female Wistar rats was given 0.48 mg Mn2+ per kg body weight intratracheally twice a week for 3 months and simultaneously exposed to a magnetic field: B = 10 mT, f = 50 Hz for 1 hr. Rats in one control group of rats received the same dose of manganese as the experimental group but were not exposed to the magnetic field. Rats in a second control group had neither exposure to manganese nor exposure to the magnetic field. After the last dose, all rats were sacrificed and their brains and other tissues were analyzed for manganese content. The results indicated that the magnetic field had a positive effect on increasing the manganese content in the brains of rats in the experimental group relative to those of the control groups. Visual evoked potentials (VEP) measured at the end of the exposure periods on randomly selected experimental and control rats showed a shortened but not statistically significant latency of the P1 peak of VEP in rats that had been exposed to both factors but not in control rats.

Distribution and excretion of cadmium and nickel after simultaneous exposure and the effect of N-benzyl-D-glucamine dithiocarbamate on their biliary and urinary excretion.

A rat model for combined exposure to cadmium and nickel is presented that involves the administration of drinking water containing these elements over a period of 90 d. Coadministration of these two ions in drinking water leads to brain levels of both elements that are significantly higher than results from the administration of equal doses of the metals individually. The enhanced biliary excretion of cadmium in rats given sodium N-benzyl-D-glucamine dithiocarbamate (BGDTC) is almost twice as great in those animals given cadmium and nickel as in those animals given cadmium only. The excretion of nickel is reduced by the administration of this chelating agent. Although equal amounts of nickel and cadmium were administered to these animals, liver and kidney cadmium levels were approximately 100 times greater than the corresponding nickel levels. The results suggest that combined exposure to these elements may lead to enhanced levels of nickel and cadmium in the brain and a level of nervous system damage not predictable from information obtained under conditions of exposure to only one of these elements.

The study of exposure to cadmium in the general population. II. Morbidity studies.

An epidemiological study was performed to assess whether environmental pollution by cadmium as found in cadmium polluted areas of CSFR (Pribram and Frýdek-Mistek) is associated with changes in biological indicators of renal dysfunction in non-occupationally exposed population groups. Polluted areas were chosen on the basis of existing sources of Cd emission. The city of Prague was selected as a control area. Environmental monitoring (Cd in air, dust fall and soil) did not confirm significant contamination of selected areas. It was found that Cd levels in urine (Cd-U) of inhabitants living in areas chosen as Cd-contaminated were significantly higher than in the control area. Differences in concentrations of Cd in blood (Cd-B) levels between individual areas were not significant. No significant differences between the study populations were noted in the urinary excretion of low molecular weight proteins (beta 2-microglobulin, retinol binding protein) and albuminuria. However, total proteinuria and aminoaciduria in persons living in Pribram area was significantly higher. This area suffers from combined contamination by cadmium and lead. In smokers of both sexes the Cd-B levels were significantly higher in all areas, no significant differences were found in Cd-U levels. However, it was found that in smokers there is higher percentage of persons excreting more than 0.9 micrograms Cd.g-1 creatinine in urine. Consumption of home-grown vegetable and fruit in Cd-polluted areas led to significantly higher levels of Cd-B and Cd-U and total proteinuria. The results of the study show that smoking and food seem to be the most important sources of Cd intake in non-occupationally exposed populations. In spite of the fact that environmental monitoring does not reveal a significant contamination of selected areas by Cd, Cd-U levels confirmed that population living in these areas is really exposed to Cd.

The study of exposure to cadmium in the general population. I. Autopsy studies.

From 1982 to 1986 samples of materials (liver tissue, kidney cortex) were collected from 438 autopsies in Prague. The age of persons was over 50 years and residence time in the area was at least 10 years Concentrations of Cd and Zn were determined in the kidney cortex and the liver tissue using the AAS method. On the basis of the Questionnaire for Relatives, data on smoking habits, and occupational history of the investigated persons were obtained. The results of the study confirmed that the concentration of Cd in analyzed tissues did not exceed values reported in the literature for people of similar age living in Cd uncontaminated areas. In smokers significant increase of Cd in the kidney cortex was found in all age and sex groups. The body burden of Cd in smokers is significantly higher.

Cadmium influence on the rat liver.

Influence of cadmium on the intestinal and hepatic tissue of rat was studied in acute injection and oral as well as subchronic and chronic oral experiments with the purpose of better understanding of the penetration mechanisms of cadmium into these tissues. Acute single oral dose of CdCl2 32.5 mg.kg-1 inhibited in vitro the respiration of intestinal scrapings (44%) and in liver slices (25.7%). In combined oral doses of 32.5 mg.kg-1 + 162.5 mg.kg-1 inhibition in the intestine increased with exposure time, while in the liver it decreased. Amount of presumable metallothionein in the liver was approximately ten times higher than that in the intestine. Respiration was measured by a Clark electrode. Binding of cadmium to metallothionein was determined by column chromatography and spectrophotometry. Physiological findings are in agreement with morphological ones. In cases when, following an acute single oral dose, a 50% change was detected in the absorptive jejunal zone, a 10% change was observed in the liver parenchyma. In the case of combined oral dose of 60-70% of absorptive villi zone is damaged by cadmium, which penetrates by passive diffusion into lamina propria and by blood to the liver, where it acts toxically in 30%. Active transport of cadmium after chronic application is preserved. Correlation of physiological and morphological findings was evident.

Effect of cadmium on the rat intestine.

The effect of cadmium on rat jejunal mucosa was observed after application of CdCl2 doses: acute single (32.5 mg.kg-1) or combined (32.5 + after 24 h 162.5 mg.kg-1) and chronic (250 mg.l-1, daily consumption 10 ml for 3 months). Inhibition of mucosal respiration, measured by a Clark electrode was 44, 50.4 and 38.4% respectively, as related to 100% of controls. Metallothionein was determined in the mucosa for combined and chronic doses. Electron X-ray microanalysis has shown Cd2+ distribution in dependence on pathological changes: greater regressive changes caused smaller Cd2+ retention. In acute experiments Cd2+ penetrate by passive diffusion through foci of damaged villi into the lamina propria. In crypt absorptive cells with preserved alcalic phosphatase and succinate dehydrogenase activity and in Paneth cells Cd2+ retention was determined. Combined dose of Cd2+ damaged homeostasis and prevented Cd2+ retention. In chronic experiments occurred a diffuse distribution of Cd2+ in the mucosa.

Effects of dithiocarbamates on cadmium distribution and excretion in chronically exposed rats.

One month after termination of a 3-mo exposure of rats to cadmium (Cd in drinking water at a concentration of 50 mg/l), the effects of dithiocarbamate analogs on the excretion and distribution of the cadmium were determined. Sodium salts of three dithiocarbamates [sodium bis(hydroxyethyl) dithiocarbamate, DEDTC; sodium N-methyl-D-glucamine dithiocarbamate, MGDTC; and sodium 4-carboxamidopiperidine dithiocarbamate, INADTC] were given to rats ip 2 times at 2.46 mmol/kg. In the following administration of the first injection of DEDTC, cadmium excretion via the urine amounted to 15.8 micrograms and via bile amounted to 124.4 micrograms Cd. Following administration of MGDTC, the urinary and biliary excretions of cadmium were 14.5 and 47 micrograms, respectively, while in the case of INADTC the corresponding values were 23.6 and 7.9 micrograms cadmium. In control animals the urinary and biliary excretion per 12 h reached 0.09 and 0.12 micrograms Cd. Gel permeation chromatography (GPC) analysis of bile revealed differences in the distribution of Cd in the elution fractions after the first injections of the individual dithiocarbamates. For all three dithiocarbamates, significant decreases of the concentrations of cadmium in the liver and kidney were found. DEDTC (but neither of the other compounds) increased the concentration of cadmium in the brain from control levels of 49 +/- 5 ppb to 105 +/- 16 ppb.

The effect of sodium diethanolamine dithiocarbamate on distribution and excretion of Cd in rats drinking Cd-containing water.

The effect of sodium diethanolamine dithiocarbamate (DEDTC) on the distribution and excretion of cadmium was studied in three sets of rats whose drinking water contained cadmium at three different concentrations (5, 10 and 50 mg Cd.l-1) for a period of three months. DEDTC administration (500 mg.kg-1, ip) in all exposed groups significantly increased the biliary excretion of cadmium. With the exception of animals drinking water containing the lowest concentration of CD (5 mg.l-1) the urinary excretion was also increased.