Maganese retention in rat brain.

Manganese retention was observed in brains and in several other tissues of female Wistar rats after the intratracheal instillation of an inorganic manganese compound: manganese dioxide. Two categories of rats, younger (180 to 200g) and older (330 to 350g), were divided into a control group, in which animals received vehicle only (0.5 mL physiological saline), and an experimental group, in which rats received a dose of 0.48 mg of Mn/kg body weight (in 0.5 mL saline), twice a week for 3 months, for a total dosage of 11.80 mg of Mn/kg body weight. At the end of the exposure period, manganese retention in selected rat organs, brain, liver, kidney, and lung, was analyzed using atomic absorption spectrophotometry. At the end of the 6-wk or 12-wk manganese dioxide exposure period, analysis of variance of the manganese retention results revealed significant differences between Mn-exposed and unexposed rats in brain, kidney, and lung tissues (p<0.01) for both experimental age categories. Moreover, at the end of the 12-wk exposure period, significant results (p<0.05) between younger and older rats were obtained for both brain and kidneys. In both types of tissue, the manganese retention in the younger group was higher than that in older animals.

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.

Regeneration in mouse skeletal muscle injured by Trichinella larvae.

During the infection caused by Trichinella pseudospiralis serious damage to muscles is partly compensated with regeneration process. Short, thin fibrillae with central position of the nuclei--regenerating myotubes originate 20--40th day post infection in endomysial tubes remaining after damaged muscle fibres, left by migrating larva. On the 10th day post infection in the vicinity of moving larva activation of nuclei and increased origin of satellite cells under basal membrane occur. With development of the infection endothelia in the vicinity of altered fibrillae are increasing in number but there is small inflammatory and fibroproductive reaction only. During the infection caused by Trichinella spiralis and T. nativa, alteration of muscle fibres is accompanied by early inflammatory and fibroproductive reaction towards immediate surroundings of larvae. In a changed segment of muscle fibre with the larva--in pseudocyst there is altered basal lamina as well, built in increased glycocalyx and in the course of 20 days encased by connective tissue. Revascularisation and regeneration in a short damaged segment does not occur even during long-lasting infection because of separation by capsule.

The effect of CdCl2 on the respiration of rat small intestine mucosa.

Process of oxygen consumption of rat small intestine have already been studied at the level of whole intestinal wall or mucosa only by means of manometric or polarographic methods. The influence of cadmium on mucosal respiration of three sections of rat small intestine was determined because of its toxicological importance. Oxygen consumption was measured polarographically with Clark electrode at 38 degrees C in Krebs Ringer phosphate medium with 0.011 mol/l glucose. Control as well as cadmium affected respiration values were measured one after the other on the same mucosa. High cadmium concentration (applied as CdCl2) that is 2.2 and 1.4 . 10(-2) mol/l significantly inhibited the respiration in duodenum, jejunum and ileum. Observed inhibition of 80 and 50% on the average approximately for these two concentrations was related (similarly as following effects) to 100% value of control respiration. Concentrations 7.8 and 4.5. 10(-3) mol/l caused mostly lower inhibition of oxygen consumption (with the exception of significant 53% inhibition of jejunal respiration for 7.8. 10(-3) mol/l CdCl2). Low concentrations 10(-4) - 10(-6) mol/l CdCl2 had either no effect or stimulated oxygen uptake in intestinal mucosa. In older rats (weight 300-350 g) the respiration of duodenal and jejunal mucosa was inhibited with cadmium chloride concentration of 10(-6) mol/l.

Effects of kerosene hydrocarbons on tissue metabolism in rats.

Kerosene hydrocarbons inhibit respiration of liver and kidney tissues in vitro simultaneously impairing biotransformation of hexobarbital and phenacetin in vivo. An increase in concentration of lactate and pyruvate in the blood and liver tissue, and a decrease in glucose concentration in the blood, reduction of glycogen content in the liver and in the skeletal muscle, with concomitant increase of lactate dehydrogenase activity in the liver were observed. These effects were noted mainly in rats acutely poisoned, while in subchronic poisoning they were less pronounced.

An X-ray, microanalytical and ultrastructural study of cadmium absorption and transport in rat liver.

Accumulation of cadmium in the liver was demonstrated by X-ray microanalysis in every type of experiment, i.e. after injecting Cd into the ligated intestine and after the peroral acute single and combined, subchronic and chronic administration of Cd. Half an hour after its injection, Cd was localized diffusely in the liver; one hour after injection its increased accumulation in the cells caused generalized changes in the endoplasmic reticulum, mitochondria and nuclei. In acute and chronic peroral tests, the hepatocytes of the intermedial and peripheral zone of the lobes were the main storage region. After an acute dose of Cd, the cells in the centrolobular zone were hydropic, or single-cell necrosis developed; after the longer effect of combined doses the latter was manifested as centrolobular focal necrosis. Cd was not demonstrated in the lesions. Chronic administration did not lead to manifest severe degenerative changes in the liver. Accretions in the mitochondria and on the membranes of the endoplasmic reticulum were identified by means of X-ray analysis with cadmium peaks. Cadmium showed up clearly as L alpha- and L beta-lines at 3.135-3.320 keV. We presume that cadmium is bound in the ribosomes of the endoplasmic reticulum, as well as the mitochondria, and is released by the invagination of swelling mitochondria of the peripheral hepatocytes into Disse's spaces.

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.