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Biomedical subjects

B Elsenhans

Publications and source records attributed to B Elsenhans.

At least 37 records · Page 2Linked to original sources
PubMed1994

Oral and subcutaneous administration of cadmium chloride and the distribution of metallothionein and cadmium along the villus-crypt axis in rat jejunum.

The route of Cd uptake influences the distribution of Cd, other metals, and metallothionein (MT). Although intestinal MT levels related to the tissue mass did not show proximodistal gradients after sc administration of CdCl2, orally administered high doses of CdCl2 increased mucosal MT levels longitudinally from the duodenum to the ileum. The gradient abolished when the mucosal MT level was related to the intestinal length. To further elucidate this finding, three groups of rats were studied: a control group, a group receiving dietary CdCl2, and a group receiving sc injections of CdCl2. The small intestine was removed after a 14-d treatment. Midjejunal segments were mounted in a cryomicrotome and cut transversally into five layers along the villus-crypt axis. Mucosal enzymes were measured to control these sections. Cd was measured by AAS and MT by RIA. Alkaline phosphatase and lactase activities exhibited the typical villus-crypt gradient. Mucosal MT levels paralleled those of Cd. Although Cd and MT concentrations were high at the tip of the villi and low in the crypts after oral administration, sc treatment reversed that profile. A molar Cd-MT ratio of approx 10 or 1 was reached after po or sc treatment, respectively. This demonstrates that only oral Cd may lead to an accumulation of Cd in the mucosal tissue fairly exceeding the binding capacity of small intestinal MT. The results show that different routes of Cd intake lead to a different MT-induction pattern in the intestinal wall and that longitudinal Cd and MT concentration gradients in the small intestine observed after high oral doses are a result of their high levels at the villus tips.

Administration, Oral↗
PubMed1993

On the capacity of the rat intestine to excrete lithium ions at therapeutic and toxic plasma lithium concentrations.

Lithium (Li) excretion into the intestinal lumen was quantitated in rats in situ by use of a pendular perfusion technique. Male Sprague-Dawley rats were injected daily (7-10 days) i.p. with 1, 3, and 6 mmol LiCl per kg body weight (n = 9-12). Jejunal as well as ileal and colonic segments were perfused with isotonic saline containing 3H-PEG-4000. Perfusate samples were taken after 0, 5, 10, 20, and 60 min. At the highest dose toxic symptoms were observed. At 6 mmol Li per kg the plasma Li concentrations were higher than those linearly extrapolated from the lower-dose groups, which may be due to inappropriate renal excretion. The Li concentration in the perfusate increased linearly over time and was not significantly different between jejunal and colonic segments. The same ratio between the Li concentration in the plasma and in the luminal perfusate was observed in all groups. Intestinal Li excretion is not impaired by high plasma concentrations. The intestinal capacity to excrete Li is considerable: 45 cm of jejunum is able to excrete the intire plasma Li content in 30-40 min, when Li is not resupplemented from intracellular stores. The renal clearance of lithium (Li) decreases when toxic Li plasma concentrations are reached. Therefore, if it were possible to trap Li in the intestinal lumen, this excretion route might be of therapeutic interest in cases of Li intoxication with impaired renal Li-excretion.

Animals↗
PubMed1993

Does intake of highly demineralized water damage the rat gastrointestinal tract?

Highly demineralized water (hd-water) is used frequently in laboratories and on an industrial scale. However, no systematic data seem available as to whether hd-water has a toxic potential beyond the physical risks of drinking water (drowning, water intoxication). This study investigated the impact of hd-water on function and morphology of the rat's gastrointestinal tract. One group of rats received hd-water together with the usual diet ad libitum for 14 d. A second group was exposed to hd-water after withdrawal of food and water for 24 h. Both experiments had control groups which were treated identically except that hd-water was replaced by tap water. Histology showed no signs of erosion, ulceration or inflammation in the esophagus, stomach or jejunum. Body weights and the uptake of food and water were not significantly different between the hd-water exposures and controls for 14 d. Tissue alkaline phosphatase activity was unaltered, and the mitotic rate in the epithelium of the esophagus and stomach were not different between controls and rats on hd-water. Exposure to hd-water caused no changes in the km or Vmax values for the uptake o of alpha-methyl-D-glucose from the upper jejunum. There findings indicate no impact of hd-water on the function or morphology of the rat gastrointestinal tract. There is no need for additional safety regulations when working with hd-water which go beyond those considered adequate to prevent drowning and water intoxication.

Animals↗
PubMed1993

Influence of low luminal cadmium-concentrations on transfer of water and cadmium in the rat small intestine in vitro.

The sensitivity of the small intestinal water transfer for cadmium (Cd) exposure and its longitudinal gradient were investigated in luminally perfused intestinal segments in vitro and in vivo. Proximal segments accumulated Cd to a higher extent and, in addition, were more sensitive to Cd exposure than distal segments. In the proximal small intestine Cd impairs the intestinal water transfer at concentrations between 0.1 and 1.0 mumol/l in vitro and 4 mumol Cd/l in vivo. In vitro the Cd transfer from the intestinal tissue into the serosal absorbate declined in parallel to the reduction of the water transfer. In proximal but not in distal segments the declining water transfer corresponded to the decreases in glucose transfer in response to Cd exposure. According to literature the Cd effect on intestinal water transfer may be mediated by interaction of Cd with the Na-glucose co-carrier or by inhibition of the oxidative phosphorylation. The involvement of both mechanisms may differ along the small intestine.

Animals↗
PubMed1992

Arsenic-copper interaction in the kidney of the rat.

1. The interaction between As and three toxic metals (Cd, Ni and Pb) and Cu (an essential trace metal) in the kidney was investigated in the rat by feeding diets containing various concentrations of As whilst maintaining constant concentrations of the other elements. After 1, 3, 7 and 15 weeks of feeding, metal contents in the renal cortex and medulla, red blood cells and plasma were determined by atomic emission spectrometry (ICP-AES). 2. As accumulated in the whole kidney, whereas Cu accumulated only in the cortex. Accumulation of Cu was found to depend on the feeding period and dietary As concentration. 3. As was also accumulated in red blood cells, where saturation was found at 550 micrograms As g-1 cells. 4. Although Cd was also accumulated in the cortex, its accumulation was independent of the dietary As concentration. Ni and Pb were not detected by ICP-AES. 5. Chromatography of the supernatants from cortical homogenates of control and As-treated rat kidney suggested that Cu accumulated in renal metallothionein (MT). Its accumulation in this fraction was independent of that of Cd, indicating that the As-Cu interaction was not a result of MT induction, but rather that it might result from altered renal handling of Cu with subsequent incorporation into MT.

Animals↗
PubMed1992

Endogenous intestinal metallothionein possibly contributes to the renal accumulation of cadmium.

At low levels of dietary cadmium chloride, cadmium accumulates directly in the kidneys and not in the liver. As dietary cadmium induces intestinal metallothionein (MT), intestinal CdMT complexes could be at least partly responsible for the renal accumulation of oral cadmium. For this to be possible, however, serosal release of mucosal CdMT would be required. To test this hypothesis, we perfused isolated rat small intestinal segments (Fisher-Parsons method) in an attempt to demonstrate the release of intestinal MT. After two weeks of feeding dietary cadmium chloride, intestinal MT was induced in amounts proportional to the dietary cadmium level. Subsequent in vitro perfusion of the small intestine revealed a concentration-dependent release of intestinal MT on the serosal side. When 109CdCl2 was present in the perfusion medium, 109Cd appeared on the serosal side mainly in the MT fraction. These results indicate that endogenous intestinal MT may deliver CdMT to the organism, thus possibly contributing to the renal accumulation of orally ingested cadmium.

Animals↗
PubMed1991

Increased copper concentrations in rat tissues after acute intoxication with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Recently, acutely toxic doses of the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have been reported to affect the hepatic distribution of essential metals in the rat. However, the reduced food intake by TCDD was not taken into account. Therefore, metal concentrations were determined in different rat tissues at the end of a toxicity study with TCDD in which a pair-fed control group was introduced. Male Sprague-Dawley rats received a single i.p. injection of corn oil/acetone with or without TCDD at 125 micrograms/kg. Controls and TCDD-treated rats were fed ad libitum; additionally, pair-fed controls received the amount of food consumed by their TCDD-treated partners 1 day before. Twenty-one days after dosing rats were killed and samples of liver, kidney and jejunum were taken for the analysis of Ca, Cu, Fe, Mg, Mn, and Zn. After acid digestion of the tissues metals were determined by atomic emission spectrometry (AES). The most outstanding effect of TCDD treatment was an increase of the copper levels in the kidney (4-fold, versus pair-fed controls) and in the liver (greater than 2-fold, versus pair-fed controls). Other metals were mainly affected by the reduced food intake only. Since Cu represents a trace metal the homeostasis of which depends on its biliary excretion and since TCDD is known to impair biliary flow and excretion, an impaired biliary excretion of Cu by TCDD is suggested as the causal mechanism.

Animals↗
PubMed1991

Intestinal iron transfer after ileojejunal transposition.

Little is known on how longitudinal differences in intestinal iron absorption develop and to what extent distal segments can adapt to a more proximal location after surgical intervention. Therefore, 3 weeks after ileojejunal transposition in rats adaptational changes of intestinal iron transfer were measured together with those of glucose and water transfer, intestinal dry weight and villus surface. In vitro iron transfer (Fisher-Parsons technique) was significantly increased in transposed segments as compared to ileal controls, when related to intestinal length. Jejunal values were not reached, though, which was confirmed by corresponding in vivo results. Increases in intestinal mass which are known to be caused by villus hyperplasia were closely correlated to increases in iron transfer after ileojejunal transposition. Thus, the increased iron transfer might partly be due to an increased number of enterocytes. In addition, transposed enterocytes took up jejunal characteristics regarding the ratio between transferred iron and water quantities which significantly increased the serosal 59Fe concentration as compared to ileal segments. Similar changes were also observed for glucose. Therefore, the adaptation of intestinal 59Fe transfer after ileojejunal transposition seems to be part of a more general adaptation process, essential parts of which are likely to be located in the brush border.

Adaptation, Physiological↗
PubMed1990

Increased intestinal iron absorption in rats with normal hepatic iron stores. Kinetic aspects of the adaptative response to parenteral iron repletion in dietary iron deficiency.

Male Sprague-Dawley rats were fed an iron-deficient diet for 8 days. After this period, iron stores were repleted in three groups of animals by intravenous administration of iron dextran. In a second set of experiments, iron was administered in the same dose as Fe nitrilotriacetic acid complex. 12 h, 24 h and 48 h thereafter, the intestinal iron transfer in vitro and in vivo as well as the non-heme iron and ferritin content were determined in both the liver and the jejunal mucosa. In iron deficiency, intestinal iron transfer is increased to 230% of untreated controls, while non-heme iron and ferritin decreased to 20% and 10% in the liver and to 55% and 25% in the mucosa, respectively. 12 h and 24 h after parenteral administration of 0.1 mmol Fe/kg body weight iron transfer was as high as in iron deficiency, while liver iron stores were not significantly different from the untreated controls. In this situation, the close link between decreases in body iron stores and increases in iron transfer was temporarily dissociated. This can be related to the time lag between the incorporation of parenterally applied iron in the liver and in the jejunal mucosa. The data provide evidence for the hypothesis that the hepatic iron stores have no means of neural or hormonal communication with the small intestine in order to adapt iron transfer to their state of repletion on short notice. Intestinal iron transfer returned to control levels after 48 h.

Adaptation, Physiological↗
PubMed1990

Rat intestinal iron transfer capacity and the longitudinal distribution of its adaptation to iron deficiency.

The longitudinal gradient of intestinal iron transfer was investigated in normal and iron-deficient male Sprague-Dawley rats in vitro and in vivo. In normal rats in vitro iron transfer in the duodenum was approximately 3 times higher than in the jejunum and decreased in the ileum to approximately half the jejunal values. Compared to the controls in vitro iron transfer was increased 3-4 times in the duodenum and in the first jejunal segment and 2-3 times in the second jejunal segment. No significant adaptation to iron deficiency was found in the rest of the small intestine. Iron transfer rates showed the same longitudinal pattern when iron was chelated with nitrilotriacetic acid (NTA) or with ascorbate. The absorbed iron quantities, however, were approximately 5 times lower when Fe-ascorbate was used, which might be due to differences in bioavailability. Omission of Fe-NTA and Fe-ascorbate had no impact on the vitality of the segments. Glucose transfer was used as vitality criterion. It was not significantly different between corresponding iron-deficient and control segments. To control these results in vivo mesenteric blood was collected from duodenal and jejunal segments in situ. Corresponding to in vitro findings iron transfer was close to linear over the experimental period. In iron deficient duodenal segments iron transfer increased approximately 3 times as compared to controls while no adaptational changes were found in the distal jejunum. No significant longitudinal gradient was found in the mucosal content of ferritin and nonheme iron. Both parameters were decreased in iron deficiency by about half. The mucosal transferrin content showed no longitudinal gradient in control animals. In iron deficiency transferrin was significantly increased in the duodenum and in the three most proximal jejunal segments. The results indicate that in rats adaptation of iron absorption to the demand can only be expected in the duodenum and in the proximal 20 cm of the jejunum. Because this process shows a steep gradient in the proximal small intestine, studies on the adaptation of intestinal iron transfer to the demand should use short and well-defined segments in order to provide reproducible results.

Adaptation, Physiological↗
PubMed1989

In-vivo inhibition by polycations of small intestinal absorption of methyl alpha-D-glucoside and leucine in the rat.

Polycations are able to inhibit active transport processes in rat small intestine in vitro. Whether this effect can also be confirmed in vivo is the concern of this study. Therefore, the effect of various polycations, e.g., protamine and polylysine, on the absorption of methyl alpha-D-glucoside and leucine was investigated in vivo by single-pass perfusion of rat jejunum. The inhibition of absorption of methyl alpha-D-glucoside and leucine by the polycations was strongly dose dependent. At a substrate concentration of 1 mmol/l a 50% inhibition was achieved with a protamine concentration of 3.2 mg/ml. The inhibition increased as the chain length of the polycation increased. In the presence of protamine the concentration-dependent leucine absorption was reduced at leucine concentrations below 60 mmol/l, but was increased at 100 mmol/l. Absorption of mannitol and 2-deoxy-D-glucose was significantly enhanced by the polycations. These results demonstrate that polycations inhibit active transport and increase passive diffusion processes in the rat small intestine in vivo. In addition, pretreatment of rats with a polycation added to the drinking water impaired the small intestinal absorption of methyl alpha-D-glucoside as subsequently measured by the tissue accumulation technique in vitro. Since polycations are hardly absorbed in the intestine, but do attach to negatively charged groups at the mucosal surface, polycations may be useful to study the influence of these negative groups on the absorption of nutrients and drugs.

Animals↗
PubMed1989

Determination of residual erythrocytes in rat tissue homogenates using commercially available anti-red blood cell sera.

A method to determine the residual erythrocyte content in rat tissue homogenates by means of radial immunodiffusion (Mancini et al., 1965) is described. The method makes use of commercially available antisera against rat erythrocytes. Tissues were homogenized after addition of digitonin and applied on Mancini plates. To measure within the linear part of the calibration curve, the tissue homogenates were diluted to concentrations between 0.062% and 2.5% wet weight content, depending on the type of tissue and on the degree of bleeding before the death of the animal. Recovery data of added blood as well as a comparison with results from organ distribution studies with 59Fe-labeled erythrocytes demonstrated that this simple method is sufficiently reliable and sensitive. The present procedure is to control experiments in which drug tissue levels (e.g., antibiotics) are to be determined and in which the drug content of residual blood is likely to bias the results to an unknown extent. It can be used as well in organ distribution studies of substances with a high affinity for erythrocytes (e.g., Pb; As in rats). It is possible to individually control the success of procedures without the use of isotopes--such as exsanguination or vascular perfusion--that are performed in order to reduce the blood content in the organs under consideration.

Animals↗
PubMed1989

Incorporation of iron from an oral dose into the ferritin of the duodenal mucosa and the liver of normal and iron-deficient rats.

To further characterize the role of ferritin in regulating iron absorption, uptake of an oral dose of 59Fe (0.2 mg Fe/kg body wt.) into duodenal and hepatic ferritin of control and iron-deficient (ID) rats was studied. Retention and uptake of 59Fe from Fe(II)-sulfate, Fe(III)-chloride, or Fe(III)-polymaltose were measured up to 28 h after dosing. Ferritin was determined by radioimmunoassay (RIA) and 59Fe ferritin-iron by gel electrophoresis. Retention and liver content of 59Fe was higher in ID rats than in controls. The mucosa of ID rats, however, retained only one third of the amount of 59Fe retained by the mucosa of controls. The mucosal and hepatic ferritin levels were lower in ID rats than in controls. The percentage of orally administered 59Fe found in the liver ferritin was therefore higher in control than in ID rats. However, when expressed as per unit of ferritin, iron uptake was eight times higher in ID rats. In contrast, mucosa ferritin of ID rats contained one-third of 59Fe per unit of ferritin than that of controls. Assuming no change in the mechanism of iron uptake into ferritin of control and ID rats, the differential uptake of oral iron into mucosa and liver ferritin indicates either a different compartmentation of the tissue ferritin or differences in the iron transport processes, but mucosal ferritin does not withdraw iron from intestinal absorption.

Administration, Oral↗
PubMed1989

Differential changes in the urinary excretion of two orally administered polyethylene glycol markers (PEG 900 and PEG 4000) in rats after feeding various carbohydrate gelling agents.

The urinary excretion of two orally administered polyethylene glycol markers (PEG 900 and PEG 4000) was measured in rats after feeding various carbohydrate gelling agents. Pectin, guaran, methylcellulose, and carrageenan were added (20% wt/wt) to a fiber-free control diet and were fed for 4 wk prior to the experiment. Excretion of 3H-PEG 900 and 14C-PEG 4000 was measured over a period of 96 h after administration of the markers in the drinking water. In general, the ratio of PEG 4000 to PEG 900 in the urine increased after fiber feeding: from 0.20 in the controls to 0.31, 0.37, 0.29, or 0.27 (medians) in the pectin-, guaran-, methylcellulose-, or carrageenan-fed group, respectively. The pattern of excretion of the two PEG markers in rats fed the fiber-free diet differed from that in the polysaccharide-fed rats. Pectin and guaran, two polysaccharides readily fermented by intestinal bacteria, led to a higher excretion of PEG 4000 but an unaltered excretion of PEG 900, whereas methylcellulose and carrageenan, two polysaccharides more inert against microbial degradation, were associated with a lower excretion of PEG 900 with unchanged excretion of PEG 4000. The study shows that polysaccharides, which may be representative of the soluble portion of dietary fiber, can influence the intestinal permeability of larger molecules. The microbiologically degradable polysaccharides in particular may lead to an increased absorption of larger molecules.

Animals↗
PubMed1989

Increase of the intestinal iron absorption in growing rats and mice after 8 days of iron-deficient feeding.

In investigations of intestinal iron absorption the combination of repetitive bleeding and iron-deficient feeding is frequently used. It induces iron deficiency which, in turn, stimulates iron absorption. When this combined procedure was compared with the effect of an 8 d iron-deficient feeding schedule in growing rats, no significant differences were found regarding the stimulating effect on intestinal iron transfer. Body iron stores, however, as represented by the hepatic ferritin and iron content are remarkably less depleted. Contrary to the effect of the combined procedure the animals growth was only marginally retarded and anaemia did not develop. This was also demonstrated in mice. The stimulation of intestinal iron absorption by iron-deficient feeding of growing animals thus seems preferable, as this procedure largely avoids the disturbing side effects observed with repetitive blood sampling.

Anemia, Hypochromic↗
PubMed1988

On the origin of intestinal transferrin.

The incorporation of 35S-L-methionine (35S-Met) into TCA-precipitable protein is used to measure protein synthesis in isolated non-vascular perfused jejunal segments and in isolated liver cells under steady-state conditions in rats. 10(5) X g supernatants of homogenates from jejunal segments and from liver cells as well as the jejunal absorbate were processed immuno-electrophoretically. Incorporation of 35S-Met radioactivity into precipitin lines with sera against transferrin, IgG and plasma proteins were autoradiographed and compared semiquantitatively with each other. Calculated on a wet-weight basis this system is sensitive enough to detect transferrin synthesis down to a level of 1% of that in the liver. Still, no transferrin synthesis was found in the jejunal mucosa, while 35S-Met incorporation into TCA precipitates and into IgG continued in isolated jejunal segments for over 2 h. A good correlation was found (r = 0.88, P less than 0.01) between mucosal and plasma transferrin in normal as well as in iron deficient rats. A complete immunologic cross-reactivity could be demonstrated between different plasma transferrins and the transferrin in three different preparations of the intestinal mucosa. Immunoblots of electropherograms after isoelectric focussing showed no distinct differences between transferrin in the plasma, bile, and in the mucosal epithelium.

Animals↗
PubMed1987

Metal-metal interactions among dietary toxic and essential trace metals in the rat.

Exposure to toxic and essential metals is thought to be reflected by corresponding metal concentrations in tissues. However, toxic and essential metals may influence each other in regard to their retention in the body. Therefore a basic diet containing four toxic metals (As 7, Cd 9, Ni 13, and Pb 20 ppm) and adequate amounts of essential metals was fed to rats for 2 weeks. Test groups received the basic diet with increasing concentrations of one of the toxic metals (up to 90 ppm As, 180 ppm Cd, 365 ppm Ni, and 394 ppm Pb). As, Cd, Ni, Pb, Cu, Fe, Mn, and Zn were determined by atomic emission spectroscopy in liver, kidney, intestine, brain, muscle, bone, skin, hair, and blood. A linear relationship between diet and tissue concentration is observed for As and Ni in the kidney, for Cd in the liver, and for Pb in the bone. In other tissues saturation was observed. While Cd-Fe interactions were common to most of the tissues, other interactions were detected only in specific tissues, e.g., As-Cu in the kidney, Cd-Zn in the liver, and As-Mn, Cd-Mn, or Ni-Cu in the intestine. Increases of renal Pb and intestinal Cd by dietary Ni, and a decrease in bone As by dietary Pb were the most pronounced interactions between the toxic metals. The results demonstrate that potential target organs for the evaluation of metal exposure need to be carefully analyzed for interfering metal-metal interactions.

Administration, Oral↗