[How useful is administration of colloidal Berlin blue for the decontamination of radio-cesium?].
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Biomedical subjects
Publications and source records attributed to W Forth.
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Isolated non blood-perfused intestinal segments from normal and iron-deficient rats were used in vitro. A modification of the luminal perfusion method according to Fisher and Parsons allowed the comparison of iron and transferrin quantities in the serosal fluid at 15 min intervals. Iron transfer in jejunal and ileal segments was directly proportional to the luminal iron concentration within a dose range of 1 to 100 mumol/l, did not show saturation characteristics and was linear over time. Jejunal segments from iron-deficient rats transferred about twice as much iron as the jejunal controls. In ileal segments there was no difference in iron transfer between iron-deficient and control rats; in both cases transfer amounted to approx. 10% of jejunal controls. An exponential correlation was found, when the decreasing transferrin content of the tissue was plotted against the cumulative water transport. Transferrin and albumin release from jejunal and ileal segments into the absorbate cumulated asymptotically, which is typical for wash-out phenomena. As iron transfer cumulated linearly while transferrin release cumulated in an asymptotic manner, the capacity of transferrin to bind iron ions is exceeded roughly 100 times by molar equivalents of iron in the last absorbate fractions. Independence of iron transfer from mucosal transferrin quantities is concluded. As the molar transferrin/albumin ratios do not show significant differences between plasma and the sequence of absorbate samples, a wash-out from the gut's interstitial space is assumed, which makes plasma the most likely origin of transferrin in the mucosa.
The content of transferrin, albumin, and iron was determined in plasma and bile from normal and iron-deficient rats. In the plasma as well as in the bile there is a decrease of iron and an increase of transferrin due to iron depletion, whereas the albumin level remains constant. No significant difference of iron contents in plasma and bile was found, but the content of transferrin and albumin in bile was markedly lower than in the plasma. Thus, in the bile the iron content substantially exceeded the binding capacity of transferrin. The ratio between transferrin and albumin was the same in bile as in blood which argues for a bulk transfer of plasma proteins into the bile.
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T-2 toxin, a major trichothecene mycotoxin, was administered intravenously to rats. At a dose of 0.75 mg/kg two thirds of the animals died. In animals that received dexamethasone (1.6 mg/kg IV) either 30 min before or 1 h after the toxin, there was a more than fourfold reduction in lethality rate. Dexamethasone injected 3 h after the toxin was less effective. At a lethal dose of T-2 toxin (1 mg/kg IV) pretreatment with dexamethasone only delayed death, whereas lethality rate was barely affected (9/10 vs 10/10 in controls). Dexamethasone markedly reduced the incidence of lung edema and diarrhea. The incidence of hemorrhages, however, was not reduced by dexamethasone. Gastrointestinal bleeding was even more frequent in treated rats than in controls.
Mucosal transferrin was determined as transferrin-like immunoreactivity (TLIR) by means of a 2-site immunoradiometric assay (IRMA). Scraped-off mucosal tissue as well as isolated mucosal cells from the duodenum and jejunum of normal and iron-deficient rats before and after a washing procedure were examined. In iron-deficient rats there was about twice as much TLIR in scraped-off mucosal tissue as in the untreated animals. In the duodenum and jejunum of normal and iron-deficient rats, TLIR contents of the isolated cells in the magnitude of 320-510 ng/mg dry weight were found. Washing isolated cells three times in ice-cold Hank's solution resulted in a nearly tenfold decrease of TLIR content in all groups. In contrast the cells' RNA content remained unchanged.
The transfer and tissue content of 3H-pteroylmonoglutamate (PteGlu) from the mucosal to the serosal side (Jms, TCm) and in the reverse direction (Jsm, TCs) was studied using the everted sac technique. In the entire intestine, except for the colon, 3H-PteGlu was transferred preferentially into the serosal solution. When 3H-PteGlu was applied to the serosal side the final tissue concentration in either jejunal, duodenal, ileal or colonic segments was not significantly different from each other and about two-fold the serosal concentration. Apparently there exists a specific transfer process from the mucosal to the serosal side in the jejunum. The transfer of 3H-PteGlu shows saturation kinetics (S0.5 = 4.9 X 10(-5) mol/l). At low concentration (2 nmol/l) 3H-PteGlu was accumulated within the mucosal epithelium (tissue/mucosal fluid ratio = 3.8). Transfer and accumulation in the mucosal tissue of 3H-PteGlu apparently need high activation energy as indicated by the temperature dependency of these processes. Finally, transfer and accumulation in the tissue of 3H-PteGlu could be inhibited by salazosulfapyridine and phenobarbital.