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In the present study, the effects of dexamethasone on cadmium-induced toxicity were evaluated in isolated rat hepatocytes. Hepatocytes were cultured for 24 h in William's E medium containing fetal calf serum (10%), insulin (0.1 IU/ml), and glucagon (0.01 microM) in the absence or presence of 0.1 microM dexamethasone. Cadmium chloride, 5 or 10 microM, was added to the medium and the toxicity was evaluated for up to 48 h after treatment. Lactate dehydrogenase (LDH) release, the reduced and oxidized glutathione ratio (GSH/GSSG), protein-SH groups, and lipid peroxidation levels were evaluated. Cadmium induced a dose- and time-dependent LDH release in control hepatocytes at 24 h (Cd 10 microM 42%) while hepatocytes pretreated with dexamethasone showed lower necrosis (Cd 10 microM 12% at 24 h). GSH/GSSH ratio and protein-SH groups were higher while lipid peroxidation was lower in dexamethasone-treated hepatocytes as compared with untreated cells. In conclusion, cadmium toxicity was associated with an increase in intracellular oxidative stress responsible for accelerated cell death. The use of dexamethasone prevented cadmium damage, suggesting that the cytoprotective action of this hormone is related to its effect in preventing changes in thiols such as glutathione and protein-SH groups.

An experimental study was carried out in an animal (New Zealand white rabbit) wound model to evaluate any effects of a hypotonic, bicarbonate-calcium-magnesium mineral water (Comano thermal water) on skin regeneration, comparing the healing rate of split-thickness skin graft donor sites treated with the thermal water wet dressing versus a standard petrolatum gauze dressing versus a saline solution wet dressing. The study was performed in two steps; an overall of 22 animals were enrolled in the study. The wound healing progress was evaluated both by the surgeons and by the histologists. Sixty-four punch biopsies were examined in all. The histological samples were examined after staining with haematoxylin and eosin, Masson's and orcein staining and under a transmission electron microscope. The data were statistically analysed. The Comano thermal water proved to improve skin regeneration, not only by increasing keratinocyte proliferation and migration but also favourably modulating the regenerated collagen and elastic fibres in the dermis. We propose that the results of the topical treatment with the thermal water could be due to the favourable combination of a local wet environment with an anti-inflammatory action and that the regenerative properties of Comano thermal water observed in rabbits could also be applied for human use.

One of the most extensively studied and best-established properties of coffee is its antioxidant activity. We have shown that coffee brew has the ability to inhibit lipid peroxidation completely in a rat liver microsome biological system. The inhibitory activity was mainly due to the high molecular weight (HMW) fraction; this consisted of five components that were isolated, purified, and seen to occur in different amounts in the brew. Each component had different spectra and element compositions, although they all contained nitrogen. HMW, nitrogen content, and brown color enabled three components to be attributed to the melanoidin family; the two nonbrown components could not be considered as melanoidins. Each melanoidin and nonmelanoidin component contributes to a different extent to the protective action exerted by coffee brew. None of the isolated components completely inhibited microsomal lipid peroxidation alone, suggesting that each acts at different sites and/or possesses different mechanisms of action. The protective activity of coffee brew is thus underpinned by the antiradical properties, reducing power, and metal chelating ability of the individual components, each contributing to a different extent.

The antiradical properties of water-soluble components of both natural and roasted barley were determined in vitro, by means of DPPH* assay and the linoleic acid-beta-carotene system, and ex vivo, in rat liver hepatocyte microsomes against lipid peroxidation induced by CCl4. The results show the occurrence in natural barley of weak antioxidant components. These are able to react against low reactive peroxyl radicals, but offer little protection against stable DPPH radicals deriving from peroxidation in microsomal lipids. Conversely, roasted barley yielded strong antioxidant components that are able to efficiently scavenge free radicals in any system used. The results show that the barley grain roasting process induces the formation of soluble Maillard reaction products with powerful antiradical activity. From roasted barley solution (barley coffee) was isolated a brown high molecular mass melanoidinic component, resistant to acidic hydrolysis, that is responsible for most of the barley coffee antioxidant activity in the biosystem.

The antiradical activity of water soluble components in six vegetables belonging to the Cichorium genus, i.e., three cultivars of red intybus species var. silvestre (Treviso, Chioggia, Verona red chicories), a white intybus species var. foliosum (Belgian chicory), and two vegetables of the endivia species var. latifolium (escarole chicory) and var. crispum (‘‘crispa’’ chicory), were studied using two biological systems consisting of: (1) microsome membrane rat hepatocyties in which oxidative damage was induced by CCl4; (2) gram-positive bacterium, Staphylococcus aureus cultures, subjected to damage with cumene hydroperoxyde. The obtained results show that in both systems the red vegetables possess the strongest antioxidant properties and contain different antioxidant compounds whether at a low or high molecular weight, but only those of high molecular-weight (MW > 3500 Da) are able to act as antioxidants in all the used systems. The lower MW fraction (MW < 3500 Da) showed itself to be pro-oxidant in the microsome system. The effects of thermal treatments such as boiling, freezing and freeze-drying were also investigated.

Several authors have demonstrated the pivotal role of proinflammatory cytokines in inducing progressive cartilage degradation and secondary inflammation of the synovial membrane in osteoarthritis (OA). It has recently been established that tumor necrosis factor (TNF)-alpha plays a well-defined role in the pathophysiology of inflammatory joint diseases and that binding to circulating soluble TNF-alpha receptors can inactivate it. We investigated the influence of mud pack treatment, which is able to diminish TNF-alpha serum values, on specific TNF receptor (sTNF-R) levels. Thirty-six patients with OA were enrolled and randomized into two groups. Group A underwent mud pack treatment and group B underwent thermal bath treatment. A group of 20 healthy untreated subjects was used as a control. Blood samples were collected at baseline and after treatment, and assays of sTNF-R55 and sTNF-R75 were performed in both groups. We found small changes in sTNF-Rs serum values but these were not statistically significant. sTNF-R55 serum values decreased by 0.4% after the therapy in group A, while in group B the decrease was -17.7%. sTNF-R75 was reduced by -21.17% in group A and by -10.6% in group B. In conclusion, through its thermic and ant/inflammatory activity mud pack treatment shows complex interaction with the most common factors of inflammatory and cartilage degradation. Our results suggest that the thermic component of this natural treatment is mainly involved in modulating inflammatory reaction and cartilage damage through binding of the circulating TNF, which controls the activation of the cells responsible for the production of proinflammatory cytokines.

Nitric oxide (NO) has recently been proposed as an important mediator in inflammatory phases and in loss of cartilage. In inflammatory arthritis NO levels are correlated with disease activity and articular cartilage is able to produce large amounts of NO with the appropriate inducing factors such as cytokines and/or endotoxin. Neutrophils also play an important role in inflammatory reactions and the level of myeloperoxidase, a constituent of neutrophil granules, is related to the intensity of the inflammation. Because there is evidence that suggests that mud packs influence the main cytokines involved in cartilage damage, we tried to determine whether NO and myeloperoxidase are involved in the mechanisms of action of mud bath treatment. We enrolled 37 subjects and randomly assigned them to two groups: 19 patients underwent mud bath treatment (group A) while 18 patients underwent bath treatment alone. Blood samples were obtained before and after the treatment cycles to assay serum levels of NO, myeloperoxidase (MPO) and glutathione (GSH)-peroxidase. The results showed a statistically significant decrease in NO and myeloperoxidase serum values in groups A and B, while GSH-peroxidase was not significantly increase in either of the groups; no correlation was found between NO, myeloperoxidase and GSH-peroxidase serum values. Mud bath treatment can exert beneficial effects on cartilage homeostasis and inflammatory reactions, influencing NO and decreasing myeloperoxidase serum values. The increase in GSH-peroxidase was not correlated with the reduction of other biochemical markers, suggesting that mud bath treatment has different mechanisms of action.

The antioxidant properties of green and roasted coffee, in relation to species (Coffea arabica and Coffea robusta) and degree of roasting (light, medium, dark), were investigated. These properties were evaluated by determining the reducing substances (RS) of coffee and its antioxidant activity (AA) in vitro (model system beta-carotene-linoleic acid) and ex vivo as protective activity (PA) against rat liver cell microsome lipid peroxidation measured as TBA-reacting substances. RS of C. robustasamples were found to be significantly higher when compared to those of C. arabica samples (p < 0.001). AA for green coffee samples were slightly higher than for the corresponding roasted samples while PA was significantly lower in green coffee compared to that of all roasted samples (p < 0.001). Extraction with three different organic solvents (ethyl acetate, ethyl ether, and dichloromethane) showed that the most protective compounds are extracted from acidified dark roasted coffee solutions with ethyl acetate. The analysis of acidic extract by gel filtration chromatography (GFC) gave five fractions. Higher molecular mass fractions were found to possess antioxidant activity while the lower molecular mass fractions showed protective activity. The small amounts of these acidic, low molecular mass protective fractions isolated indicate that they contain very strong protective agents.

The water soluble antioxidant properties of Cichorium intybus var. Silvestre, whose production zone is around Chioggia, Italy, were investigated. Vegetable juices were obtained by centrifugation, and (1) filtration at 2 degrees C; (2) filtration at 25 degrees C, and stored for 3 h; (3) boiled for 30 min at 102 degrees C, and then analysed. The antioxidant properties were evaluated in vitro as antioxidant activity (AA) (model system beta-carotene-linoleic acid) and ex vivo as protective activity (PA) against rat liver cell microsome lipid peroxidation measured as 2-thiobarbituric acid-reactive substances (TBA-RS) generated by peroxide degradation. All the vegetable juices showed high but very variable AA (83%) and PA (64%). After dialysis and analysis of fractions it was shown that the vegetable contained both biological antioxidant and prooxidant compounds. The prooxidants had MW3000, conversely the very active antioxidants (PA = 100%) had MW15,000. Electrophoretic analysis revealed that the most active fraction was a complex mixture of brown components at MW300,000.

The water soluble antioxidant properties of carrot, cauliflower, celery, eggplant, mushroom, garlic, onion, white cabbage, white potato, tomato, yellow bell pepper, and zucchini were investigated. Vegetable juices were obtained by centrifugation, and each antioxidant property was determined in terms of the protective activity (PA%) against rat liver microsome lipid peroxidation induced by CCl4 and measured by malondialdehyde release. All juices were found to be active. PA was very high (90−100%) and constant (relative standard deviation (RSD) = 4−7) for mushroom, garlic, cauliflower, and potato. For white cabbage, zucchini, and eggplant the PA reached similar values (80%) but was less constant (RSD = 12−15). Onion and yellow bell pepper showed high PA (75%) which was more variable (RSD = 20−24), and the PA for tomato and celery was less high (50%) and very variable (RSD = 25), especially in the case of carrot juice (6%) (RSD = 50). The juices were also analyzed after different technological treatments (bo...

The objective of this in vitro study was to examine the response of mixed cultures of Sertoli and germ cells to treatment with thallium (Tl) at the range of concentrations that, in previous studies, was shown in vivo to affect reproduction. Cultures were prepared from the testis of Sprague-Dawley rats. Cultures containing approximately 3.75 x 10(6) cells/ml were treated with Tl concentrations corresponding to 35, 7, and 1.4 micrograms Tl/g testis, estimated from protein content of cultures. Observations at 24, 48, and 72 h after treatment showed a significant release of germ cells into the culture medium that was both concentration and time dependent. Cultures treated with 35 micrograms Tl/g testis showed a threefold increase in germ-cell detachment compared with controls after only 24 h of exposure. As the treatment time increased to 48 h of exposure, even cultures exposed at the lowest Tl concentration (1.4 micrograms Tl/g testis) showed significant loss of germ cells. After 48 h, cultures exposed to 7 micrograms Tl/g testis exhibited a 2.5-fold increase in germ-cell detachment, and those exposed to 35 micrograms Tl/g testis exhibited a 10-fold increase over controls. Morphological investigations of cell cultures showed evident loss of germ cells with significant reduction in prepachytene and pachytene spermatocytes and changes in the shape of Sertoli cells. These results are in agreement with in vivo studies, in which thallium treatment at comparable exposure levels manifested its earliest toxic testicular effects in Sertoli and germ cells. They also demonstrate the usefulness of this in vitro culture technique to assess toxic testicular damage rapidly.

The hepatic effects of 1,2-dichloropropane (DCP) were investigated in male Wistar rats exposed to 15, 50, 100, 250, 450, 1000, 1300, 1800 or 4900 mg DCP m-3. At the end of a 4-h period of exposure, average blood DCP levels were 0.025 and 5.38 micrograms ml-1 in animals treated with 15 and 1300 mg m-3, respectively. Blood DCP concentrations were correlated with the air DCP concentrations in the inhalation chamber. At DCP concentrations of 100 mg m-3 or higher, the liver non-protein thiol (NPT) content was significantly reduced. Assays performed 20 h after 4-h DCP exposure showed that exposure to 100-1000 mg DCP m-3 had no effect on hepatic NPT levels. The NPT content increased only in the liver of rats exposed to higher (1300-4900 mg m-3) DCP concentrations. Treatment with DCP did not cause hepatic lipid peroxidation and did not modify total protein content. The observed changes in liver cell thiol homeostasis are likely to reflect the action of reactive intermediates formed during DCP metabolism. These changes can occur in rats following exposure to considerably low levels of DCP vapour.

Placental transfer of thallium was evidenced in rats treated with a single intraperitoneal dose of 2 micrograms 201T1-labelled thallium/rat on the 13th day of pregnancy. Both maternal and fetal organs showed remarkable thallium retention, approx. 10% of the dose being unexcreted 8 days after injection. The highest thallium accumulation was found in maternal muscle and brain tissues. Fetal brain exhibits higher thallium uptake and faster decay rate of thallium levels than maternal brain. It is suggested that the reduced activity of the mechanisms regulating ion movements and composition of nervous tissue and the immaturity of the blood-brain barrier play a role in the peculiar pattern of thallium kinetics in the developing rat brain.

Different [ 201+202 Tl] labelled thallium compounds such as inorganic mono-(I) and trivalent Tl(III) ions as well as organic dimethylthallium (III) species have been prepared and administered intraperitoneally or orally to rats. The 201+202 Tl radioactivity was measured in the tissues as well as in the kidney and liver intracellular fractions such as nuclei, mitochondria, lysosomes, microsomes and cytosol. The results also suggest analogies in the metabolic behaviour of the dissimilar inorganic Tl + and Tl 3+ chemical forms when they were administered by different routes. Qualitative similarities have also been observed in the tissue distribution of inorganic Tl + and Tl 3+ and dimethylthallium forms, the latter being much less absorbed by the gastro-intestinal tract. However the renal and hepatic subcellular distribution of the organic dimethylthallium were identical with respect to those of the inorganic thallium-treated animals. The present findings suggest that the oxidation state of thallium does not influence its metabolism in vivo. The similar biochemical behaviour of the different thallium species is probably related to a mechanism which transforms the different species to a single form. At present it is not possible to predict the most probable oxidation state of thallium in vivo, because both Tl(I) and Tl(III) have been shown biochemically active in vitro.

The administration of phenobarbitone to the rat (8 mg/100 g BW) once daily for 3 days significantly decreased the serum and tissue levels of erythromycin administered intraperitoneally (5 mg/100 g BW). Furthermore, phenobarbitone stimulated the hepatic microsomal N-demethylation of erythromycin and increased the biliary concentration and the biliary excretion rate of the unmetabolized antibiotic. These effects were accompanied by augmented liver mass and bile flow. The possibility is discussed that erythromycin concentrates in the bile through a specialized hepatic drug transport system, activated by phenobarbitone.

Selected enzyme activities were investigated in adult Wistar rats given 10 ppm thallium as the sulphate in the drinking water. The activity of β-glucuronidase, an enzyme primarily located in Sertoli cells and spermatogonia, was significantly reduced after 60 days of treatment with thallium whereas the activity of acid phosphatase (an ubiquitous testicular enzyme) did not differ from that of controls. Thallium did not affect food and water consumption, absolute and relative weight of testes, testicular protein content or the plasma levels of testosterone over the 60-day period of treatment. It is suggested that disorders in energy metabolism primarily involving Sertoli cells may, at least in part, account for the abnormal testicular biochemistry in thallium treated rats.

The administration to the rat of the inhibitors of microsomal mixed function oxidases, SKF 52S-A and Oxine-5-sulphonic acid (OSA) caused a significant decrease of the hepatic aminopyrine N-demethylase activity, as well as an increase in the plasma levels and antipyretic activity of orally administered aminopyrine. The plasma concentrations of the aminopyrine metabolite 4-aminoantipyrine were reduced in SKF S2S-A treated animals while they were slightly increased in those pretreated with OSA. These findings suggest that the in vivo changes of aminopyrine disposition and activity brought about by SKF 525-A were the result of an inhibited hepatic drug metabolism, while the effects produced by OSA were due to a more rapid intestinal absorption of aminopyrine.

1,2-Dichloropropane (DCP) is an industrial solvent widely used as a component of household dry-cleaning products, in the paint industry, and in agriculture as a soil fumigant. In recent years, intoxications and fatalities have been described as the result of abuse (“sniffing”) and accidental or deliberate ingestion of commercial household products containing varying concentrations of DCP (Pozzi et al. 1985). Clinical features of poisoning by DCP-containing products have included blood disorders, renal failure, and hepatic damage (Ghezzi Laurenzi et al. 1987).

The presence of high concentrations of boron in community water supplies has been reported as a localized problem in certain areas of United States, USSR and Italy. In this paper, current information on sources, occurrence, pollution potential and toxicity of environmental boron is reviewed. In animals, chronic low-level boron exposure has been shown to cause reduced growth, cutaneous disorders and suppression of male reproductive system function. The mechanisms underlying these effects and available data on dose-response relationships are discussed in connection with human health hazards possibly associated with continuous low-level absorption of boron compounds.

Rats treated intravenously with 51Cr-labelled sodium chromate, 0.1 or 100 microgram Cr/rat, excreted more 51Cr into bile in a 2-hr period than did the animals given equal amounts of chromium in the trivalent state. Distinct patterns of hepatic intracellular distribution of the radiotracer were also observed. In the Cr-VI rats over 50% of the liver chromium was present in the supernatant fraction whereas in the Cr-III rats almost all the liver radioactivity was localized in the cell organelles. Fractionation of bile on Sephadex G-75 demonstrated binding of chromium to low-molecular weight substances. It is suggested that complexes of chromium with low-molecular weight components of liver cytosol are involved in the passage of this element from the liver to bile. A low cytosolic content of diffusable Cr-complexes associated with the incorporation of a large fraction of liver chromium in cell organelles may be a factor contributing to the low rates of 51Cr biliary excretion in the animals given Cr-III. 24 hr after the injection of 51Cr to bile duct-ligated rats appreciable levels of radiotracer were found in the gastrointestinal tract. The animals given Cr-VI exhibited significantly higher values of chromium content in the gut than those treated with Cr-III.

Hepatic microsomal aniline hydroxylase and aminopyrine N-demethylase in vitro activities and the biliary excretion of sulfobromophthalein (BSP) were significantly reduced in rats treated with triphenyl tin (TPT) in daily doses of 1 mg/kg i.p. for 3 days. Bile flow, liver weight, serum enzyme activities, and hepatic sulfhydryl groups and thiobarbituric reactant levels were unaffected in TPT-treated animals. Moreover, TPT failed to induce any appreciable change in the biliary excretion of both the organic base procainamide ethobromide and the organic acid amaranth which is excreted into the bile in the unmetabolized form. TPT has been shown to be an effective inhibitor of rat liver glutathione-S-transferase activity. Reduced conjugation with glutathione may play a role as a factor determining the low rate of biliary BSP excretion in the TPT-treated rats.

The gastrointestinal transport of 201Tl-labelled monovalent thallium has been studied in normal and rats with cannulated bile ducts using an in vivo ligated loop technique. A marked difference in the Tl absorptive capacity among the various sections of the gut was observed. 201Tl was taken up more quickly from the colon than from any other segment and the uptake from the ileum and jejunum was higher than from the stomach. In addition, considerable amounts of the intravenously administered thallium were excreted into the intestinal lumen. The biliary excretion was very low compared with the direct transfer of 201T1 across the gastrointestinal wall that occurred against a tissue-to-plasma concentration gradient. In the rat, the large intestine seems to be the major area for the enteral reabsorption and recycling of thallium (I) ions.

Hepatic microsomal aniline hydroxylase and aminopyrine N-demethylase in vitro activities and the biliary excretion of sulfobromophthalein (BSP) were significantly reduced in rats treated with triphenyl tin (TPT) in daily doses of 1 mg/kg i.p. for 3 days. Bile flow, liver weight, serum enzyme activities, and hepatic sulfhydryl groups and thiobarbituric reactant levels were unaffected in TPT-treated animals. Moreover, TPT failed to induce any appreciable change in the biliary excretion of both the organic base procainamide ethobromide and the organic acid amaranth which is excreted into the bile in the unmetabolized form. TPT has been shown to be an effective inhibitor of rat liver glutathione-S-transferase activity. Reduced conjugation with glutathione may play a role as a factor determining the low rate of biliary BSP excretion in the TPT-treated rats.

The biliary excretion of vanadium was studied in bile duct cannulated rats at various times after the iv administration of a single dose of 48V-labelled pentavalent vanadium. The tissue disposition, hepatic intracellular distribution and binding of 48V to plasma, bile and liver components were also investigated. During the first 6 hours after the injection of V, 0.9 to 30 microgram/kg, less than 2 per cent of the dose was excreted into the bile and up to 20 per cent of vanadium was eliminated in urine. The bile flow was markedly decreased in rats cannulated 24 hours after the injection of V, 30 microgram/kg, while higher doses produced signs of severe toxicity immediately after the administration. Evidence was also obtained that a concentration gradient triggers the passage of vanadium from plasma to the liver, where only a fractional amount becomes available from canalicular excretion, due to the extensive binding of the metal to organelles and other tissue ligands.

The placental transfer of thallium was studied in rats treated with a toxic dose of thallium sulphate (10 mg Ti/kg b.wt. p.o.), as well as in animals injected intraperitoneally with 201T1-labelled thallium in amounts as low as 2 μg Tl/rat. Rapid uptake and retention of thallium in both maternal and fetal organs were observed. The administration of potassium ferrihexacyanoferrate II (100 mg/kg b.wt. twice daily by gavage) to rats acutely intoxicated with thallium on day 17 of pregnancy resulted in significant decrease of thallium concentrations in various maternal tissues including brain, in the placenta as well as in the fetal liver and brain. Potassium ferrihexacyanoferrate II also reduced the mortality of pregnant animals in the 72-h interval after the intoxication.

Different aspects of the biochemistry of chromium in laboratory animals have been investigated using 51 Cr radiotracer methods. 51 Cr-labelled chromium compounds such as cationic trivalent 51 Cr 3+ and anionic hexavalent 51 Cr 6− were prepared and administered I.V. to rats in doses ranging from 0.1 to 100 μg/rat. The results show remarkably different metabolic patterns in the two chemical species. They refer (1) to the distribution in the blood. More than 95% of the 51 Cr in the blood of rats administered with the trivalent form was present in the plasma while the corresponding value in the case of the hexavalent species was of about 25%. Gel permeation chromatography on sephadex G-150 and ion exchange chromatography in DEAE show that the 51 Cr plasma of rats treated with 51 Cr 3+ is associated with β-globulin transferrin. Dialysis experiments indicate the strong nature of the binding of chromium to transferrin. They also refer (2) to the biliary excretion patterns. The biliary excretion of 51 Cr has been studied in the bile duct-cannulated rats 120 min after the intravenous administration of 0.1 μg Cr/rat to 100 μg Cr/rat as trivalent or hexavalent chromium. The biliary levels of 51 Cr-derived radioactivity reached their peak 30 min after injection of both Cr III and Cr VI and decreased slowly thereafter. The 2 hour biliary concentrations of Cr in the animals treated with Cr VI were up to 60 times higher than those found in the rats given the same amount of the trivalent Cr form 2.6 per cent of the dose was recovered in the bile of rats injected with Cr VI within 2 hours while the 2 hours cumulative excretion of 51 Cr in the bile of Cr III treated animals was approximately 50 times lower. In the first 120 min period after treatment of the bile-fistula rats the urinary excretion of 51 Cr ranged from 7 to 15% of the administered dose without any obvious relation to the chemical form and the dosage level. Chromium had no effect on the rate of biliary flow. The plasma levels of 51 Cr-radioactivity of the animals treated with Cr VI were significantly lower than those detected after injection of the same doses of Cr in the trivalent form. No valency-related differences were found with respect to the liver concentrations of 51 Cr labelled chromium. These findings indicate that the distinctive pattern of Cr biliary excretion observed in the rat after treatment with Cr III and Cr VI are independent of the plasma-to-bile and liver-to-bile concentration gradients of this chemical species. In this study, evidence has also been obtained for a direct excretion of Cr across the intestinal wall as indicated by the presence of appreciable levels of 51 Cr activity in feces in the gastrointestinal segments of rats with ligated bile duct after intravenous injection of 100 μg of 51 Cr-labelled chromium. Average values of 4% and 1.5% of the injected Cr dose were measured in the gut(stomach and intestine plus contents) 24 hrs after the injection of Cr VI and Cr III , respectively. This findings provided further support for the concept that the trivalent and hexavalent forms of Cr exhibit different behaviour in their elimination patterns by the digestive tract.