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At least 19 recordsLinked to original sources
PubMed1991

[Significance of urinary cadmium concentration as an indicator of cadmium exposure in a population exposed to cadmium in a general environment].

Study was made on the significance of urinary cadmium concentration as an indicator of internal dose in a general environment polluted by cadmium. As an index of external dose, the mean rice cadmium concentration in each of 23 villages was employed. Morning urine samples were collected from 3,178 inhabitants of 23 cadmium-polluted villages of Kakehashi River basin in Ishikawa Prefecture and 294 inhabitants of two nonpolluted villages. Cadmium concentration in urine was determined. In addition, their residential history and intake of cadmium-polluted rice were obtained. All the subjects were 50 years of age or over. Participation rates were 91% for the polluted area and 94% for the nonpolluted area. Urinary cadmium concentrations were higher in the inhabitants of the cadmium-polluted area than in those of the nonpolluted area. Among the inhabitants in the cadmium-polluted area, urinary cadmium concentrations were higher in the subjects who had consumed cadmium polluted rice than in those who had not. The mean urinary cadmium concentrations in each village increased proportionally to increase in mean village rice cadmium concentration (intensity of exposure) when the inhabitants were classified according to period of residence at their present address. The mean urinary cadmium concentrations in each village were also significantly correlated with period of residence at the present address (duration of exposure) when the inhabitants were classified according to mean rice cadmium concentration of their village. It is concluded that urinary cadmium concentration mainly reflects the body burden of cadmium in a general environment polluted by cadmium.

Adult↗
PubMed1990

Retention of cadmium in cadmium-naive normal and iron-deficient rats as well as in cadmium-induced iron-deficient animals.

The retention of cadmium was investigated in cadmium-naive normal and iron-deficient rats in comparison to rats with cadmium-induced iron deficiency. Rats subchronically (4 weeks) exposed to dietary cadmium (28, 56, 112 ppm Cd and 28 ppm Fe) received a radioactively labeled dose of 2 mumol Cd/kg body wt; acutely (no cadmium exposure with diet) treated rats received doses between 1 and 8 mumol Cd/kg body wt. Two animals of each group received iron (1 mumol/kg as 59FeSO4 in order to monitor iron absorption in parallel. After a period of 4 weeks of feeding a cadmium-fortified diet, the test dose was administered and after a 2-weeks period 109Cd and of 59Fe retention was determined. The results showed in part an unexpected pattern of cadmium retention: subchronic feeding of cadmium induced iron deficiency. This implies an immediate interaction between the two metals with regard to intestinal transfer of iron. The retention of iron was increased in the Cd-induced anemia to the same extent as that in iron deficiency induced by iron restriction. Cadmium retention in iron deficiency induced by iron withdrawal also showed a marked increase, which implies that iron deficiency stimulates the intestinal transfer system for both metals in a similar way. Contrary to this effect, the cadmium retention in cadmium-induced iron deficiency was reduced to about 30% of control values. A self-induced aggravation of the body cadmium burden, as a consequence of the iron deficiency which is known to result from subchronic exposure to feeding of dietary cadmium, was thus excluded.

Anemia, Hypochromic↗
PubMed1977

Cadmium-induced enteropathy: comparative toxicity of cadmium chloride and cadmium-thionein.

In protecting the body against the noxious effects of dietary cadmium ions, cadmium is bound to metallothionein in the proximal intestine, and subsequently excreted into the lumen with desquamation of the epithelium. The purpose of this study was to determine the extent to which cadmium in the form of intestinal cadmium-thionein is absorbed from the intestinal lumen and to appraise the toxicity of cadmium-thionein on the intestinal mucosa. With open-ended duodenal perfusion, equivalent amounts of cadmium administered as CdCl2 or cadmium-thionein entered the mucosa, but significantly less cadmium from the perfusate of cadmium-thionein passed into the body. Exposure of the mucosa to CdCl2 for 1 hr led to minor abnormalities in the form of broadening of villi with pseudostratification of epithelium, and swelling of mitochondria, whereas cadmium-thionein produced extensive necrosis of absorptive cells. The results suggest that cadmium-thionein may play a paradoxical role, providing protection against the cadmium ion in the intracellular milieu, but promoting cadmium toxicity when it is present in sufficient amounts in the lumen of the intestine.

Animals↗
PubMed1975

Accumulation of cadmium in rat liver cadmium binding protein following single and repeated cadmium administration.

The accumulation of cadmium in rat liver cadmium binding protein induced by single and repeated intraperitoneal injections of CdCl2 and the de novo biosynthesis of CdBP were studied by using 109Cd to measure cadmium binding in the CdBP and 35S incorporation as indicator of protein synthesis. The biosynthesis of CdBP is controlled by the cadmium concentrations. For single doses up to 1 mg Cd2+/Kg b.w. about 50% of the cadmium is present in the soluble fraction of liver bound to CdBP and the incorporation of 35S-cysteine is linear with the cadmium concentration. When single doses ranging from 1 to 3 mg Cd2+/Kg b.w. are administered the fractions of both 35S-cysteine and cadmium incorporated into de novo synthesized CdBP gradually decrease. For single doses higher than 3 mg Cd2+/Kg b.w. the biosynthesis capability is maximum and 20 mug Cd/g liver can be incorporated into the de novo biosynthesized CdBP. When rats are treated every day with amounts of cadmium of about 0.8 mg Cd2+/Kg b.w. for up to 8 days a dose-proportional increase in both Cd incorporation and CdBP biosynthesis are observed. This shows a cumulative incorporation of cadmium in the de novo biosynthesized CdBP. Experiments carried out by injecting 65ZnCl2 and 203HgCl2 every day showed that they are not accumulated like cadmium and do not induce the biosynthesis of rat liver CdBP after repeated administration over 7 days.

Animals↗
PubMed1992

Effect of ethanol on the distribution of cadmium between the cadmium metallothionein- and non-metallothionein-bound cadmium pools in cadmium-exposed rats.

In an attempt to assess the effect of ethanol on cadmium accumulation, metallothionein (MT) synthesis, Cd-binding capacity and lipid peroxidation, rats were administered either Cd, ethanol or their combination for a period of 4 weeks. A significant increase in Cd accumulation was observed in all the organs of rats under study co-exposed to Cd and ethanol as compared to only Cd-treated rats. Increased MT levels in response to Cd were associated with a marked alteration in the distribution of Cd amongst the two pools of intracellular Cd i.e. Cd bound to MT (Cd-MT) and Cd not bound to MT (non-MT-Cd). Higher levels of non-MT-Cd were observed in liver, kidney and heart of Cd+ethanol-exposed rats as compared to only Cd-exposed rats. Lesser binding of 109Cd to the protein peak was observed in Cd+ethanol-exposed rats than the Cd-treated rats when hepatic supernatants from all the groups were chromatographed on Sephadex G-75 columns, suggesting that ethanol has a redistributing effect on Cd amongst the two pools. A marked increase in lipid peroxidation was observed which was linear to the increase in non-MT-Cd levels. A positive correlation between non-MT-Cd levels and lipid peroxidation was observed in liver, kidney and heart suggesting that non-MT-Cd levels are more crucial and toxicologically more important than total Cd levels.

Animals↗
PubMed1979

[Accumulation of cadmium in organs of mice by a long-term injection of cadmium and interactions of cadmium with copper, manganese and zinc already present in the animals (author's transl)].

It is well known that the greater part of the administered cadmium is accumulated in liver and kidneys. But, in considering the toxicity of cadmium, it is important to make clear the time pattern of cadmium accumulation not only in liver and kidneys but in the other organs. Male mice were injected subcutaneously 1 mg/kg of cadmium daily for 25 weeks except one day in every week. Five mice at a time were killed in the suitable time during this experiment, and Cd, Cu, Mn, and Zn concentrations in several organs were determined by atomic absorption spectrophotometry. Cadmium content in liver and kidneys increased remarkably during the first 30 days, and it is scarcely increased after that period. Cadmium content in other organs, that is, heart, lungs, spleen, testes and femurs, increased slowly during the first 20 days, and this content increased hardly after that. The results show further that: Cd administered at the early stage accumulated mainly in liver an in kidneys. As Cd concentration in liver and kidneys arrives at saturation, Cd content in other orbans increased remarkably. And, after 30th day, Cd content in all the organs increased little in spite of the continuous injection of Cd. Concentrations of Cu, Mn, and Zn in the organs of mice injected with Cd were as follows: Cu concentration increased significantly in heart, liver, and kidneys, Zn concentration increased in heart, lungs, liver, and kidneys, whereas Mn concentration decreased remarkably in kidneys. Cadmium content in the organs of mice injected with Zn (0.5 mg/kg) or Mn (0.5 mg/kg) together with Cd (1 mg/kg) showed a tendency to increase remarkably compared with single injection of Cd.

Animals↗
PubMed1991

Cadmium accumulation and metallothionein concentrations after 4-week dietary exposure to cadmium chloride or cadmium-metallothionein in rats.

The distribution of cadmium was examined in rats fed diets containing either cadmium-metallothionein (CdMt) or cadmium chloride (CdCl2) for 4 weeks. The test diets contained 3, 10, or 30 mg Cd/kg diet (3, 10, or 30 ppm) as CdMt or 30 mg Cd/kg diet (30 ppm) as CdCl2. A second study was performed to establish the Cd content in liver and kidneys after exposure to low doses of both CdMt and CdCl2 (1.5 and 8 ppm Cd). The feeding of CdMt resulted in a dose- and time-dependent increase of the Cd concentration in liver, kidneys, and intestinal mucosa. Rats fed 30 ppm CdMt consistently showed less Cd accumulation in liver and intestinal mucosa than did rats fed 30 ppm CdCl2. However, renal accumulation in rats fed 30 ppm was similar until Day 28 regardless of Cd form. At lower dietary Cd levels (1.5 and 8 ppm), relatively more Cd is deposited in the kidneys, although even at these doses the kidney/liver ratio of Cd is still higher with CdMt than with CdCl2. Tissue metallothionein (Mt) levels in the intestinal mucosa were relatively constant but always higher after CdCl2 exposure than after CdMt exposure. Mt levels in both liver and kidney increased after CdCl2 or CdMt exposure during the course of study. Although Mt levels in liver were higher after CdCl2 intake (30 ppm) than after CdMt intake (30 ppm), renal Mt concentrations were the same for both groups. In fact on Day 7, CdMt administration resulted in slightly higher Mt levels than CdCl2 administration, suggesting a direct accumulation of exogenous CdMt in the kidneys. In conclusion, after oral exposure to CdMt in the diet there is a relatively higher Cd accumulation in the kidneys. However, the indirect renal accumulation via redistribution of Cd from the liver might be lower than after CdCl2 exposure. Which of these two phenomena is decisive in the eventual level of renal toxicity of Cd after long-term oral intake could determine the toxicological risk of the chronic intake of biologically incorporated Cd.

Animals↗
PubMed1979

Cadmium effects in rats on tissue iron, selenium, and blood pressure; blood and hair cadmium in some oregon residents.

Exposure of rats to cadmium causes a marked depletion of iron in liver and kidney. Selenium neither counteracts or intensifies the influence of cadmium on tissue iron levels. Selenium injections protect against cadmium-induced testicular damage but cause this element to accumulate in the testes at higher concentration than in animals exposed to cadmium without selenium. Selenium injection diverts the binding of cadmium from low molecular weight proteins to high molecular weight ones. Dosing rats with selenium and cadmium or inclusion of Se or Cd in the diet did not result in altered cadmium binding in tissues, raising some questions concerning the environmental significance of these injection experiments. Addition of selenium to a diet containing cadmium decreased the accumulation of cadmium in liver and kidney, but increased its deposition in testes. The metabolism of cadmium bound to metallothionein was markedly different as compared to the inorganic salt of this element. Dietary ascorbate, but not citrate or cysteine, decreased the deposition of cadmium in rat tissues. In some low-level exposure experiments with cadmium (1 to 1000 ppb), no differences were found in the percentage of dose absorbed or rate of cadmium accumulation when provided in food versus water. Female rats tended to absorb more cadmium than males. The binding of cadmium to cytosolic proteins was found to be different between rats fed low levels of cadmium (up to 1 ppm) as compared to those fed high levels of this element (100 ppm). Cadmium was not found to contribute to hypertension in rats, and a summary of results by various investigators is presented. Blood and hair cadmium levels in Oregon residents were found to be highest in employees of a mine, and hair cadmium was found to be respectively higher in smokers than nonsmokers and in metal workers than office workers. No relationships were observed in humans between blood or hair cadmium levels and blood pressure.

Animals↗
PubMed1991

Absorption of cadmium after a long-term oral administration of cadmium to dogs.

A long-term experiment using beagle dogs to investigate the absorption of cadmium was conducted. The dogs in the experimental groups were given a commercial diet and pelleted food containing 1, 3, 10, 50, and 100 mg of cadmium per day. The cadmium concentration in the blood increased continuously, gradually reaching a steady state following the administration of cadmium. The cadmium excreted daily in urine increased continuously. The cumulative excreted amount of cadmium in urine was calculated by using the trapezoidal rule based on the data of excretion of cadmium in urine. Then the absorbed fraction of administered cadmium was estimated on the basis of the relationship between the cumulative excreted amount of cadmium in urine and the cumulative administered dose of cadmium after the cadmium concentration in blood reached a steady state. The absorbed fraction of cadmium decreased with an increase in the administered dose of cadmium. A dose-dependent increase between the absorbed amount and the administered dose was observed.

Administration, Oral↗
PubMed1991

Biological half-time and body burden of cadmium in dogs after a long-term oral administration of cadmium.

To investigate the kinetic behavior of cadmium, we conducted a long-term oral administration experiment, using beagle dogs. The experimental animals were given a commercial diet and pelleted food containing 1, 3, 10, 50, and 100 mg of cadmium per day in the form of cadmium chloride for 8 yr. A single injection of cadmium (as CdCl2) into dogs was also performed in order to obtain fundamental kinetic information for a dog. The kinetic behavior of cadmium in chronic experiment is described theoretically, using a two-compartment model. The model was selected based on the elimination pattern of cadmium from the blood in the single injection experiment. The parameters of the model were estimated from the acute and chronic experimental data. The theoretical value of the cumulative amount of cadmium excreted in urine agreed with the experimental one. This result suggests that the two-compartment model used in this study is useful to elucidate the kinetic behavior of cadmium after a long-term exposure to cadmium. The terminal biological half-time in the two-compartment model was estimated at about 1 to 2 yr for both male and female dogs given 1, 3, 10, and 50 mg of cadmium, and for the male dog given 100 mg of cadmium, but only 0.3 to 0.5 yr for the female dog given 100 mg of cadmium. The amount of cadmium in the central compartment and tissue compartment increased continuously and then gradually reached a steady state. The amount of tissue compartment was much higher than that of the central compartment for each beagle dog.

Administration, Oral↗
PubMed1977

Biliary excretion of cadmium in rat. II. The role of metallothionein in the hepatobiliary transport of cadmium.

Intravenous injection of 109Cd-labeled CdCl2 (1 mg/kg) to control rats and rats that had been injected with CdCl2 (0.25 mg/kg) 24 hr earlier showed that there was a decrease in the biliary excretion of 109Cd in the latter group. The 24 hr pretreatment with CdCl2 resulted in induced synthesis of metallothionein in rat liver and kidney. The binding of cadmium to liver tissue was increased and the renal accumulation of cadmium was unaltered on cadmium pretreatment. Rat liver metallothionein was isolated from rats injected repeatedly with CdCl2. Intravenous injection of cadmium-bound metallothionein gave a different distribution of cadmium in the tissues and biological fluids as compared to injection of CdCl2. A major percentage of cadmium was deposited in the kidney with urinary excretion after injection of rat cadmium-metallothionein to control rats. The biliary excretion of cadmium after cadmium-metallothionein injection was minimal. About 90% of cadmium in the kidney cortex and urine could be recovered as cadmium-thionein in sephadex gel filtration, 3 hr after cadmium-thionein injection.

Animals↗
PubMed1977

Biliary excretion of cadmium in rat. I. Dose-dependent biliary excretion and the form of cadmium in the bile.

Biliary excretion of cadmium was studied in rats after intravenous injection of different doses of cadmium chloride (0.1-2 mg Cd/kg). The rate of bile flow was not affected by cadmium injection and cadmium was excreted into bile during the first 2 hr after injection. The biliary excretion of cadmium increased with increasing dose of CdCl2. Cumulative biliary excretion of cadmium for 5 hr was 0.065% of the administered dose for groups injected with 0.1 mg Cd/kg as compared to 16.9% of the administered dose for 2 mg Cd/kg. During the 5 hr experimental period, most of the cadmium in liver cytosol was bound to high-molecular-weight proteins and less than 10% was bound to the metallothionein fraction. The biliary cadmium was recovered as a low-molecular-weight compound (less than 4,000) in experiments with various doses of cadmium and no cadmium was attached to high-molecular-weight proteins or metallothionein in the bile. The low-molecular-weight cadmium complex in bile was partially characterized as Cd-glutathione by thin-layer chromatography and amino acid analysis.

Animals↗
PubMed1991

The origin of high cadmium loads in some bivalve molluscs from Shark Bay, Western Australia: a new mechanism for cadmium uptake by filter feeding organisms.

Although Shark Bay is remote from all known industrial and geological sources of heavy metals, the cadmium content of several species of Shark Bay molluscs may exceed 10 mg/kg. The cadmium load in these molluscs varies geographically within the bay, but possible explanations for cadmium distribution involving variation in salinity, saline groundwater influx, the dissolved cadmium concentration, the cadmium concentration in substrate sediments, species, or an anthropogenic source are not supported by analytical data. The cadmium concentration is normal in Shark Bay seawater (0.04 microgram/L to about 0.35 microgram/L), rarely exceeds 0.25 microgram/L in ground waters, bore waters, and salt lake brines, and very seldom exceeds 1 mg/kg in sediments. No direct link between the cadmium loads in molluscs and its concentration in the water or substrate sediment is evident, but the cadmium load in molluscs is usually highest where turbulence is high and the substrate sediment contains fine hematite. Over about 2,000 km2, the water depth in Shark Bay is less than 1 m and fine sediment is readily suspended by strong winds. The iron-oxides (superfine hematite) are eroded from the Peron Sandstone exposed in some coastal cliffs and constitute up to 2% of substrate sediments near these cliffs. This study reveals that cadmium in the water adsorbs extremely efficiently onto the surface of the hematite, which is negatively charged at the prevailing seawater pH of 8.15, and that suspended hematite particles are ingested by the molluscs. Inside the molluscs, lower pH conditions cause reversal of the hematite charge and the cadmium is released and accumulated by the organism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Cadmium levels in hair and other tissues during continuous cadmium intake.

Rats that received cadmium 300 ppm in drinking water (average daily cadmium intake = 4.5 mg/rat) for 12 wk attained peak cadmium levels of 112, 34, and 19 mug/g in hair, liver, and kidney, respectively, at week 4. Rats that ingested cadmium 200 ppm (average daily cadmium intake = 3.6 mg/rat) for 13 wk attained peak cadmium levels of 29 mug/g in kidney at week 7, and 94 and 27 mug/g in hair and liver, respectively, at week 9. Despite continuous exposure to the heavy metal, tissue cadmium concentrations declined to steady-state levels of 24-33 mug/g in hair and 10-17 mug/g in liver and kidney. Histopathologic effects were not observed in liver or kidney. In contrast to cadmium in hair, blood cadmium levels, which remained consistently low (less than 0.04 mug/ml) throughout the study, did not correlate with changes in cadmium levels in liver and kidney.

Animals↗