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PubMed1985

[Evaluation of occupational exposure to cadmium based on air analysis of the work area. I. Cadmium oxide level in the air of work areas in a cadmium and nickel cumulator factory].

Results of evaluation of occupational exposure carried on by individual dosimetry and stationary measurements were compared. The former method yielded higher values for airborne cadmium concentrations. The investigations exhibited high cadmium oxide dust concentrations at most workplaces within the alkaline accumulator plant. Time-weighted average (per 8 h) concentrations of this compound in the workers' breathing zone ranged between 0.040-1.5 mg/m3, 85% of the obtained results exceeding the TLV value (0.1 mg Cd/m3).

Air Pollutants, Occupational↗
PubMed1999

Tissue distribution of cadmium in rats given minimum amounts of cadmium-polluted rice or cadmium chloride for 8 months.

To investigate the relationship between cadmium (Cd) toxicity, intestinal absorption, and its distribution to various tissues in rats treated orally with minimum amounts of Cd, 14 female rats per dose group per time point were given diets consisting of 28% purified diet and 72% ordinary rice containing Cd-polluted rice (0. 02, 0.04, 0.12, or 1.01 ppm of Cd) or CdCl(2) (5.08, 19.8, or 40.0 ppm of Cd) for up to 8 months. At 1, 4, and 8 months after the commencement of Cd treatment, seven rats per group were euthanized for pathological examinations to determine the Cd concentrations in the liver and kidneys and metallothionein (MT) in the liver, kidneys, intestinal mucosa, serum, and urine. One week before each period of 1, 4, and 8 months, the remaining seven rats in each group were administered a single dosage of (109)Cd, a tracer, to match the amounts of the designated Cd doses (about 1.2 to 2400 microg/kg body wt). They were euthanized 5 days later to determine the distribution of Cd to various tissues. No Cd-related toxic changes were observed. The concentrations of Cd in the liver and kidneys at any time point and MT in the liver, kidney, serum, and urine at 4 and 8 months increased dose-dependently, whereas MT in the intestinal mucosa did not alter markedly at any time point. The distribution rates of Cd to the liver increased dose-dependently (40% at lower doses to 60% at higher doses), whereas those to the kidney decreased dose-dependently (20% at lower doses to 10% at higher doses). The Cd retention rates 5 days after (109)Cd administration (amounts of Cd in various tissues/amounts of Cd administered) ranged from 0.2 to 1. 0% at any time point. These results suggest that the distribution of Cd to the liver and kidneys after the oral administration vary depending on the dosage levels of Cd. The difference of the distribution pattern of Cd to the liver and kidney is probably due to the difference in the form of the absorbed Cd, i.e., free ion or Cd-MT complex, although not closely related to the MT in the intestinal mucosa.

Administration, Oral↗
PubMed1981

Distribution of cadmium in heavily cadmium-accumulated rat liver cytosols: metallothionein and related cadmium-binding proteins.

Distribution profiles of cadmium (Cd) in the cytosols of livers prepared from repeatedly Cd-injected rats (3.0 mg Cd/kg body weight, 4 times a week for 1, 2, 3, or 4 weeks) were characterized by high-performance liquid chromatography with a flame atomic absorption spectrophotometer (HPLC-AAS). The accumulation of Cd and decrease of relative zinc (Zn) to Cd ratio in metallothionein were accompanied by the change of distribution profile of Cd in the cytosol fraction. Cd distributed to the heat-unstable high molecular weight proteins was assumed to be non-selectively bound free Cd and a toxic chemical form. Two kinds of heat-stable Cd-binding proteins other than metallothionein increased with the accumulation of Cd; one was metallothionein dimers, and the other was thought to be Cd-binding proteins of shorter amino acid chain than metallothionein and related to metallothionein.

Animals↗
PubMed1983

Altered subcellular distribution of cadmium following cadmium pretreatment: possible mechanism of tolerance to cadmium-induced lethality.

Animals pretreated with cadmium (Cd) subsequently develop tolerance to an otherwise lethal dose of Cd. Possible mechanisms for this tolerance include reduced absorption, an altered tissue distribution, and an altered subcellular distribution of Cd. Male rats received a single Cd pretreatment (2.0 mg/kg, sc) 24 hr prior to administration of a typically lethal challenge dose of Cd (3.9 mg/kg, iv). Tolerance was evident because no mortality was observed in Cd-pretreated rats. Since Cd induces synthesis of hepatic metallothionein (MT), a higher percentage of the challenge dose might be sequestered in the liver of Cd-pretreated animals with less distributed to target organs of toxicity. At 2 and 24 hr following Cd challenge, no marked changes in organ distribution of the challenge dose of Cd were observed as a result of Cd pretreatment. However, isolation of hepatic subcellular fractions 2 hr following injection of the challenge dose revealed less Cd in nuclei, mitochondria, and endoplasmic reticulum, and more in cytosol as a result of Cd pretreatment. The increased cytosolic Cd was bound primarily to MT which had been induced markedly by Cd pretreatment. These data indicate that differences in absorption or tissue distribution of Cd are unlikely explanations for development of tolerance to Cd. Rather, tolerance appears to result from an MT-related change in the hepatic subcellular distribution of Cd, evidenced by lower concentrations of Cd in nuclei, mitochondria, endoplasmic reticulum, and cytosolic high-molecular-weight proteins and higher concentrations bound to MT in cytosol.

Animals↗
PubMed2004

Comprehensive study of the effects of age, iron deficiency, diabetes mellitus, and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.

The absorption rate of dietary cadmium (Cd) was investigated among 38 female farmers who had been exposed to Cd at levels close to the current provisional tolerable weekly intake (PTWI); these levels were much higher than those examined in previous studies. The study group composed of 7 diabetics and their 13 age-matched controls and 6 anemic subjects and their 12 controls. With their informed consent, the study participants were confined in an inn for 7 nights and 8 days to collect all feces and urine and duplicates of all food consumed. The dietary Cd absorption rate was calculated for each subject from her total Cd intake and fecal excretion. The means and 95% confidence intervals (CI) of the diabetic group and the anemic group did not differ significantly from those of their respective controls. By individual analysis using all 38 subjects, however, significant Pearson's correlation coefficients were observed between Cd absorption rate and age, serum ferritin, serum iron, and blood and urine Cd levels. Among these, multiple regression analysis revealed that only age was a significant factor contributing to Cd absorption rate. The actual Cd absorption rate in the youngest age group (20-39 years) was 44.0%, which was highly accelerated compared with the rate in the total subject group of 6.5%, while zero to negative balance was observed in the older subjects. These results demonstrate that age, rather than iron deficiency, diabetes mellitus (DM), or Cd burden, is the only independent factor affecting the Cd absorption rate, suggesting that young women are always at high risk.

Adult↗
PubMed2001

Relationship between toxicity and cadmium accumulation in rats given low amounts of cadmium chloride or cadmium-polluted rice for 22 months.

To clarify toxic effects of long-term oral administration of low dose cadmium (Cd) on the liver and kidney, six groups of female Sprague-Dawley rats were fed a diet containing Cd-polluted rice or CdCl2 at concentrations up to 40 ppm, and killed after 12, 18, and 22 months. With toxicological parameters, including histopathology, there was no evidence of Cd-related hepato-renal toxicity, despite a slight decrease of mean corpuscular volume and mean corpuscular hemoglobin of red blood cells with 40 ppm CdCl2. Dose-dependent accumulation of Cd was observed in the liver and kidneys with peak levels of 130 +/- 42 micrograms/g and 120 +/- 20 micrograms/g, respectively, at 18 months in animals treated with 40 ppm CdCl2. A dose-dependent increase in urinary Cd levels became evident with time. Induction of metallothionein (MT) was also observed in the liver and kidney with a high correlation to the corresponding Cd levels. In the proximal renal tubular epithelia of 40 ppm CdCl2-treated rats at 22 months, prominent accumulation of Cd was observed in secondary lysosomes associated with MT deposits in their exocytotic residual bodies. The results demonstrated that, in contrast to the case with high-dose Cd-administration, renal toxicity is not induced by long-term oral administration of low amounts of Cd, although tissue accumulation does occur. Possible protective mechanisms may be operating.

Animals↗
PubMed1995

Complex study of the physiological role of cadmium. II. Effect of cadmium load on the cadmium content of eggs.

The possibility of "cadmium (Cd) contamination" of eggs and the dynamics of Cd accumulation were studied. A total of 40 (4 x 10) Japanese quails weighing 155-200 g, being at the middle phase of egg production and kept on batteries in a climatized animal house were used. The birds were fed a standard quail layer diet and drank tap-water ad libitum. With the exception of the control group (Cd-0), the diet of the other three groups was supplemented with Cd sulphate homogeneously mixed in the diet so that it contained 75 mg (Cd-75), 150 mg (Cd-150) and 300 mg (Cd-300) per kg. During the 37-day feeding trial the quails' behaviour, health status and daily egg production were monitored and the birds were weighed weekly. The egg production of the experimental groups, particularly of those exposed to a high Cd load, rapidly decreased: at the highest Cd load (300 ppm) egg production completely ceased at days 10-11 of the trial. The total Cd content of the eggs rose already from the 3rd day of the feeding trial and by day 10 it reached a value of 0.777 mg/kg dry matter in the eggs of quails of group Cd-75. This was about five times the value measured in the control quails' eggs (0.165 mg/kg dry matter). The Cd content of the egg-white and egg-yolk (maximum values: 0.212 and 0.107 mg/kg dry matter) also increased to about 2 or 3 times that measured in the control eggs. The Cd content of eggs reached the peak in the 2nd week of the feeding trial, then started to decrease, and in the 3rd and 4th weeks not even the eggs laid by quails exposed to a high Cd load contained more Cd than about twice the concentration measured in the controls' eggs. The elucidation of this hitherto not studied process requires further investigations. The phenomenon may be due to a lack of the protein necessary for Cd transport and to the impairment of Cd absorption and of the excretory activity of the oviduct. The higher Cd concentrations measured in the egg were accompanied by markedly elevated Fe, K and S values. In the egg samples collected in the 4th week a substantial reduction in Ca and P concentration was observed. As regards the mineral elements measured in the egg-shell, a significant negative correlation was established between the concentration of Cd and those of Zn, Mg and Ca.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

Murine strain differences and the effects of zinc on cadmium concentrations in tissues after acute cadmium exposure.

The role of strain differences in cadmium tissue distribution was studied using sensitive (129/J) and resistant (A/J) mice. These murine strains have previously been shown to differ in their susceptibility to cadmium-induced testicular toxicity. Cadmium concentration was measured in testis, epididymis, seminal vesicle, liver, and kidney at 24 h after cadmium chloride exposure (4, 10, and 20 micromol/kg CdCl2). The 129/J mice exhibited a significant increase in cadmium concentration in testis, epididymis, and seminal vesicle at all cadmium doses used, compared to A/J mice. However, cadmium concentrations in liver and kidney were not different between the strains, at any dose, indicating that cadmium uptake is similar in these organs at 24 h. These murine strains demonstrate similar hepatic and renal cadmium uptake but significantly different cadmium accumulation in the reproductive organs at 24 h. The mechanism of the protective effect of zinc on cadmium toxicity was studied by assessing the impact of zinc acetate (ZnAc) treatment on cadmium concentrations in 129/J mice after 24 h. Zinc pretreatment (250 micromol/kg ZnAc), given 24 h prior to 20 micromol/kg CdCl2 administration, significantly decreased the amount of cadmium in the testis, epididymis, and seminal vesicle of 129/J mice, and significantly increased the cadmium content of the liver after 24 h. Cadmium levels in the kidney were unaffected at this time. Zinc pretreatment also prevented the cadmium-induced decrease in testicular sperm concentration and epididymal sperm motility seen in 129/J mice. These findings suggest that the differences in the two murine strains may be attributed partly to the differential accumulation of cadmium in murine gonads. This may be caused by strain differences in the specificity of cadmium transport mechanisms. The protective role of zinc in cadmium-induced testicular toxicity in the sensitive strain may be due to an interference in the cadmium uptake by susceptible reproductive organs.

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↗
PubMed1984

Cadmium - a complex environmental problem. Part II. Cadmium in sludges used as fertilizer.

In intensively populated countries efficient sewage treatment is essential to protect river quality. An inevitable by-product is sewage sludge which has to be disposed of safely and economically. Utilisation of sludge as a fertilizer of agricultural land is the most economic disposal route for inland sewage-treatment works and also benefits farmers by providing a cheap manure. Much of the cadmium in wastewater is concentrated into sludge which consequently contains higher concentrations of cadmium than soil does. It is impracticable to reduce cadmium concentrations in sludge below certain levels. When sludge is used on farmland rates of application must be controlled so that cadmium concentrations in soil never reach levels that could significantly contaminate food crops. Cadmium is a principal factor limiting the use of sludge on land. Nevertheless, it is a local problem since agricultural land in general receives more cadmium from aerial deposition and phosphatic fertilizers. The significance of accumulations of cadmium in soil depends mainly on its availability for crop uptake. Investigations are described which have attempted to identify and to determine the availability of forms of cadmium in soil. There is considerable research interest in cadmium in soil solution which is likely to be directly available for crop uptake. Another area of interest is the apparent disappearance of cadmium from sludge-treated soil. Soil analysis often cannot fully account for the cadmium added in sludge. Apart from the effect of soil conditions, especially pH value, crop uptake varies according to the particular crop examined. Highest concentrations of cadmium occur in tobacco, lettuce, spinach and other leafy vegetables. Using crop uptake data from field trials it is possible to relate potential human dietary intake of cadmium, on which hazard depends, to soil concentrations of cadmium, which can be controlled by regulating applications of sludge. This provides an objective basis for limits for cadmium concentrations in soils receiving sludge. Transfer of cadmium via farm animals to meat and dairy products for human consumption is thought to be minimal, even allowing for some direct ingestion of sludge-treated soil by the animals. Evidence from these and other investigations suggests that a loading rate limit of 5 kg Cd/ha (equivalent to a soil concentration of about 3.5 mg Cd/kg) affords adequate protection to the foodchain where sludge is used on agricultural land. More research work is needed to provide a basis for predicting the long-term availability of cadmium introduced to the soil in sludge.

Animal Feed↗
PubMed2001

Cyproterone acetate induces a cellular tolerance to cadmium in rat liver epithelial cells involving reduced cadmium accumulation.

Several reports indicate that some steroids, in particular sex steroid hormones, can modify cadmium toxicity. We recently reported that cyproterone acetate (CA), a synthetic steroidal antiandrogen that is closely related in structure to progesterone, affects cadmium toxicity in mice. In the present study, we investigated the effect of CA on cadmium toxicity in a rat liver epithelial cell line (TRL 1215) in vitro. Cells were exposed to various concentrations of CA (0,1,10, or 50 microM) for 24 h and subsequently exposed to cadmium (0,50, or 100 microM; as CdCl2) for an additional 24 h. CA pretreatment resulted in a clear decrease in the sensitivity to cadmium. Additional time course study showed CA pretreatment provided protection against cadmium toxicity but only when given for 6 or more hours prior to cadmium exposure. Cellular cadmium accumulation was markedly reduced (60% decrease) in cells pretreated for 6 or more hours with CA. In the presence of protein synthesis inhibitors the protective effect of CA toward cadmium toxicity was abolished. However, in the presence of the GSH synthesis inhibitor, L-buthionine (S,R)-sulfoximide (BSO), the protective effect of CA toward cadmium toxicity remained. CA alone increased metallothionein (MT) levels 2.4-fold, while cadmium (50 microM) alone resulted in a 8.9-fold increase over control. However, cadmium-induced MT synthesis was markedly decreased by CA pretreatment probably because of reduced cadmium accumulation. Analysis of various metal transporters by bDNA signal amplification assay revealed that the ZnT-1 transporter gene, which encodes for a membrane protein associated with zinc efflux, was expressed three-fold more in CA treated cells than control. These data show that CA pretreatment provides protection against cadmium toxicity in vitro and indicate that this protection is due to a decreased accumulation of cadmium rather than through activation of MT synthesis. This decrease of cellular cadmium accumulation appears to be related to events that require protein synthesis and may be due to activation of the genes associated with zinc efflux.

Androgen Antagonists↗
PubMed2001

Urinary cadmium elimination as a biomarker of exposure for evaluating a cadmium dietary exposure--biokinetics model.

The Cadmium Dietary Exposure Model (CDEM) utilizes national survey data on food cadmium concentrations and food consumption patterns to estimate dietary intakes in the U.S. population. The CDEM has been linked to a modification of the cadmium biokinetic model of Kjellström and Nordlberg (KNM) to derive predictions of kidney and urinary cadmium that reflect U.S. dietary cadmium intake and related variability. Variability in dietary cadmium intake was propagated through the KNM using a Monte Carlo approach. The model predicts a mean peak kidney cadmium burden of approximately 3.5 mg and a 5th-95th percentile range of 2.2-5.1 mg in males. The corresponding peak renal cortex cadmium concentration in males is 15 microg/g wet cortex (10-22, 5th-95th percentile). Predicted kidney cadmium levels in females were higher than males: 5.1 (3.3-7.6) mg total kidney, 29 (19-43) microg/g wet cortex. Predicted urinary cadmium in males and females agreed with empirical estimates based on the NHANES III, with females predicted and observed to excrete approximately twice the amount of cadmium in urine than males. An explanation for the higher urinary cadmium excretion in females is proposed that is consistent with the NHANES III data as well as experimental studies in humans and animals. Females may absorb a larger fraction of ingested dietary cadmium than males, and this difference may be the result of lower iron body stores in females compared to males. This would suggest that females may be at greater risk of developing cadmium toxicity than males. The predicted 5th-95th percentile values for peak kidney cadmium burden are approximately 60% of the peak kidney burden (8-11 mg) predicted for a chronic intake at the U.S. Environmental Protection Agency (EPA) chronic reference dose of 1 microg/kg-d.

Adolescent↗
PubMed1997

Cadmium burden of men and women who report regular consumption of confectionery sunflower kernels containing a natural abundance of cadmium.

Because of inherent genetic and physiological characteristics, the natural concentration of cadmium in the kernels of sunflowers grown in uncontaminated soils of the northern Great Plains region of the United States is higher than in most other grains. We tested the hypothesis that a habitual consumption of sunflower kernels will increase the body burden and health effects of cadmium in humans. Sixty-six men and women who reported consuming various amounts of sunflower kernels were recruited and divided by sex and kernel consumption: those who consumed less than or equal to 1 ounce(oz)/week and those who consumed more than 1 oz/week. Cadmium intake was assessed by calculation from 7-day food diaries, cadmium burden by whole blood cadmium, red blood cell (RBC) cadmium and urine cadmium concentrations, and health effects by urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) activity and beta2-microglobulin (beta2MG). The results showed that high intakes of sunflower kernels (>1 oz/day) significantly increased the intake of cadmium (p<0.004). However, the amount of cadmium in whole blood or RBCs was not affected by cadmium intake. Urinary excretion of cadmium also was not affected by cadmium intake. Urine NAG activity and the amount of urinary beta2MG were significantly elevated in the urine of high sunflower kernel consumers when the values were expressed on a urine volume basis (p<0.03), but not when expressed on a creatinine basis (p>0.05). Because normal ranges for the excretion of these protein markers have not been established, it was not possible to determine if these elevated values were meaningful. However, given the knowledge that habitual consumption of sunflower kernels with natural cadmium concentrations higher than most other food products will increase the average intake of dietary cadmium, the potential exists for an increased body burden of cadmium. Controlled feeding studies in humans should be pursued in order to determine if the body burden does indeed increase and, if so, is it a cause for concern.

Adult↗
PubMed1984

Reduced cadmium body burden in cadmium-exposed calves fed supplemental zinc.

The objectives of this study were to evaluate the use of practical supplemental dietary zinc to modify the cadmium content in edible bovine tissues and to identify copper interactions with cadmium and zinc. The effect of supplemental zinc (200 or 600 micrograms/g) on the concentrations of cadmium, zinc, and copper in liver, kidney cortex, muscle, and blood of calves fed 50 micrograms/g cadmium for 60 days was evaluated. Blood samples were collected before and eight times after starting to feed cadmium or cadmium plus zinc. Liver, kidney, and muscle samples were collected when calves were slaughtered (baseline, at beginning of experimental feeding; cadmium-fed, at end of 60 days feeding). The cadmium concentrations of all sample types collected were markedly increased by the feeding of cadmium. Feeding 600 micrograms/g supplemental zinc significantly increased the zinc concentrations of liver, kidney cortex, and blood and decreased the cadmium accumulation in these organs as well as muscle. The copper concentrations of muscle or blood were not altered by feeding cadmium with or without zinc but those of liver and kidney cortex were significantly increased by higher dietary levels of zinc and cadmium. The potential use of dietary zinc salts in reducing cadmium body burden in food animals suspected or known to have high cadmium intakes is suggested.

Animals↗
PubMed2000

Activation of androgen response element by cadmium: a potential mechanism for a carcinogenic effect of cadmium in the prostate.

Cadmium is a transition metal that has been widely used in industry. Epidemiological and animal studies have demonstrated a carcinogenic effect of cadmium on the prostate. Although it has been established that androgen is required for this cancer-inducing process, it is not clear how cadmium interacts with androgen. In this study, the carcinogenic mechanism of cadmium was explored with a focus on interaction of androgen and cadmium at the gene transcription level. An androgen response luciferase reporter was used for analysis of the cadmium activity in the transient transfection assay. Human prostate epithelial cells (LNCap) and liver cells (HepG2) were transfected by the reporter. The result showed that cadmium was able to activate the reporter in the absence of androgen, and that this activation was dependent on the presence of androgen receptor. Cadmium could enhance the androgen response when both androgen and cadmium were applied together to the reporter-transfected cells. Activation of the reporter by cadmium was not associated with cell proliferation or interleukin 6 (IL-6) production, which was proposed to be involved in cadmium-induced carcinogenesis in other experimental systems. Cadmium exhibited a weak ability to induce AP-1. The results demonstrate that cadmium has an androgen-like activity in prostate epithelial cells, and this activity implies a new mechanism for the carcinogenic effect of cadmium in the prostate.

Androgens↗
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↗