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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↗
PubMed1983

Effects of cadmium on glutathione metabolism in cadmium sensitive and cadmium resistant Chinese hamster cell lines.

Three cadmium resistant sublines, Cdr20F4, Cdr30F9, and Cdr200T1, resistant to 26, 40, and 145 micron CdCl2, respectively, have been derived from the cadmium sensitive Chinese hamster cell line CHO (resistant to 0.2 microM CdCl2). The resistance appears to be largely a function of the increased ability of the variant cells to induce the synthesis of metallothioneins (MTs) in response to cadmium, as the incorporation of [35S]cysteine into MTs ranges from an undetectable level to nearly 60% of the total cysteine incorporation into proteins in the CHO and Cdr200T1 cell lines, respectively. Treatment of the cadmium resistant sublines and the parent line with maximal subtoxic levels of Cdcl2 produced increases in the concentration of glutathione and glutathione S-transferase activity. In the parent, cadmium-sensitive CHO cell, the glutathione concentration began to increase after 9 h of exposure to 0.22 microM CdCl2 to over 250% of control level by 12 h. In 1 cadmium resistant line (Cdr20F4) the increase, again at 9 h, was preceded by a decrease, possibly due to depletion of the cysteine pools by the cadmium-induced MT synthesis. The second cadmium-resistant cell line (Cdr30F9) displayed no decrease, and the most cadmium-resistant line (Cdr200T1) showed the decrease and a recovery, but no significant increase by 12 h. In all cell lines there was a small but significant increase in glutathione S-transferase activity by 9 or 12 h. These responses may be specific for the thiol-reactive metal, cadmium, or may represent more general responses to cellular toxicity.

Animals↗
PubMed1981

Differential induction by cadmium of a low-complexity ribonucleic acid class in cadmium-resistant and cadmium-sensitive mammalian cells.

The Chinese hamster ovary (CHO) cell line and the subline Cdr20F4 have been used to compare cadmium-induced ribonucleic acid (RNA) synthesis in cadmium-sensitive and cadmium-resistant cells, respectively. Gel electrophoresis of the cell-free translation products directed by polyadenylated [poly(A+)] messenger RNA (mRNA) from cadmium-induced Cdr20F4 cells revealed four low molecular weight species (Mr 7000-21 000), including metallothionein, whose synthesis was not detected after translation of either cadmium-induced or uninduced CHO cell poly(A+) mRNA. At least two of these species were also detected after translation of an abundant 400-nucleotide (NT) RNA class purified from the cadmium-induced Cdr20F4 cell RNA. Molecular hybridization of complementary deoxyribonucleic acid (cDNA) complementary to this abundant, cadmium-induced 400-NT RNA fraction indicates that the cadmium-induced RNA class possesses a total kinetic complexity of about 2000 NT's. At least half of these inducible sequences are also represented constitutively in less abundant RNA classes of both uninduced CHO and Cdr20F4 cells. Induction of Cdr20F4 cells with cadmium increases the cellular concentration of the 2000-NT-complexity RNA class to a level at least 2 x 10(3)-fold greater than its constitutive level in uninduced Cdr20F4 cells. Induction of CHO cells with cadmium increases the cellular concentration of a subset of the sequences in the 2000-NT-complexity class, but only to a level 100-fold over the constitutive level in uninduced CHO cells. The remainder of these sequences belongs to the least abundant CHO cell poly(A+) RNA class.

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↗
PubMed1985

[Evaluation of occupational exposure to cadmium based on analysis of air in the work area. II. Cadmium oxide levels in the air of work areas during cadmium production in a non-ferrous metal foundry].

By stationary measurements the levels of cadmium oxide aerosols concentrations in air at particular workplaces related to cadmium production at non-ferrous metals mill have been determined. High concentrations of that compound have been found at such technological operations as unloading of cadmium-bearing raw materials, batching of cadmium sponge in the induction furnace and casting of fused cadmium into moulds. With the personal dosimetry technique, concentrations of that compound in the workers' breathing zone have been determined. Those were within 0.16-1.84 mg/m3, so--above the TLV values. However, those concentrations do not necessarily reflect the occupational exposure magnitude, as the workers had respirators.

Air Pollutants, Occupational↗
PubMed1982

Cadmium inhibition of in vitro hepatic oxidative drug metabolism in the rat: comparison between ionic cadmium and cadmium-thionein.

The effectiveness of cadmium added in vitro in inhibiting the microsomal oxidative metabolism of ethylmorphine or aniline in rat hepatic microsomes was markedly decreased if the metal was added as cadmium-thionein when compared to ionic cadmium. These data are consistent with the hypothesis that cadmium thionein is less active biologically than ionic cadmium.

Aniline Hydroxylase↗
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↗
PubMed1995

Discrepancy between the nephrotoxic potencies of cadmium-metallothionein and cadmium chloride and the renal concentration of cadmium in the proximal convoluted tubules.

Acute exposure to inorganic cadmium produces hepatotoxicity, but no renal injury. In contrast, chronic exposure to Cd produces nephrotoxic effects. However, a single injection of cadmium bound to metallothionein (CdMT) can produce nephrotoxicity similar to that seen with chronic exposure to Cd. It is generally thought that CdMT is nephrotoxic because more CdMT than CdCl2 distributes to the kidney. To test this hypothesis, the toxic effects and distribution of Cd were compared after iv injection of CdMT and CdCl2 to mice. CdMT increased urinary excretion of glucose, and protein indicating renal injury. This dysfunction occurred with dosages as low as 0.2 mg Cd/kg. In contrast, renal function was unaltered by CdCl2 administration, even at dosages as high as 3 mg Cd/kg. CdMT distributed almost exclusively to the kidney, whereas CdCl2 preferentially distributed to the liver. However, a high concentration of Cd was also found in the kidneys after CdCl2 administration. In fact, the renal Cd concentration after administration of a high but nonnephrotoxic dose of CdCl2 was equal to or higher than that obtained after injection of nephrotoxic doses of CdMT. Light microscopic autoradiography studies, using 0.3 mg Cd/kg as CdMT and 3 mg Cd/kg as CdCl2, indicated that Cd from CdMT preferentially distributed to the convoluted segments (S1 and S2) of the proximal tubules, whereas Cd from CdCl2 distributed equally to the various segments (convoluted and straight) of the proximal tubules. However, the concentration of Cd at the site of nephrotoxicity, the proximal convoluted tubules, was higher after CdCl2 than after CdMT administration. A higher Cd concentration in both apical and basal parts of the proximal cells was found after CdCl2 than after CdMT administration. Therefore, the reason why CdMT is nephrotoxic and CdCl2 is not nephrotoxic is not due to a higher concentration of Cd in the target cells after CdMT than after CdCl2 administration.

Analysis of Variance↗
PubMed2003

Synthesis and spectroscopic and structural studies of a new cadmium(II)-citrate aqueous complex. Potential relevance to cadmium(II)-citrate speciation and links to cadmium toxicity.

The presence of cadmium in the environment undoubtedly contributes to an increased risk of exposure and ultimate toxic influence on humans. In an effort to comprehend the chemical and biological interactions of Cd(II) with physiological ligands, like citric acid, we explored the requisite aqueous chemistry, which afforded the first aqueous Cd(II)-citrate complex [Cd(C(6)H(6)O(7))(H(2)O)](n)() (1). Compound 1 was characterized by elemental analysis, and spectroscopically by FT-IR and (113)Cd MAS NMR. Compound 1 crystallizes in the orthorhombic space group P2(1)2(1)2(1), with a = 6.166(2) A, b = 10.508(3) A, c = 13.599(5) A, V = 881.2(5) A(3), and Z = 4. The X-ray structure of 1 reveals the presence of octahedral Cd(II) ions bound to citrate ligands in a molecular crystal lattice. Citrate acts as a tridentate binder promoting coordination to one Cd(II) through the central alcoholic moiety, one terminal carboxylate group, and the central carboxylate group. In addition, the central carboxylate binds to three Cd(II) ions. Specifically, one of the oxygens of the central carboxylate serves as a bridge to two neighboring Cd(II) ions, while the other oxygen binds to a third Cd(II). A bound water molecule completes the coordination requirements of Cd(II). (113)Cd MAS NMR studies project the spectroscopic signature of the nature of the coordination environment around Cd(II) in 1, thus corroborating the X-ray findings. Collectively, the data at hand are in line with past solution studies. The latter predict that other similar low molecular mass Cd(II)-citrate complexes may exist in the acidic pH region, thus influencing the uptake of cadmium by living (micro)organisms, their ability to metabolize organic substrates, and possibly Cd(II) toxicity.

Cadmium↗
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↗