• Journal of Preventive Medicine and Public Health
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• 제15권1호
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• pp.89-94
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• 1982

Among the environmental pollutants, cadmium and lead compounds may impair human health. These compounds may inhibit the biological metabolic function of human body and may furthermore cause the disease directly or indirectly. This study was undertaken to investigate the effects of the immune response by intoxication of cadmium chloride and lead acetate. Cadmium chloride (8.8mg/kg, in saline 10ml) and lead acetate (15mg/kg, in saline 10ml) were administered by intraperitoneal injection. After 3 weeks, the rats were intoxicated with the above chemicals and immunized with sheep RBC. After 4 weeks, the immune response of rat spleen cells was measured by the Jerne's technique. The results were obtained as follows; 1. There was no change in leukocyte counts by the intoxication of cadmium chloride or lead acetate. 2. Cadmium chloride or lead acetate reduced hemoglobin contents for most intoxicated and immunized groups. 3. Hematocrits were decreased by the intoxication of cadmium chloride or lead acetate significantly. 4. It was determined that total protein, A/G (Albumin/Globulin), ${\alpha}-,\;{\beta}-\;and\;{\gamma}$-globulins in rat serum were not changed. 5. Intoxication by cadmium chloride or lead acetate reduced the number of hemolytic plaque to the sheep RBC in rat spleen cells. Therefore, antibody producing of rat spleen cells was suppressed by the intoxication of cadmium chloride and lead acetate.

• Journal of Nutrition and Health
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• 제25권5호
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• pp.360-378
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• 1992

This study was performed to investigate effect of dietary protein and calcium levels on cad-mium intoxication in rats. Adult Sprague-Dawley male rate(245$\pm$21g) were blocked into 18 groups of 7 animals according to body weight Nine experimental diets different with protein(40%, 15%, 7%) and calcium (1.3%, 0.6%, 0.1%) levels were prepared. Nine groups of animals were fed each diet with 50ppm cadmium in drinking water and the other 9 groups without cadmium for 30days. Results were summarized as follows: 1) Body weight gain F. E. R(Food Efficiency Ratio) and weights of liver kidney and femur were higher in high protein groups among cadmium exposed groups. 2) Cadmium contents in liver and intestine were higher in rats fed high protein diet or low calcium diet among cadmium exposed groups. Fecal cadmium excretion was highest in high protein-high calcium diet group among cadmium exposed animals. Metallothionein contents in liver kidney and intestine were higher in animals exposed to cadmium and fed high protein diets. 3) Gel filtration chromatography of cytosolic solution showed that the higher dietary protein and calcium levels were the more cadmium was found in metallothionein fractions. 4) No gross histopathological change was seen in liver kidney and intestine of cadmium exposed rats. However a significant increase of smooth endoplasmic reticulum which was alleveated by high protein-high calcium diet was observed. Results obtained indicated that not only high protein diet but also high calcium diet showed preventive effect on cadmium intoxication by increasing the induction of metallothionein syn-thesis and decreasing the cadmium absorption.

• Safety and Health at Work
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• 제11권2호
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• pp.235-240
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• 2020

Background: Cadmium exposure may induce chronic intoxication with renal damage. Silver soldering may be a source of cadmium exposure. Methods: We analyzed working environment measurement data and periodic health screening data from a small-scale silver soldering company with ten workers. Concentrations of cadmium in air from working environment measurement data were obtained. Concentrations of blood and urinary cadmium, urine protein, and urine β2-microglobulin (β2M) were obtained. The generalized linear model was used to identify the association between blood and urine cadmium and urine β2M concentrations. Clinical features of chronic cadmium intoxication focused with toxicological renal effects were described. Results: The mean duration of work was 8.5 years (standard deviation [SD] = 6.9, range = 3-20 years). Cadmium concentrations in air were ranged from 0.006 to 0.015 mg/㎥. Blood cadmium concentration was elevated in all ten workers, with a highest level of 34.6 ㎍/L (mean = 21.288 ㎍/L, SD = 11.304, range = 9.641-34.630 ㎍/L). Urinary cadmium concentration was elevated in nine workers, with a highest level of 62.9 ㎍/g Cr (mean = 22.151 ㎍/g creatinine, SD = 19.889, range = 3.228-62.971 ㎍/g creatinine). Urine β2M concentration was elevated in three workers. Urinary cadmium concentration was positively associated with urine protein concentration (beta coefficient = 10.27, 95% confidence interval = [4.36, 16.18]). Other clinical parameters were compatible with renal tubular damage. Conclusion: Cadmium intoxication may occur at quite low air concentrations. Exposure limit may be needed to be lowered.

• Nutrition Research and Practice
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• 제10권1호
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• pp.19-25
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• 2016

BACKGROUND/OBJECTIVES: Cadmium is a toxic metal that is an occupational and environmental concern especially because of its human carcinogenicity; it induces serious adverse effects in various organs and tissues. Even low levels of exposure to cadmium could be harmful owing to its extremely long half-life in the body. Cadmium intoxication may be prevented by the consumption of dietary components that potentially reduce its accumulation in the body. Dietary chitosan is a polysaccharide derived from animal sources; it has been known for its ability to bind to divalent cations including cadmium, in addition to other beneficial effects including hypocholesterolemic and anticancer effects. Therefore, we aimed to investigate the role of dietary chitosan in reducing cadmium accumulation using an in vivo system. MATERIALS/METHODS: Cadmium was administered orally at 2 mg (three times per week) to three groups of Sprague-Dawley rats: control, low-dose, and high-dose (0, 3, and 5%, respectively) chitosan diet groups for eight weeks. Cadmium accumulation, as well as tissue functional and histological changes, was determined. RESULTS: Compared to the control group, rats fed the chitosan diet showed significantly lower levels of cadmium in blood and tissues including the kidneys, liver, and femur. Biochemical analysis of liver function including the determination of aspartate aminotransferase and total bilirubin levels showed that dietary chitosan reduced hepatic tissue damage caused by cadmium intoxication and prevented the associated bone disorder. CONCLUSIONS: These results suggest that dietary chitosan has the potential to reduce cadmium accumulation in the body as well as protect liver function and bone health against cadmium intoxication.

• 대한가정학회지
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• 제30권1호
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• pp.99-113
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• 1992

This study was performed to investigate the effect of dietary protein and calcium levels on cadmium detoxication in rats. Seventy male Sprague-Dawley rats weighing 208 $\pm$ 19 g were blocked into 10 groups of 7 animals according to body weight. Five groups were fed 15% protein-0.6% calcium diet with 100ppm cadmium in drinking water for first 15days and the other 5groups fed same diet without cadmium in drinking water for same period and served as controls. After this 15-day intoxication period, each one of cadmium intoxication and control groups were fed each of 4 kinds of detoxifying diets different with protein(40%, 15%) and calcium(1.3%, 0.6%) levels without cadmimum in drinking water for following 15 days of detoxifying period. Results were summarized as follows: 1) Food intake, body weight gain, F.E.R. and weights of liver, kidney and femur were increased by detoxifying diets and high protein diet was most effective in weight gains of liver and kidney. 2) When cadmium and metallothionein contents of initial intoxication group and those of all detoxication groups were compared, cadmium and metallothionein contents in the liver were not changed, but those in kidney increased, and those in intestine decreased markedly. 3) Only dietary protein level affected cadmium and metallothionein distribution among organs, and cadmium contents of whole blood, liver, kidney and femur were lower in high protein diet, but metallothionein contents in liver and kidney were higher in high protein diet. 4) Gel filtration chromatogram showed that most of cadmium in the cytosol was bound to metallothionein fractions in high protein-high calcium group. Results obtained indicated that high protein diet was effective in cadmium detoxication by increasing the induction of metallothionein synthesis. But high calcium diet did not play a role in cadmium detoxication.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.107-107
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• 2002

It has been reported that antinatriuresis is induced by acute cadmium intoxication. However, the mechanisms related to the increase in renal sodium reabsorption by cadmium exposure is not clear yet although it has been suggested that the elevated aldosterone might involve in this process.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.503-510
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• 1998

Effects of cadmium exposure on renal $Na^+$ and $K^+$ transports were studied in rats. During the course of cadmium treatment (2 mg Cd/kg/day, s.c. injections for 3 weeks) renal tubular transports of $Na^+$ and $K^+$ were evaluated by lithium clearance technique. During the early phase (first week) of cadmium treatment, urinary $Na^+$ excretion decreased drastically and this was due to an increased $Na^+$ reabsorption both in the proximal and distal nephrons. During the late phase (third week) of cadmium treatment, filtered $Na^+$ load was decreased by reduction in GFR, but the renal $Na^+$ excretion returned to the control level due to impaired $Na^+$ transport in the proximal tubule. Urinary excretion of $K^+$ did not change during the early phase, but it rose markedly during the late phase of cadmium treatment. These results indicate that a light cadmium intoxication induces a $Na^+$ retention, and a heavy intoxication results in a $K^+$ loss. Possible mechanisms for these changes are discussed.

• BMB Reports
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• 제41권9호
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• pp.657-663
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• 2008

The present study was undertaken to investigate the protective role of taurine (2-aminoethanesulfonic acid) against cadmium (Cd) induced oxidative stress in murine erythrocytes. Cadmium chloride ($CdCl_2$) was chosen as the source of Cd. Experimental animals were treated with either $CdCl_2$ alone or taurine, followed by Cd exposure. Cd intoxication reduced hemoglobin content and the intracellular Ferric Reducing/Antioxidant Power of erythrocytes, along with the activities of antioxidant enzymes, glutathione content, and total thiols. Conversely, intracellular Cd content, lipid peroxidation, protein carbonylation, and glutathione disulphides were significantly enhanced in these cells. Treatment with taurine before Cd intoxication prevented the toxin-induced oxidative impairments in the erythrocytes of the experimental animals. Overall, the results suggest that Cd could cause oxidative damage in murine erythrocytes and that taurine may play a protective role in reducing the toxic effects of this particular metal.

• The Korean Journal of Physiology and Pharmacology
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• 제6권1호
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• pp.41-46
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• 2002

Effect of cadmium (Cd) intoxication on renal acid-base regulation was studied in adult male Sprague-Dawley rats. Cd intoxication was induced by subcutaneous injections of $CdCl_2$ at a dose of 2 mg Cd/kg/day for $3{\sim}4$ weeks. In Cd-intoxicated animals, arterial pH, $PCO_2$ and plasma bicarbonate concentration decreased, showing a metabolic acidosis. Urine pH and urinary bicarbonate excretion increased and titratable acid excretion decreased with no change in ammonium excretion. In renal cortical brush-border membrane vesicles derived from Cd-exposed animals, the $Na^+/H^+$ antiporter activity was significantly attenuated. These results indicate that chronic exposures to Cd impair the proximal tubular mechanism for $H^+$ secretion (i.e., $Na^+/H^+$ antiport), leading to a metabolic acidosis.

• The Korean Journal of Physiology
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• 제30권2호
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• pp.279-288
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• 1996

Chronic exposure to cadmium impairs various renal tubular functions, including organic acid (anion) secretion. To investigate the mechanism of cadmium-induced alterations in the organic anion transport system, kinetics of p-aminohippurate (PAH) uptake was studied in renal cortical basolateral membrane vesicles (BLMV) isolated from cadmium-intoxicated rats (adult male Sprague-Dawley). Cadmium intoxication was induced by subcutaneous injections of $CdCl_{2}$ (2 mg Cd/kg per day) for 3 weeks. The renal plasma membrane vesicles were prepared by Percoll gradient centrifugation. The vesicular uptake of $^{14}C$-PAH was determined by rapid filtration technique using Millipore filter. Cadmium intoxication resulted in a marked attenuation of $Na^{+}$-dependent, ${\alpha}$-ketoglutarate (${\alpha}$KG)-driven PAH uptake with no changes in $Na^{+}$ and ${\alpha}$KG-independent transport component. Kinetic analysis indicated that Vmax, but not Km, of the $Na^{+}$-dependent, ${\alpha}$KG-driven component was reduced. A similar reduction of $Na^{+}$-dependent, ${\alpha}$KG-driven PAH uptake was observed in normal membrane vesicles directly exposed to inorganic cadmium in vitro, and this was accompanied by an inhibition of both $Na^{+}$-dependent ${\alpha}$KG uptake and ${\alpha}$KG-PAH exchange activity. These results indicate that during chronic exposure to cadmium, free cadmium ions liberated in the proximal tubular cytoplasm directly interact with the basolateral membrane and impair the active transport capacity for organic anions, most likely due to an inhibition of both $Na^{+}$-dicarboxylate cotransporter and dicarboxylate-organic anion antiporter activities.