Experimental animals were divided into 5 groups; normal, cadmium control, and 3 experimental groups. Cadmium control and experimental groups were exposed to 1 mg/㎥ of cadmium aerosol in air by inhalation exposure for 6 hours/day, 5 days/week during 4 weeks. Dosages of 20, 40, and 80mg/kg of extracts of persimmon leaves were intraperitoneally injected to experimental groups respectively and several toxicological parameters and induction of metallothionein were measured from the rats that inhaled cadmium aerosol in air. The results of this study were as follows. Cadmium concentration that cadmium control and experimental groups were inhaled was 0.980±0.061 mg/㎥. Mass median diameter of cadmium aerosol for inhalation exposure was 4.93±0.483㎛. Cadmium content of normal group in lung was 0.088㎍/g and the highest cadmium content in lung, 55.492㎍/g was from 80mg/kg dose group. Cadmium concentration of normal group in blood was 0.348㎍/100㎖ and the highest cadmium concentration in blood, 2.642㎍/100㎖ was from cadmium control. Cadmium concentration of normal group in liver was 0.010㎍/g and the highest cadmium concentration in liver, 31.100㎍/g was from 20mg/kg dose group. Cadmium concentration of normal group in kidney was 0.030㎍/g and the highest cadmium concentration in kidney, 2.526㎍/g was from cadmium control. Cadmium concentration of normal group in intestine was O.064㎍/g and the highest cadmium concentration in intestine, 0.300㎍/g was from 80mg/kg dose group. The highest cadmium concentration in urine by week was 6.080㎍/day from 20mg/kg dose group in the fouth week and the highest cadmium concentration in feces by week was 341.731㎍/day from 20mg/kg dose group in the fouth week. Metallothionein concentration of normal group in lung was 5.769㎍/g and the highest in lung, 30.986㎍/g was from 80mg/kg dose group. Metallothionein concentration of normal group in liver was 38.856㎍/g and the highest in liver, 169.378㎍/g was from 40mg/kg dose group. Metallothionein concentration of normal group in kidney was 22.228㎍/g and the highest in kidney, 47.898㎍/g was from 80mg/kg dose group. Metallothionein concentration of normal group in intestine was 2.170㎍/g and the highest in intestine, 13.642㎍/g was from 80mg dose group.
Thirty five male Sprague-Dawley rats were treated with cadmium chloride solution ranging from 0.2 to 3.2mg $CdCl_2/kg$ by intravenous single injection. At 48 hours after administration of cadmium, total cadmium, MT bound cadmium and histopathologic finding in liver, kidney, lung, heart, testis, metallothionein in liver, kidney and total cadmium in bleed were examined. Tissue cadmium concentration was highest in liver, followed by in kidney, heart, lung and testis. Cadmium bound to rnetallothionein (MT-Cd) and ratio of MT-Cd to total cadmium were increased in liver and kidney dependently of cadmium exposure dose, but not significantly changed in other organs. On histopathologic finding, the most susceptible organ was heart in considering cadmium exposed dose, but testis in considering cadmium concentration. Blood cadmium concentration was increased with dose-dependent pattern, and significantly correlated with tissue cadmium concentration, so that we may estimate tissue cadmium concentration by measurement of blood cadmium concentration. Metallothionein in liver and kidney was increased with dose-dependent pattern, higher in liver than in kidney, and was significantly correlated with tissue cadmium concentration. However, metallothionein induction efficiency of tissue cadmium(${\mu}g\;MT/{\mu}g\;Cd$) was eater in liver than in kidney, and reverse to tissue concentration or exposed dose of cadmium.
A low level exposure experiment was conducted on growing rats to investigate the accumulation and organ distribution of protein bound cadmium compared with cadmium chloride. Male Sprague-Dawley rats were fed for 21days with one of the semisynthetic diets, which contains cadmium as either bovine liver- or kidney meal bound cadmium, cadmium chloride with uncontaminated liver meal or cadmium chloride without organ meal, in the levels of ca. 0.5, 1 and 1.5mg/kg diet, respectively. After 21days of exposure cadmium was accumulated in liver, kidney and gastrointestinal tracts depending upon cadmium levels in diet. Inspite of very low cadmium accumulation in whole blood, it tends also to increase with dietary cadmium levels. The blood cadmium concentration of animals fed organ meal containing diets was about 4-7 fold higher than that without organ meal, regardless of cadmium was intrinsically bound to protein or not. However, significant effects of organ protein on cadmium accumulation in liver, kidney and digestive tracts were not detectable, when cadmium was supplemented as cadmium chloride. On the other hands, animals fed diet containing ca. 1.5mg Cd/kg as organ bound cadmium retained more cadmium in liver, kidney and digestive tracts compared to cadmium chloride with organ meal, whereby the increase of cadmium concentration in kidney was greater then in liver. However, when the concentration of protein bound cadmium was<1mg/kg diet, organ bound cadmium was not significantly different from cadmium chloride in bioavailability and organ distribution. From this result it is suggested that the intestinal absorption of protein bound cadmium is influenced of the amount of cadmium bound in protein. When cadmium concentration in protein is relatively low, protein bound cadmium seems to be absorbed in the same way as cadmium ions are absorbed. However, when the concentration is high, at least a small amount of intact protein bound cadmium could be absorbed and accumulated selectively in kidney.
This experiment was carried out to investigate the effects of cadmium on the growth of Arabidopsis thaliana when they were treated with different concentrations of cadmium. The growth of stem was stimulated in the concentrations up to fifty times higher than the official standard concentration of cadmium of pollutant exhaust notified by the Ministry of Environment, but it decreased in the concentration one hundred fifty times or more higher in proportion to the degree of concentration. The growth of root was similar to that of stem, except that the decrease was gradual in the concentration fifty times or more higher. The growth of leaf was almost the same as that of stem, that is, it was stimulated the increase of leaf surface area in the concentration fifty times higher, but decreased in the concentration one hundred fifty times or more higher in proportion to the degree of concentration. The fresh weights of the plants were increased in accord with the degree of growth of the stem and leaf. Concentration of cadmium accumulated in the plants was increased in proportion to the concentration of cadmium. These results show that the growth of plants was stimulated in the soil polluted by cadmium up to fifty times higher than the official standard concentration, but it was decreased in proportion to the degree of concentration in the plants grown in the presence of cadmium more than one hundred fifty times.
We have examined the bioaccumulation patterns and the ecophysiological responses (photosynthetic pigment and total antioxidative capacity) of Monochoria korsakowi exposed to various cadmium concentrations, one of major environmental pollutants. Cadmium ion contents in M. korsakowi increased significantly with higher cadmium concentration, and most of the accumulated cadmium was found in the root parts. Biomass of each part decreased with higher cadmium concentration. As cadmium treatment concentration was increased, chlorophyll a content was decreased, whereas chlorophyll b content was increased. However, the variations of total chlorophyll and carotenoid contents were not evident. Total antioxidative capacity in the leaves of cadmium treated M. korsakowi increased greatly with higher cadmium concentration. We considered these results as indicative of the ability of M. Korsakowi plants to take up cadmium from wetlands.
This study is performed to find out the effects of selenium against cadmium toxicity. The experimental mice were divided into 6 gruops such as control group, cadmium alone treatment group, selenium treatment groups and two simultaneous treatment groups of selenium and cadmium. Mice were given intraperitoneal administration with two dosage of sodium selenite such as 1.0 mg/kg, 2.5 mg/kg body weight and cadmium chloride was administered 3.0 mg/kg body weight. After giving the challenge dose, the concentration of cadmium and metallothionein and histopathological change of liver and kidney were determined. The results were summarized as follows on 1. The simultaneously administration of selenium and cadmium significantly more decreased cadmium concentration in kidney and iiver tissues compared to the administration of cadmium only(P<0.05). 2. The simultaneously administration of selenium and cadmium more increased metallothionein concentration compared to administration of cadmium only. 3. The simultaneously administration of selenium and cadmium more decreased cadmium concentration in urine compared to the administration of cadmium only. 4. When liver and kidney tissues were observed with optical microscope, no obvious changes were visible in those tissues.
The natural weathered sand of basalt (WSB) has been used for the removal of cadmium from aqueous solution. The influence of various parameters i.e., contact time, pH, weathered sand of basalt dosage, particle size of the weathered sand of basalt, temperature and initial cadmium concentration were analyzed. Cadmium adsorption kinetics was well described by the pseudo second order model. Adsorption equilibrium for cadmium was properly well fitted to Langmuir isotherm model with maximum adsorption capacity 0.50 mg/g. Compared with the other experimental results using various kinds of adsorbents at a low concentration (1.0 mg/L or so) similar to that of this study, the cadmium removal efficiency using weathered sand of basalt was higher. It has been demonstrated that weathered sand of basalt has a available alternative adsorbent for cadmium when its initial concentration is low.
In this study, we analyzed the blood cadmium concentration in general population of Korea, and followed the analyses the relations with epidemiologic factors, life-style and body iron store. The geometric mean concentration of blood cadmium was 1.20 ${\mu}g/L$ in study subject, the level of blood cadmium was higher in female (1.27 ${\mu}g/L$) than in male (1.11 ${\mu}g/L$). The mean concentration of blood cadmium was the highest in coastal area (1.80 ${\mu}g/L$) and followed in urban (1.01 ${\mu}g/L$) and rural area (0.90 ${\mu}g/L$). The cadmium concentration in whole blood was increased with age-dependent pattern, such as 0.64 ${\mu}g/L$ in the below 30 years, 0.95 ${\mu}g/L$ in the 30~44 years, 1.28 ${\mu}g/L$ in the 45~59 years and 1.31 ${\mu}g/L$ in the over 60 years. The level of blood cadmium was higher in smokers than in non-smokers, but was not significant by alcoholic habit. The blood cadmium level was different from occupations, which was the highest in the fishers as 1.87 ${\mu}g/L$. The inversed relation was observed between blood cadmium and serum Fe, while was correlated positively with the ferritin level. In summary, the environmental exposure to cadmium in Korean is not so much compared to other countries, and the blood cadmium is influenced by genetic factors (age and sex), life-styles (dietary habit, occupation and smoking habit) and nutrition such as serum iron.
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.
The rate of metallothionein synthesis on cadmium-poisoned rats reflects the level of toxicity, and also it reduces the toxicity which is caused by the uptake of cadmium. Chlorella supplementation in the diets of the cadmium-poisoned rats decreased the concentration of cadmium in blood and urine compared with the control group. Although the liver and kidneys of rats are major target organs of cadmium and coherence of metallothionein and cadmium, no previous study has determined the correlation between the rate of metallothionein synthesis in the liver and kidneys of rats and dietary supplementation of chlorella with cadmium uptake. This study analyzed total metallothionein level on the tissue of the liver and kidneys, the concentration of cadmium bound to the metallothionein, and the total concentration of cadmium on the tissue of the liver and kidneys after dietary supplementation with 1%, 5%, and 10% dried chlorella and 40 ppm of cadmium to 46 male SD rats (mean weight: $150\pm20\;g$) for 4 weeks. According to the data analysis of the total rate of metallothionein synthesis in the liver and kidneys, the group of SD rats on the supplementation with 1% chlorella and 40 ppm of cadmium showed a rate of $93.2\pm8.9\;ng/g$, a significant decrease of 58.8% compared to that of the control group of SD rats on the supplementation with cadmium only, which showed a rate of $227.3\pm32.5 ng/g$ (P=0.0001). In contrast, no significant difference was observed through the changing of chlorella concentrations between 5% and 10% chlorella supplementation with cadmium. The group supplemented with 1% or greater chlorella levels represented a greater decrease in the total cadmium concentration of the kidney and liver tissues, the amount of total metallothionein synthesis, the amount of metallothionein with binding to cadmium, and the concentration of free cadmium without binding to metallothionein. Consequently, the supplementation of 1% and 5% chlorella was effective in reducing the synthesis of metallothionein for cadmium uptake, but increased the rate of binding of cadmium to metallothionein.
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