• Journal of Environmental Health Sciences
• /
• v.23 no.4
• /
• pp.26-32
• /
• 1997

To evaluate the cytogenetic toxicity, of cadmium and the reducing effect of selenium or zinc on cadmium toxicity, the induction of SCEs in cultured human lymphocytes by the concentraion of 0.5 $\mu$M to 16.0 $\mu$M of cadmium chloride and those of cadmium chloride combined with sodium selenite or zinc chloride 1.2 $\mu$M, respectively was investigated. The induction of SCEs by cadmium chloride in the range of 0.5 $\mu$M to 16.0 $\mu$M increased in a dose-dependent manner. A notable increase in SCEs by sodium selenite as well as zinc chloride was also observed. However, the frequency of SCEs by cadmium chloride was inhibited by the simultaneous addition of sodium selenite and zinc chloride 1.2 $\mu$M, respectively. The mitotic index significantly decreased in higher concentration of cadmium chloride but not was significantly different in any concentration of cadmium chloride with the simultaneous addition of sodium selenite or zinc chloride. The results showed that the decreased additive SCE effect was observed when induced by the combined treatment which could suggest that sodium selenite and zinc chloride have a protective effect on cadmium chloride.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.33 no.9
• /
• pp.1486-1491
• /
• 2004

The estrogenicities of six heavy metal compounds, which contaminate frequently in foods, were assayed using a combination of in vitro and in vivo assays. The assays were 1) estrogen receptor dependent transcriptional expression assay, 2) E-screen assay and, 3) the uterotropic assay in mice. The chemicals studied were 17$\beta$ -estradiol, diethylstilbestrol (DES), arsenic oxide, bis(tri-n-butyltin), cadmium chloride, chromium chloride, lead acetate, and mercuric chloride. Using the estrogen receptor dependent transcriptional expression assay, the following estrogenicity ranking was measured: bis(tri-n-butyltin) > cadmium chloride > chromium chloride >> mercuric chloride >lead acetate = arsenic oxide. Using E-screen test, the following estrogenicity ranking was measured: bis(tri-n-butyltin) > cadmium chloride > chromium chloride >> mercuric chloride > lead acetate = arsenic oxide. Results from the uterotropic assay showed that bis(tri-n-butyltin), cadmium chloride, chromium chloride caused an increase in uterine wet weight, while lead acetate, mercuric chloride, and arsenic oxide failed to do so. Bis(tri-n-butyltin), cadmium chloride and chromium chloride showed the highest estrogenicity in three assay systems. Recent studies suggesting that bis(tri-n-butyltin), cadmium chloride have estrogenicities are compatible with the present finding. Furthermore, our study is suggesting that chromium chloride may be estrogenic. The results demonstrate that this three level-assay combination (transcriptional activation, cell proliferation, and an in vivo effect in an estrogen-responsive tissue) could serve as a useful method to assess the estrogenicity of heavy metals.

• Journal of Nutrition and Health
• /
• v.27 no.8
• /
• pp.828-836
• /
• 1994

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.

• Applied Microscopy
• /
• v.23 no.1
• /
• pp.125-138
• /
• 1993

This study was carried out to investigate the effects of cadmium chloride on the spermatogenesis of male mouse. Cadmium chloride was administered as a single dose of 5mg/kg body weight by intraperitoneal injection. The testes were isolated from the experimental animals at 3 hours, 8 hours, 12 hours, and 24 hours respectively after administration of cadmium chloride. The major changes in ultrastructures of the seminiferous tubules observed after cadmium chloride administration include dilation of smooth endoplasmic reticulum, swelling of mitochondria and vacuolation in cytoplasm of the germ cells. Especially, cadmium chloride caused direct damages to spermatogonia such as degeneration of nuclei, nuclear membrane and plasma membrane. In addition, necrotic changes were observed in most germ cells at 24 hours after cadmium chloride administration. Therefore, it seems clear from these results that cadmium chloride induces acute irreversible degenerative changes in the seminiferous tubules of the mouse testis, so that the cadmium chloride ultimately causes necrosis in germ cells at all stages of the spermatogenesis.

• Toxicological Research
• /
• v.12 no.1
• /
• pp.59-68
• /
• 1996

This study was conducted to investigate the antitoxic effects of Radix Menispermi extracts against cadmium toxicity. The experimental rats were divided into 5 groups such as control group, cadmium alone treatment group and simultaneous treatment groups of cadmium and three doses of Radix Menispermi extracts. Each group was administered with different dose of Radix Menispermi extracts such as 0.55 mg, 1.10 mg, 1.65 mg/kg wet weight in pallets for 12 weeks. Cadmium Chloride $(CdCl_2)$ was administered by 4 mg/kg body weight. The results were summarized as follows: 1. The simultaneous administration of cadmium and Radix Menispermi significantly more decreased cadmium concentration in liver tissues compared to the administration of cadmium only (P < 0.05). 2. When blood were measured, no significantly difference in haemoglobin, haematocrit, erythrocyte values compared to the administration of cadmium only. 3. The simultaneous administration of cadmium and Radix Menispermi more increased metallothionein concentration in liver than the administration of cadmium only (P < 0.05). 4. There were the histopathological slight changes in the liver and kidney tissues of rats.

• Journal of Preventive Medicine and Public Health
• /
• v.15 no.1
• /
• pp.89-94
• /
• 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 Environmental Health Sciences
• /
• v.21 no.3
• /
• pp.16-22
• /
• 1995

This study was designed to investigate the antibody production to sheep red blood cells(SRBC) and proliferation of mitogen-stimulated spleen cells in Balb/c mice which received cadmium chloride. The mice were divided into three independent groups which were one control and two experimental groups by the cadmium treatment or not. No specific treatment was done for the control group. One of two experimental groups, which is called 'pre-treatment group' in this paper, was subcutaneously injected with low dose of cadmium chloride(0.5 mg/kg/day) for 5 consecutive days before the primary SRBC immunization. The other called 'non-pretreatment group' was only pretreated with normal saline. Both experimental groups were intraperitoneally injected with high dose of cadmium chloride(5 mg/kg) 8 hours before the primary immunization. Mice were intraperitoneally immunized twice with 2% SRBC suspension containing $10^8$ cells. The results obtained were as follows, 1. The PFG responses to SRBC were significantly increased in two experimental groups, cadmium pretreatment and non-pretreatment compared with that of control group(p<0.05). 2. The total antibody titers to SRBC in cadmium treated groups were similar to that of control group, but titers of IgG antibody were significantly elevated(p<0.01). 3. The proliferation response of spleen lymphocytes to various mitogens was suppressed in proportion to the concentration of cadmium and the degree of cadmium accumulation in liver was increased in the cadmium treated groups. These results suggest that cadmium chloride could affect on mouse immune response, especially its cell mediated immune response could be decreased while its humoral immune response could be increased, which may not be influenced by the administration methods or pretreatment of cadmium to mouse.

• Environmental Mutagens and Carcinogens
• /
• v.22 no.4
• /
• pp.255-258
• /
• 2002

In order to determine the safety of chemicals and pharmaceutical products, various methods can be used to evaluate the toxicity. In this study the genotoxic effect of the widely used industrial chemical, cadmium chloride, was assessed using the micronucleus test in peripheral blood of mice. The presence of micronucleated reticulocytes by microscopic observation following acridine orange staining indicated a potential genotoxic effect. The genotoxicity of intraperitoneally (i.p.) administered cadmium chloride (0.5, 1, 2 mg/kg) appeared to be dose dependent, with the maximum tolerated dose (MTD) found to be 2 mg/kg. Compared to the negative control (saline), cadmium chloride (2 mg/kg) exhibited statistically significant genotoxic potential (P<0.05) but was found to be less than the positive control of mitomycin C (0.5 mg/kg) and was not statistically significant compared to historical negative controls (P>0.05).

• Journal of environmental and Sanitary engineering
• /
• v.12 no.2
• /
• pp.37-42
• /
• 1997

The toxic and detoxifying effects of cadmium and zinc on rat plasma ACTH and serum cortisol levels were investigated in rats. Rats were injected by i.p. with saline (0.9%), cadmium chloride (0.25 or 0.5mg/kg body weight) and pretreated with zinc chloride (4mg/kg body weight) before cadmium chloride treatment 1 or 2 weeks, respectively. The ACTH levels were no significant differences in cadmium 0.25mg/kg-treated group, but were significantly decreased in cadmium 0.5mg/kg-treated group compared with normal group. The ACTH levels after zinc pretreatment for 1 week were significantly increased but zinc pretreatment for 2 week were no difference. The serum cortisol levels of cadmium treated rats were significantly decreased, but were increased in zinc pretreated rats. The results showed that the zinc have some protective effect on cadmium toxicity in rats.

• Applied Microscopy
• /
• v.21 no.2
• /
• pp.76-95
• /
• 1991

A single injection of cadmium chloride (3.75 mg/kg) was made into the peritoneal cavities of albino rats. The cortices of kidney were obtained from the experimental animals at 3 hr., 6 hr., 12 hr., 24 hr. and 36 hr. after administration of cadmium chloride, respectively. The specimens of each experimental animal were prefixed in 2% glutaraldehyde-4% paraformaldehyde solution for $2{\sim}4$ hours, and these specimens were post-fixed in 1% osmic acid. After fixation, the specimens were dehydrated with alcohol and acetate and embedded in Epon 812. Ultrathin sections, $600{\sim}800{\AA}$ thickness were made and stained with uranyl acetate and lead citrate. And all the preparations were observed with Hitachi-600 transmission electron microscope. The results obtained were as follows: 1. The main changes in ultrastructures of the glomeruli observed at 3 hr. after cadmium chloride administration include loss of filtration slit and fenestrae of capillary endothelium that was resulted from thickings of the basal lamina and fusion of pedicels of the podocytes. At 12 hr. after cadmium chloride administration the Bowman's capsules were mostly filled with abnormally thickened and fused pedicels. After 24 hr. however, the only recognized change was loss of fenestrae of the capillary endothelium. And the ultrastructure of the glomeruli were almost normal in 36 hr. after cadmium chloride treatment. 2. At 3 hr. after treatment with cadmium chloride, in the renal tubular cells the vesicles and vacuoles increased in number at the apical portion, of the tubular epithelial cells, the basal infoldings were reduced and the basal lamina was thickened. After 12 hr., a number of phagosomes appeared at the apical portion and the cisternae of rough endoplasmic reticulum were swollen. At 24 hr. after cadmium chloride administration irregularly shaped mitochondria were observed in the apical area, and mitochondria with swollen cristae were found at the basal portion. And after 36 hr. The ultrastructures of the epithelial cells appeared almost normal except for a moderate increase in the number of vesicles and vacuoles. Consequently it is suggested that in albino rats, cadmium chloride induces acute reversible degenerative changes in the glomeruli as well as in the epithelial cells of the proximal convoluted tubules.