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

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.2
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• pp.249-257
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• 2010

Crataegii Fructus is commonly used as a improving digestion, removing retention of food, promoting blood circulation and resolving blood stasis agent in East Asia. Cadmium (Cd) is widely distributed in the environment due to its use in industry. An exposure to Cd causes dysuria, polyuria, chest pain, hepatic and renal tubular diseases. The liver is the most important target organ when considering Cd-induced toxicity because Cd primarily accumulates in the liver. This study investigated the protective effect of Crataegii Fructus water extract against cadmium ($CdCl_2$, Cd)-induced liver toxicity in H4IIE cells, a rat hepatocyte-derived cell line and in rats. Cell viability was significantly reduced in Cd-treated H4IIE cells in a time and concentration-dependent manner. However, Crataegii Fructus water extract (CFE) protected the cells from Cd-induced cytotoxicity via inhibition of PARP cleavage. To induce acute toxicity in rats, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously injected into rats. The rats then received either a vehicle or silymarin (as a positive control) or CFE (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with CFE reduced ALT, AST and LDH. In histopathological analysis, CFE reduced the hepatic degenerative regions and the number of degenerative hepatocytes. These are considered as direct evidences that Crataegii Fructus has favorable inhibitory effects on the Cd-intoxicated liver damages. The efficacy of Crataegii Fructus shows slight lower than that of silymarin in the present study.

• The Korean Journal of Ecology
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• v.27 no.5
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• pp.301-306
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• 2004

The sensitivity to Cd of three ectomycorrhizal fungi, Paxillus involutus, Suillus bovinus and Rhizopogon subcaerulescens, was assessed and compared in terms of radial growth and dry mass production, using both agar and liquid culture. The radial growth of S. bovinus and R. subcaerulescens was significantly reduced at the lowest concentration (0.1mg Cd/L). The 50% effective concentration (EC$_{50}$) values calculated from radial growth rates of the ectomycorrhizal fungi showed that the sensitivity of the fungi to Cd was greatest in S. bovinus and lowest in R. subcaerulescens. Cadmium addition also significantly decreased dry mass production of the ectomycorrhizal fungi. The sensitivity of the fungi to Cd in terms of dry mass production, was greatest in S. bovinus and lowest in P. involutus. Higher growth rates of P. involutus and melanisation of R. subcaerulescens appeared to contribute to reduced Cd toxicity.

• Journal of Microbiology
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• v.37 no.1
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• pp.45-49
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• 1999

To investigate the mechanism of cadmium tolerance in a cadmium-resistant Azomonas agilis PY101 that produces a specific fluorescent pigment promoted by cadmium, we carried out Tn5 mutagenesis and isolated four pigment-deficient mutants. In these mutants, Ppg1, Ppg2, and Ppg3 remarkably reduced the pigment production to 15.3%, 11.2%, and 13.9%, respectively. Especially, Ppg4 mutant did not produce the pigment at all. None of the mutants grew in the presence of 1500 ppm of CdCl2 in growth medium, and they exhibited differential sensitivities to cadmium. Ppg1, Ppg2, Ppg3, and Ppg4 mutants were sensitive to 900 ppm, 1100 ppm, 1000 ppm, and 800 ppm of CdCl2, respectively. These mutants also showed noticeable increase, from 8.8-fold to 13.2-fold, in the size of growth inhibition zone compared with that of the will type after treatment with cadmium. Therefore, the pigment production of A. agilis PY101 was found to decrease the toxic effects of cadmium to the bacterium.

• Korean Journal of Environmental Biology
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• v.20 no.3
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• pp.232-236
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• 2002

The morphological patterns and the cytopathogenicity time of the Vero cells induced by free $Cd^{2+}$ and pigment-bound $Cd^{2+}$ were observed by inverted microscope in order to investigate the difference of cadmium toxicity. The Vero cells induced by Hee $Cd^{2+}$ of 0.1 mM were shown to have a fatal toxic effect and the cytopathogenicity could be seen early after 6$\pm$2 hours of incubation. Partially affected cells induced by pigment-bound $Cd^{2+}$ of 0.1 mM were shown and the cytopathogenicity could be seen after 20 hours of incubation. The Vero cells grown with free 0.001 mM $Cd^{2+}$ were also affected and the cytopathogenicity could be seen after 17 hours of incubation, whereas the Vero cells grown with 0.001 mM pigment- bound $Cd^{2+}$ were unaffected. The sensitivity of Escherichia coli DH5$\alpha$ bacterial cells was also examined after a short treatment with free $Cd^{2+}$ or pigment-bound $Cd^{2+}$. About 5% of cells survived after 0.01 mM of free $Cd^{2+}$ treatment, while about 68% of cells survived after 0.01 mM of pigment- bound $Cd^{2+}$.

• Journal of the Korean Society of Food Science and Nutrition
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• v.19 no.1
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• pp.27-34
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• 1990

This study was undertatken to investigate the effects of dietary vitamin E on the toxicity of cadmium(Cd) in rats. The two variables were the supplmentary vitamin E(400lU/kg) and the protein amount(10.5% in the low protein diet and 18.0% in the normal protein diet) In cadmium treated rats net weight gain and food intake were decreased but improved by supplementation with vitamin E in the normal protein, hematocrit values reduced by Cd were significantly increased by the addition of vitamin E to normal protein diet in Cd intoxicated rats, The supplementation with vitamin E diminished the effect of Cd on aspartate aminotransf-rase and alanine aminotransferase activities in serum In Cd treated rats fed normal protein diet with vitamin E the contents of triglyceride were decreased and total-cholesterol contents were significantly reduced in serum and both of them in liver were markedly decreased. The activity of alcohol dehydrogenase in liver was decreased by Cd however supplementation with vitamin E reduced the effects of Cd on hepatic alcohol dehydrogenase. the results of this experiment indicated that there was some interaction between vitamin E and protein levels and supplementation with vitamin E had an effect more than protein levels oncd toxicity.

• Korean Journal of Environmental Agriculture
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• v.22 no.2
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• pp.94-99
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• 2003

The objective of present study was to investigate the antioxidative and hepatoprotective effects of selenium on cadmium-induced toxicity and lipid peroxidation in rat hepatocyte primary culture. To do this, two separate experiments were conducted. In Experiment 1, primary cultures of rat hepatocytes were incubated for 6 hr in the presence of various concentrations (1, 10, 50, 100, and $500\;{\mu}M$) of cadmium chloride. Cytotoxicity and lipid peroxidation were evaluated using the MTT assay and TBARS assay, respectively. Antioxidative and hepatoprotective effects were determined by measuring the activity of GOT and GSH-Px, respectively. Cell viability was reduced and lipid peroxidation was increased by cadmium in dose-dependent manners. There was significantly negative correlation (r=-0.943, p<0.01) between cell viability and lipid peroxidation GOT activity was increased and GSH-Px activity was decreased by cadmium at the concentration of $50\;{\mu}M$. In Experiment 2, primary cultures of rat hepatocytes were incubated for 6hr in the presence of 100\;{\mu}M$ of cadmium chloride and various concentrations (0.01, 0.1 and 1 ppm) of sodium selenite to assess the effect of selenium on cadmium-induced toxicity and lipid peroxidation. Cell viability and GSH-Px activity were increased by sodium selenite at the concentration of 1 ppm Whereas, lipid peroxidation and GOT activity were reduced by 0.1 ppm of sodium selenite. These results demonstrate that selenium has an antioxidative and hepatoprotective potentials against cadmium.

• Proceedings of the Korean Society of Applied Entomolohy Conference
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• 2005.05a
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• pp.166-166
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• 2005

• Journal of Environmental Health Sciences
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• v.18 no.1
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• pp.95-104
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• 1992

The influence of selenium to several toxic effects of cadmum, including lethality has been shown following pretreatment with cadmium, zinc and seleniurm Five groups of rats, each consisting of 16 rats, were studied and each group was divided into four subgroups, 4 rats for each subgroup. After subcutaneous pretreatment during 5 days with saline, CdCl$_{2}$ (0.5mg/kg, ZnCl$_{2}$ (13.0mg/kg) and $Na_{2}SeO_{3}$(1.0mg/kg), rats were given intraperitioneal administration of various dosage of or cadium of cadmium and selenium. After giving the challenge dose, cadmium and metallothionein(MT) concentrations were determined in liver and kidney The concentration of cadmium in liver and kideny increased proportionally to the increase of challenge dosage. The simultaneous administration of cadmium and selenium significantly more decrease cadmium concentrations in liver and kidney than those of the administration of cadmium only. However, MT concentrations in liver and kideny were increased by the pretreatment of cacmium, zinc and selenium. Our results suggest that increasing cadmium concentrations, gradully accumulating in the tissues of liver and kidney as a result of the pretreatment, served to induced the synthesis of MT, thus making them resistant to the challenge from cadmium.

• Toxicological Research
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• v.28 no.2
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• pp.129-137
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• 2012

Probabilistic ecological risk assessment (PERA) for deriving ecological protective concentration (EPC) was previously suggested in USA, Australia, New Zealand, Canada, and Netherland. This study suggested the EPC of cadmium (Cd) based on the PERA to be suitable to Korean aquatic ecosystem. First, we collected reliable ecotoxicity data from reliable data without restriction and reliable data with restrictions. Next, we sorted the ecotoxicity data based on the site-specific locations, exposure duration, and water hardness. To correct toxicity by the water hardness, EU's hardness corrected algorithm was used with slope factor 0.89 and a benchmark of water hardness 100. EPC was calculated according to statistical extrapolation method (SEM), statistical extrapolation $method_{Acute\;to\;chronic\;ratio}$ ($SEM_{ACR}$), and assessment factor method (AFM). As a result, aquatic toxicity data of Cd were collected from 43 acute toxicity data (4 Actinopterygill, 29 Branchiopoda, 1 Polychaeta, 2 Bryozoa, 6 Chlorophyceae, 1 Chanophyceae) and 40 chronic toxicity data (2 Actinopterygill, 23 Branchiopoda, 9 Chlorophyceae, 6 Macrophytes). Because toxicity data of Cd belongs to 4 classes in taxonomical classification, acute and chronic EPC (11.07 ${\mu}g/l$ and 0.034 ${\mu}g/l$, respectively) was calculated according to SEM technique. These values were included in the range of international EPCs. This study would be useful to establish the ecological standard for the protection of aquatic ecosystem in Korea.