No abstract available.
Animals ; Cadmium Chloride* ; Cadmium* ; Nasal Mucosa* ; Rats*

OBJECTIVES: This research was intended to verify hepatic effect of simutaneously combined exposure of nickel chloride and cadmium chloride with IPRL(Isolated Perfused Rat Liver) method. METHODS: AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity and oxygen consumption rate were used as the indicator of viability. 300(+/-50) g weighted rats were allocated randomly to each group (control group, 50 microM 200 microM separately exposure group of NiC1, and CdC1, simultaneously combined exposure group of NiC1 and CdC1) by 5, totally 35. Buffer which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. In order to verify difference among groups, two way repeated ANOVA was used. With comparing mean summation of separate exposure group with mean of simultaneous exposure group, possibility that combined effect could be synergistic effect was verified. RESULTS: AST, ALT, LDH increased in both of separate exposure group and simultaneous exposure group. Perfusion flow rate and oxygen consumption rate decreased but statistically significant difference among groups was not found, In each exposure group, AST, ALT, LDH, oxygen consumption rate of simultaneous exposure group increased more than sum of separate exposure group after any sampling time. CONCLUSIONS: It was found that simultaneous combined effect could be synergistic effect through the biochemical indicator of hepatotoxicity.
Animals ; Cadmium Chloride ; Cadmium* ; Liver ; Nickel* ; Oxygen Consumption ; Perfusion ; Rats*

In order to elucidate the mechanism of oxidative damage of cadimu(Cd) on culturedmouse preimplantation embyors.The embryotoxocity of Cd was examined after cultured mouse preimplantation embryoswere exposed to various concentrations of CdCl2. In addition, the protected effect of antioxidant,catalase against Cd-induced embryotoxicity was investigated.CdCl2 decreased the development of cultured mouse preimplantation embryos in dose andtime-dependent manners, and also oxidative damage was involoved in Cd-induced embryotoxicityin mouse preimplantation embryos by the prevention of catalase on Cd-induced toxicity.
Animals ; Blastocyst ; Cadmium Chloride ; Cadmium* ; Catalase ; Embryonic Structures* ; Mice

In order to elucidate the mechanism of oxidative damage of cadimu(Cd) on culturedmouse preimplantation embyors.The embryotoxocity of Cd was examined after cultured mouse preimplantation embryoswere exposed to various concentrations of CdCl2. In addition, the protected effect of antioxidant,catalase against Cd-induced embryotoxicity was investigated.CdCl2 decreased the development of cultured mouse preimplantation embryos in dose andtime-dependent manners, and also oxidative damage was involoved in Cd-induced embryotoxicityin mouse preimplantation embryos by the prevention of catalase on Cd-induced toxicity.
Animals ; Blastocyst ; Cadmium Chloride ; Cadmium* ; Catalase ; Embryonic Structures* ; Mice

Tolerance to several toxic effects of cadmium, including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicity and renal toxicity. Three groups of rats (A, B, C), each consisting of 16 rats, were studied and each group was divided into four subgroups (1, 2, 3, 4), 4 rats for each subgroup. Rats were subcutaneously pretreated with saline (A), CdCl2(0.5 mg/kg, B), and ZnCl2 (13.0 mg/kg, C) during time periods of 1~6 weeks. At the end of the period, rats were challenged with CdCl2 (3.0, 6.0 and 9.0 mg/kg, ip). After giving the challenge dose, cadmium and metallothionein (MT) concentrations were determined and also observed the histologic change in liver and kidney. The concentration of cadmium in liver and also observed the increased dose-dependently to the challenge dosage. These data indicate the kidney is a major target organ of chronic cadmium poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play and important role in the nephrotoxicity observed in response to long-term exposure to cadmium. In addition, histologic examination of group A2, A3 and A4 revealed moderate to severe cadmium toxicity, evidenced by infiltration of inflammatory cells, cell swelling, pyknosis, enlarged sinusoids and necrosis in liver, and tubule cell necrosis and degeneration in kidney. However, MT concentrations in liver and kidney were increased by the pretreatment of CdCl2 and ZnCl2 and their morphological findings were not significantly changed, comparing with control group. Higher MT concentration in liver and kidney observed in the pretreated groups constitutes a plausible explanation of the protective effects of pretreatment against the cadmium toxicity after challenge dosing.
Animals ; Cadmium Chloride* ; Cadmium Poisoning ; Cadmium* ; Kidney* ; Liver* ; Metallothionein* ; Necrosis ; Rats* ; Zinc

OBJECTIVES: To evaluate the protective effects of glutathione (GSH) on the cytotoxicity of mercurial compounds(CH3HgCl, HgCl2) or cadmium chloride(CdCl2) in EMT-6 cells. METHODS: The compounds investigated were CH3HgCl, HgCl2, CdCl2, GSH, buthionine sulfoximine(BSO), L-2-oxothiazolidine-4-carboxylic acid(OTC). Cytotoxicity analysis consist of nitric oxide(NO) production, ATP production and cell viability. RESULTS: Mercurial compounds and cadmium chloride significantly decreased cell viability and the synthesis of NO and cellular ATP in EMT-6 cells. GSH was not toxic at concentrations of 0 - 1.6 mM. In the presence of GSH, mercurial compounds and cadmium did not decrease the production of ATP and nitrite in EMT-6 cells. The protective effects of GSH against the cytotoxicity of mercurial compounds and cadmium depended on the concentration of added GSH to the culture medium for EMT-6 cells. We evaluated the effects of intracellular GSH level on mercury- or cadmium-induced cytotoxicity by the pretreatment experiments. Pretreatment of GSH was not changed NO2- and ATP production, and pretreatment of BSO was decreased in dose- and time-dependent manner. Pretreatment of OTC was increased NO2- and ATP production in dose- and time-dependent manner. Because intracellular GSH level was increased by OTC pretreatment, the protective effect on mercury- and cadmium-induced cytotoxicity was increased. CONCLUSIONS: These results indicated that sulfhydryl compounds had the protective effects against mercury-induced cytotoxicity by the intracellular GSH levels.
Adenosine Triphosphate ; Cadmium Chloride ; Cadmium* ; Cell Survival ; Glutathione* ; Mercuric Chloride ; Nitric Oxide ; Sulfhydryl Compounds

OBJECTIVES: To investigate the role of superoxide dismutase(SOD) in the pathogenesis of cadmium-induced acute nephrotoxicity. METHODS: Rats treated with a single intraperitoneal injection of cadmium(as CdCl2, 1 mg/kg) were included in the cadmium-treated group; the control group comprised untreated rats. 24-hour urine samples were obtained prior to sacrifice on days 1, 2, 4, 8 and 16(N = 10 per group), respectively. The activity of SOD and concentration of cadmium were measured in the homogenates of the renal cortex. Nephrotoxicity indices such as N-acetyl-beta-D-glucosaminidase(NAG) activity, total protein, and 24-hour urine volume, and the cadmium concentrations in the urine were measured. RESULTS: The cadmium injection caused a significant increase of cadmium concentration in the renal cortex on days 1 and 2, and in the urine on days 1, 2 and 4. The NAG activities and total protein concentrations in urine were significantly increased on days 1, 2 and 4, and on days 1, 4 and 8, respectively. The peak values of NAG activity and total protein in urine were observed on days 1 and 4, respectively. A significant decrease of 24- hour urinary volume was induced on day 1. Renal SOD activity was significantly inhibited on day 1. Finally, on day 8, SOD activity was significantly increased and all nephrotoxicity indices except urinary total protein returned to the control level. CONCLUSIONS: These results suggest that cadmium induces initial depression of SOD enzyme activities in the renal cortex followed by a later activation, and that the initial depression of this enzyme plays an important role in mediating the proteinuric injury of cadmium-induced acute nephrotoxicity.
Acetylglucosaminidase ; Animals ; Cadmium ; Cadmium Chloride ; Depression ; Injections, Intraperitoneal ; Negotiating ; Rats* ; Superoxide Dismutase* ; Superoxides*

BACKGROUND: To investigate the relationship between malondialdehyde in renal cortex and Urinary NAG activity of rats exposed to cadmium. METHODS: Rats were treated with a single intraperitoneal injection of cadmium (as CdCl2, 1 mg/kg) for cadmium-treated group and 24-hour urine were obtained prior to sacrifice on days 1, 2, 4, 8 and 16 (N=10 per each group), respectively. The concentration of malondialdehyde by thiobarbituric acid reaction and cadmium were measured in the homogenates of renal cortex. Nephrotoxocity indices such as N-acetyl--D-glucosaminidase (NAG) activity, total protein, and 24 hours urine volume, and cadmium concentration were measured in the urine. RESULT: The cadmium injection caused significant increase of cadmium concentration in the renal cortex on days 1 and 2, and in urine on days 1, 2 and 4. NAG activity and total protein concentration in urine were significantly increased on days 1, 2 and 4, and on days 1, 4 and 8, respectively. The peak values of NAG activity and total protein in urine were observed on days 1 and 4, respectively. Significant decrease of 24 hours urinary volume was induced on day 1. These results indicated that cadmium induced acute nephrotoxicity in the rats. Urinary NAG activity was changed earlier and at a higher rate than urinary total protein, which suggest that NAG activity is a more sensitive biological index in terms of early diagnosis of cadmium-induced nephrotoxicity. Renal MDA concentration was significantly increased on day 2 and on day 4, and on day 8, MDA concentration and nephrotoxicity indices except urinary total protein were returned to control level. CONCLUSION: Based on the results obtained as above, it was concluded that the malondialdehyde in renal cortex, product of lipid peroxidation was related with the changes of urinary NAG activity indicating nephrotoxic injury.
Animals ; Cadmium Chloride ; Cadmium* ; Early Diagnosis ; Injections, Intraperitoneal ; Lipid Peroxidation ; Malondialdehyde* ; Rats*

Among the environmental pollutants, cadmium and lead compounds may impair human health. These compounds may inhibit the biological metabolic function of bum.an 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 chloride acetate. Cadmium chloride (8.8 mg/kg, in saline 10 ml) and lead acetate (15 mg/kg, in saline 10 ml) were administered by lntraperitoneal 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.
Animals ; Cadmium Chloride* ; Cadmium* ; Environmental Pollutants ; gamma-Globulins ; Hematocrit ; Humans ; Leukocyte Count ; Rats* ; Sheep ; Spleen

OBJECTIVES: It is the objective of this study to compare hepatotoxicity of nickel chloride and cadmium chloride with each other through IPRL(Isolated Perfused Rat Liver) method. METHODS: Biochemical indicator of hepatic function such as AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity. Oxygen consumption rate were used as viability indicator. 300(+/-50) g - weighted rats were allocated randomly to each group(0 micrometer, 50 micrometer, 200 micrometer NiCl2 and CdCl2 exposure) by 5, totally 25. After Krebs-Ringer bicarbonate buffer solution flowed into the portal vein and passed the liver cell, it flowed out of vena cava. Liver was administered with each NiCl2 and CdCl2 of each concentration and observed with buffer solution sampling time. Buffer which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. RESULTS: AST, ALT, and LDH in buffer increased with sampling time much more in CdCl2 exposure group than NiCl2 exposure group in both 50 and 200 micrometer and statistical significance was verified with 2-way repeated ANOVA. Viability was decreased more and more in all substances during passed time. CONCLUSIONS: It is inferred that CdCl2 has stronger hepatotoxicity than NiCl2. IPRL method would be used widely for acute hepatotoxicity when considerating the benefit of it.
Animals ; Cadmium Chloride ; Cadmium* ; Liver ; Nickel* ; Oxygen Consumption ; Perfusion ; Portal Vein ; Rats*