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

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*

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*

Thirty five male Sprague-Dawley rats were treated with cadmium chloride solution ranging from 0.2 to 3.2mg CdCl2/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 blood were examined. Tissue cadmium concentration was highest in liver, followed by in kidney, heart, lung and testis. Cadmium bound to metallothionein(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(microgram MT/microgram Cd) was greater in liver than in kidney, and reverse to tissue concentration or exposed dose of cadmium.
Animals ; Cadmium Chloride ; Cadmium* ; Heart ; Humans ; Kidney ; Liver ; Lung ; Male ; Metallothionein* ; Rats* ; Rats, Sprague-Dawley ; Testis

BACKGROUND: Cadmium, an environmental pollutant, has implicated in the pathogenesis of cardiovascular diseases. Biochemical and pathophysiological changes characterized by arterial hypertension, accelerated cholesterol plaque formation on arterial walls, cardiac conduction abnormalities, and reduction in myocardial contractility have been reported in experimental animals chronically exposed to low concentration of cadmium. This study was undertaken to evaluate the ultrastructural changes of the cardiac muscle in rats exposed to cadmium chloride and to ascertain whether these changes are modified after discontinuation of cadmium feeding. METHOD: Wistar strain rats(body weight 200~250gram) were injected intraperitoneally once weekly with 3.75mg/kg of cadmium chloride for 10 weeks and were sacrificed at 1 day, 1 week and 2 weeks after discontinuation of cadmium administration. RESULT: Ultrastructure if rat cardiac muscle fibers after cadmium administration revealed that mitochondria were increased in number and their cristae were severely damaged. Cardiac myofibrils and myofilaments were reduced. Z-disc were partly dislocated and A-bands and I-bands were not clearly defined. Irregularly arranged intercalated disc and disrupted sarcolemma were also found. These structural alterations resulting from cadmium feeding were partly reduced after removal of cadmium exposure for 2 weeks. These structural alterations resulting from cadmium feeding were partly reduced after removal of cadmium exposure for 2 weeks. CONCLUSIONS: It is suggested that exposure to cadmium chloride was associated with cardiac ultrastructural changes which might be responsible for physiologic abnormalities and these alterations may be partly reversible after discontinuation of cadmium administration.
Animals ; Cadmium Chloride* ; Cadmium* ; Cardiovascular Diseases ; Cholesterol ; Hypertension ; Mitochondria ; Myocardium* ; Myofibrils ; Rats* ; Sarcolemma

OBJECTIVE: To verify the separate and combined effects of cadmium and nickel on blood pressure in rats. METHODS: Following the daily administration of cadmium chloride(CdCl2) and nickel chloride(NiCl2) to rats both individually and in combination with intraperitoneal injection method for one week, systolic blood pressure of the tail was measured at 1 day and 5, 10, 20, 30 days after administration. Each substance was injected into the rats with 0.1 mg/kg bw and 1.0 mg/kg bw concentration. RESULTS: After 0.1 mg/kg bw CdCl2 was injected, a statistically significant difference was found as compared with the control group(only saline) after 1, 5 and 10 days. After 0.1 mg/kg bw NiCl2 was injected, a statistically significant difference was not found compared with the control group. After 0.1 mg/kg bw CdCl2 and 0.1 mg/kg bw NiCl2 were injected simultaneously, a statistically significant difference was found as compared with the control group after 1, 5 and 10 days and compared with 0.1 mg/kg bw CdCl2 group after 5 days and as compared with 0.1 mg/kg bw NiCl2 group after 5 and 10 days. After 1.0 mg/kg bw CdCl2 was injected, a statistically significant difference was found as compared with the control group after 1, 5, 10 and 20 days. After 1.0 mg/kg bw NiCl2 was injected, a statistically significant difference was found as compared with the control group after 1 day and 5 days. After 1.0 mg/kg bw CdCl2 and 1.0 mg/kg bw NiCl2 were injected in combination, a statistically significant difference was found after 1, 5, 10, 20 and 30 days as compared with 1.0 mg/kg bw CdCl2 after 10, 20 and 30 days and as compared with 1.0 mg/kg bw NiCl2 after 5, 10, 20 and 30 days. CONCLUSION: It was found that the effect of CdCl2 on blood pressure was much more than NiCl2 and a high concentration CdCl2 and NiCl2 in combination delayed the recovery of blood pressure.
Animals ; Blood Pressure* ; Cadmium Chloride ; Cadmium* ; Injections, Intraperitoneal ; Nickel* ; Rats* ; Tail