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Original Articles
- Comparative Hepatotoxicity Assessment of Cadmium and Nickel with Isolated Perfused Rat Liver(IPRL).
- Bong Suk Cha, Seung Jun Wang, Sei Jin Chang, Jung Woo Lee
- Korean J Prev Med. 2000;33(1):117-124.
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Abstract
PDF - 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. -
Summary
- Metallothionein induction and its protective effect in liver and kidney of rats exposed to cadmium chloride.
- Nam Song Kim, Jae Hyung Lee, Dai Ha Koh, No Suk Ki, In Dam Hwang
- Korean J Prev Med. 1991;24(3):287-304.
- 2,162 View
- 21 Download
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Abstract
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- 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.
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