| ObjectiveMercury is an ancient toxicant, is a venenous metal distributed widely in environment. Kidney is a principle target of mercury. Although people have cognizance of the severe harm of mercury and mercuric compound, people ha vent created the similar or higher functional substitutes for them. Mercury and its compounds still have been extensively used in medicine, agriculture and industry. Numerous clinic observations and animal experiments have confirmed the neurotoxic symptom, genital toxicity, embryo toxicity and immune toxicity of mercury, but the investigative materials of its nephrotoxicity is rare and the mechanisms of renal damage induced by mercury is still unclear. So this study established mercury chloride as the research object, to explore the effect of glu-tathione and taurine on acute nephrotoxicity caused by mercury, the effect of glutathione and taurine on renal acute oxidative damage caused by mercury, the dose-effect relation of renal cell apoptosis induced by mercury and the effect of glutathione and taurine on renal cell apoptosis induced by mercury, accordingly, to provide farther academic evidences for the molecular biological mechanism of mercuric renal damage.Methods1. Experimental study on the effect of GSH and taurine on acute nephrotoxicity of mercuryWistar rats were randomly divided into four groups. The rats of control were given subcutaneous injections with 0. 9% saline. The rats in mercuric chloride (HgCl2) group were subcutaneously injected with 2. 5mg HgCl2/kg. Other twogroups of rats were pretreated with 3mmol/kg GSH and 4mmol/kg taurine, respectively and two hours later injected subcutaneously with 2.5mg HgCl2/kg. U-rine activities of NAG, ALP, LDH, urine protein contents and urine mercury level were determined. Serum BUN contents and level of mercury in the renal cortex of rats were measured.2. Study on the effect of GSH and taurine on renal oxidative damage of mercuryWistar rats were randomly divided into four groups. The rats of control group were given subcutaneous injections with 0. 9% saline. The rats in mercuric chloride ( HgCl2) group were subcutaneously injected with 2.5mg HgCl2/kg. Other two groups of rats were pretreated with 3mmol/kg GSH and 4mmol/kg taurine, respectively and two hours later injected subcutaneously with 2. 5mg HgCl2/kg. Urine creatine and mercury contents were determined; mercury level , content of GSH, MDA and GSH-Px in kidney was evaluated.3. The study of the dose-effect relation of renal apoptosis induced by mercuryMice were randomly divided into four groups. The mice of control were given intraperitoneal injections with 0. 9% saline. The different mercuric chloride (HgCl2) group was administrated respectively with 0. 75mg HgCl2/kg, 1.5mg HgCl2/kg and 3.0mg HgCl2/kg. Twenty-four hours later both kidneys were exposed by laparotomyand excised. After longitudinal bisection, the renal cortex was removed by sharp dissection. The larger section of right kidney was fixed in 10% formalin, with immunochemistry to detect apoptosis related gene expression of bcl-2 and bax. The smaller section of right kidney was fixed in 2.5% glutar-aldehyde, with Transmission electron microscope to observe the renal cell apoptosis morphologic changes. The left renal cortex was made of single cell suspend solution, then was fixed in 70% alcohol at 4ct, stained with propidium iodide and the percent of the apoptosis cell was analyzed by Flowcytometry.4. The effect of glutathione and taurine on renal cell apoptosis induced by mercuryMice were randomly divided into four groups. The mice of control were with 0. 9% saline. The mice in mercuric chloride (HgCl2) group were intraperitone-ally injected with 3. Omg HgCl2/kg. Other two groups of rats were pretreated with 3mmol/kg GSH and 4mmol/kg taurine, respectively and two hours later injected with 3. Omg HgCl2/kg. The methods of morphologic changes, apoptosis related gene expression and the percent of the apoptosis cell analysis are similar to the third section.Results1. Ex... |
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