口服二巯基丙磺酸钠对亚急性汞中毒大鼠防治效果的实验研究

给大鼠腹腔注射氯化汞溶液（０．５μｍｏｌＨｇ／ｋｇ体重），并同时经口投与０．１ｍｍｏｌ／ｋｇ的ＤＭＰＳ，每天一次，连续５天；或给大鼠腹腔注射氯化汞溶液（２．０μｍｏｌＨｇ／ｋｇ体重），每天一次，连续５天后再经口投与３次０．２ｍｍｏｌ／ｋｇ的ＤＭＰＳ，观察口服ＤＭＰＳ对尿汞和肝肾汞含量以及尿ＡＬＰ和尿ＮＡＧ酶活性的影响。实验结果显示口服ＤＭＰＳ能够促进染汞大鼠的尿汞排泄，降低肝脏、肾皮质的汞含量，减     

硒、镉对小鼠大脑脂质过氧化作用的交互影响

昆明种雄鼠７０只，体重１８～２４ｇ，随机分为５组，每天分别给予腹腔注射０．０５、０．１０ｍｇ／ｋｇ硒，０．２３ｍｇ／ｋｇ镉，０．１０ｍｇ／ｋｇ硒＋０．２３ｍｇ／ｋｇ镉，对照组给予等体积的生理盐水，实验期５０天。末次注射２４ｈ后断头取脑，分离脑区（小脑、脑桥、四叠体、丘脑、皮质），加０．２５ｍｏｌ／Ｌ蔗糖制匀浆，取上清液测定ＧＳＨ和ＭＤＡ含量。结果显示，各组脑组织ＧＳＨ含量都呈降低趋势，单纯镉组脑组织ＭＤＡ含量显著增高，硒具有降低镉致脂质过氧化代谢产物生成增加的作用，但其自身也可使脑组织的ＧＳＨ消耗增加。     

刺梨利康饮对慢性汞中毒脂质过氧化损害的拮抗作用

用８３７－４９μｍｏｌ／Ｌ 含汞水饲养大鼠８ 周,复制出慢性汞中毒模型,然后分别自由饮用含维生素Ｃ６８１２－７６μｍｏｌ／Ｌ 的利康饮和ｉｐ １２５ｍｇ／ｋｇ 二巯基丙磺酸钠（ＤＭＰＳ）３ 周,探讨利康饮和ＤＭＰＳ 对慢性汞中毒大鼠尿汞排泄和脂质过氧化损害的影响。结果发现,慢性汞中毒引起血清、肝、脑和肾还原型谷胱甘肽（ＧＳＨ） 含量显著降低,血清、肝、脑和肾丙二醛（ ＭＤＡ） 含量、尿蛋白含量及尿碱性磷酸酶（ＡＫＰ） 活性显著升高;利康饮可显著增加尿汞排泄和血清维生素Ｃ 含量,并使慢性汞中毒引起的血清、肝、脑和肾ＧＳＨ 含量显著回升,血清、脑和肾ＭＤＡ 含量、尿蛋白含量及尿ＡＫＰ 活性显著回降;ＤＭＰＳ 虽有明显促进尿汞排泄效果和使血清ＭＤＡ 含量显著回降的作用,但对慢性汞中毒引起的其它脂质过氧化损害指标影响不明显。结果表明,刺梨利康饮具有一定排汞效果,并对慢性汞中毒引起的机体抗氧化功能降低和脂质过氧化损害具有明显拮抗作用。     

硒多糖、亚硒酸钠对大鼠血硒浓度和肝细胞色素P_(450)单加氧酶系的影响

研究了一次和连续７天腹腔注射硒多糖、亚硒酸钠对大鼠血硒浓度及肝细胞色素Ｐ４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响；并比较了硒多糖与亚硒酸钠的作用。结果表明：一次腹腔注射Ｓｅ０．６ｍｇ／ｋｇ体重的硒多糖和亚硒酸钠后，血硒浓度迅速增加，在注射后２小时血硒浓度达到高峰，随后血硒浓度逐渐下降。亚硒酸钠在大鼠体内的吸收和排出均较硒多糖快。连续７天腹腔注射０．２ｍｇ／ｋｇ体重剂量硒多糖和亚硒酸钠后，硒多糖和亚硒酸钠组大鼠血硒浓度分别为对照组的２．６倍和２．１倍，其中硒多糖组的血硒含量显著高于亚硒酸钠组（Ｐ＜０．０５）；硒多糖和亚硒酸钠在体内、外均降低肝细胞色素Ｐ４５０、ｂ５的含量，抑制ＧＳＴ的活性，硒多糖的作用尤为显著，分别为对照组的５７％、７０％和６２％（Ｐ＜０．０５）。两种硒化合物对ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶无明显影响。硒多糖和亚硒酸钠均能显著增强ＧＳＨ－Ｐｘ的活性（Ｐ＜０．０５）。     

甲基汞诱发大鼠肾脏脂质过氧化作用的探讨

采用ＴＢＡ及ＤＴＮＢ比色法，测定不同染毒时间和染毒剂量，甲基汞对大鼠肾脏丙二醛（ＭＤＡ）含量及谷胱甘肽过氧化物酶（ＧＳＨ—ＰＸ）活性的影响。结果发现染毒组ＭＤＡ含量均显著高于对照组（Ｐ＜０．０２～Ｐ＜０．０１），染毒后２４ｈ处死动物，除５．０ｍｇ／ｋｇ·ｗｔ组ＭＤＡ含量显著低于对照组外（Ｐ＜０．００１），其余各剂量组ＭＤＡ含量均分别高于各自的对照组（Ｐ＜０．０１～Ｐ＜０．０５）。另外，雌性大鼠肾脏ＧＳＨ－Ｐｘ活性于染毒后２４ｈ、７２ｈ显著低于对照组（Ｐ＜０．００１，Ｐ＜０．０１）。     

β-胡萝卜素对二甲基亚硝胺致大鼠脂质过氧化的影响

探讨了给予二甲基亚硝胺（ＮＤＭＮ），同时补充β－胡萝卜素（β－Ｃ）后，大鼠体内抗氧化酶活性和脂质过氧化物含量的变化。结果显示，一定剂量的ＮＤＭＮ可使大鼠血红细胞、肝肾匀浆ＳＯＤ活性和全血ＧＳＨ－Ｐｘ活性下降（Ｐ＜０．０５），血清和肝ＭＤＡ和血清ＲＯＯＨ产生增多（Ｐ＜０．０５）。添加β－Ｃ（２５ｍｇ／ｋｇ）后，ＳＯＤ和ＧＳＨ－Ｐｘ活性均比单纯ＮＤＭＮ组有明显提高（Ｐ＜０．０５）。ＭＤＡ和ＲＯＯＨ含量明显低于ＮＤＭＮ组（Ｐ＜０．０５）。提示自由基和脂质过氧化反应可能也是ＮＤＭＮ及其它亚硝胺致癌的途径之一；一定剂量的β－Ｃ可对抗ＮＤＭＮ引起的自由基和脂质过氧化。     

放射性^153Sm—EDTMP对动物及人血细胞影响的研究

目的：探讨骨肿瘤治疗药物１５３Ｓｍ－ＥＤＴＭＰ对血细胞的影响。方法：用小鼠、Ｗｉｓｔａｒ大鼠和大白兔作实验。给小鼠注射的ＥＤＴＭＴ、１５３Ｓｍ－ＥＤＴＭＰ的量相当于人用量的２０００倍、２０倍，观察化学毒性和放射损伤反应。给大鼠和大白兔注射１５３Ｓｍ－ＥＤＴＭＰ的剂量相当于人用量的３０和７．５倍，于不同时间内取血测定血色素（Ｈｂ）、白细胞（ＷＢＣ）和血小板（ｐｌｔ）计数。按３７ＭＢｑ／ｋｇ注射患者，也于注射后不同时间取血检查血细胞计数的变化。结果：ＥＤＴＭＰ、１５３Ｓｍ－ＥＤＴＭＰ剂量分别大于人用量的２０００、２０倍时，未发现动物有化学毒性和放射损伤反应。给于１５３Ｓｍ－ＥＤＴＭＰ的剂量大于人用量的３０倍时，用药后第１天和第７天，动物的白细胞和血小板计数均有降低（Ｐ＜０．０５），但１６天以后恢复到正常。７天和３０天时，９３例患者的血色素、白细胞、淋巴细胞计数与治疗前比较，均无显著性差异（Ｐ＞０．０５）。７天时血小板有减少，３０天以后已恢复到正常。结论：按３７ＭＢｑ／ｋｇ的剂量注射人体，１５３Ｓｍ－ＥＤＴＭＰ对患者的血细胞（主要是血小板）有轻微影响，但１月以后可恢复到正常。使用比较安全。     

锰对仔鼠血液,脑及睾丸组织中微量元素的影响

为研究大鼠孕期染锰后对其仔鼠血液、脑及睾丸组织中微量元素的影响,将妊娠雌性大鼠随机分为３组,腹腔注射氯化锰,剂量分别为０、７．５和１５ｍｇ／ｋｇ,测定出生２０天仔鼠的血液、脑及睾丸组织中锰、锌、铜的含量,结果与对照组比较,１５ｍｇ／ｋｇ染锰组脑及睾丸组织中锰含量明显增高（Ｐ〈０．０１,Ｐ〈０．０５）;血清锌含量两实验组均明显降低（Ｐ〈０．０１）,１５ｍｇ／ｋｇ染锰组脑及睾丸组织中锌含量均明显降低（Ｐ〈０．０１）;１５ｍｇ／ｋｇ染锰组脑组织中铜含量明显增高（Ｐ〈０．０５）。说明孕期染锰后通过胎盘和乳汗转运可影响仔鼠体内锰、锌、铜的代谢,从而对仔鼠神经、生殖系统等产生危害。     

用计算机辅助精子分析系统测定TCDD对大鼠精子运动能力的影响

利用计算机辅助的精子分析系统（ＣＡＳＡ）研究了２,３,７,８—四氯二苯－Ｐ－二口恶口英（ＴＣＤＤ）对大鼠精子运动能力的影响。给２１天龄幼鼠腹腔注射ＴＣＤＤ０．１、１．０和５．０μｇ／ｋｇ,对照组注射等量体积的溶媒。在性成熟后（９０天）,用扩散法收集附睾尾精子,测定其运行速度（ＶＣＬ、ＶＳＬ、ＶＡＰ）、运动方式（ＳＴＲ、ＬＩＮ、ＢＣＦ、ＡＬＨ、ＭＡＤ等）及活动精子的比率（Ｍｏｔ％）。结果表明,ＴＣＤＤ１．０μｇ／ｋｇ组,精子的运动速度明显低于对照组（ＶＣＬＰ＜０．０５;ＶＡＰ、ＶＳＬ、ＢＣＦＰ＜０．０１）,０．５μｇ／ｋｇ时精子的运动速度、及前向性和直线性运动性能均明显降低（Ｐ＜０．０１）,活动精子的比率也明显低于对照组（Ｐ＜０．０１）。本研究结果为ＴＣＤＤ的男性生殖毒理学研究,以及ＣＡＳＡ在男性生殖毒理学研究中的应用提供了进一步参考依据     

甲醛染毒大鼠脂质过氧化水平分析

用不同剂量（５，１０，２０，５０，１００ｍｇ／ｋｇ）甲醛经腹腔注射染毒ＳＤ大鼠后２４小时，以及１０ｍｇ／ｋｇ染毒后２，６，２４小时收集大鼠血和肝脏。对样品的测定结果显示，红细胞ＳＯＤ活性，全血ＧＳＨ－ＰＸ活性，红细胞内谷胱甘肽含量以及血浆与肝组织ＭＤＡ浓度等五项指标与染毒剂量均有不同程度相关，其中红细胞ＳＯＤ对甲醛最为敏感，５ｍｇ／ｋｇ时就比对照组有明显降低，在时间效应关系中可以见到红细胞内ＳＯＤ     

D-青霉胺和二巯基丙磺酸钠对急性汞氧化损伤的影响

目的 研究预投D-青霉胺(DPA)和二巯基丙磺酸钠(DMPS)对急性汞氧化损伤的保护作用,进一步探讨无机汞氧化损伤的作用机制。方法 48只Wistar大鼠随机分成6组。第1组以5ml／kg皮下注射0．9％氯化钠溶液,第2～4组分别皮下注射0．75,1．5,2．5mg／kgHgCl2溶液。第5,6组大鼠分别腹腔注射DMPS、DPA200μmol／kg,2h后再投与2．5mg／kg HgCl2溶液。染毒12h后,收集12h尿样,测定尿汞含量。染毒48h后。切取肾脏和肝脏,测定丙二醛(MDA)和谷胱甘肽(GSH)含量及谷胱甘肽过氧化物酶(GSH-Px)活力。结果DMPS可显著降低肾脏MDA含量,而DPA对肾脏MDA含量没有影响。DMPS和DPA对肝脏MDA的变化没有影响。DMPS和DPA两干预组在肾脏和肝脏中GSH含量和GSH-Px活力都明显高于2．5mg／kg染汞组,差异有显著性。DPA能显著降低肾脏汞的含量。结论 DMPS可显著减轻汞在肾脏的氧化损伤,但对肝脏没有影响。DPA对汞在肾脏和肝脏氧化反应都没有影响。DMPS能减少肾脏和肝脏GSH的耗竭,而给予DPA只能防止肾脏GSH的耗竭,对肝脏GSH影响不大。DMPS和DPA能防止GSH-Px耗竭。DPA可减少汞在肾脏的蓄积量,致使汞分布到其他组织器官中,而DMPS不能引起汞的这种分布。     

BSO、GSH、VC和DMPS对汞肾毒性影响的实验研究

目的探讨一次染汞的肾脏毒性作用并观察2氨基4(S丁基磺酰亚氨)丁酸(BSO)、还原型谷胱甘肽(GSH)、维生素C(VC)和二巯基丙磺酸钠(DMPS)预处理对汞肾脏毒性的影响。方法Wistar大鼠64只,随机分成8组。第1组为对照组,第2～4组为低、中、高剂量染汞组,分别皮下注射0.75、1.5和2.5mg kg的氯化汞溶液,第5～8组为预处理干预组。BSO预处理组先腹腔注射BSO0.5mmol kgbw,4h后皮下注射0.75mg kgHgCl2溶液。其他3个预处理组中,先分别腹腔注射GSH3mmol kg,VC4mmol kg或DMPS200μmol kgbw,2h后皮下注射2.5mg kgHgCl2溶液。注射容量均为5ml kgbw。对照组皮下注射生理盐水。注射12h后收集大鼠12h尿液,采集血液,分离血清,切取肝脏和肾皮质样品。测定肝脏、肾皮质和尿中汞含量;尿NAG、ALP、LDH活性和尿蛋白,血清尿素氮(BUN)含量。结果染汞后肝、肾皮质和尿汞含量随染汞剂量加大而逐渐增加。肾皮质汞含量有明显的剂量-效应关系,高剂量组肝汞含量显著高于中低剂量组和对照组。中高剂量组尿汞含量显著高于对照组。BSO预处理组和单纯0.75mg kgHgCl2组比,使肝汞含量增加,肾皮质和尿汞含量降低。GSH、VC和DMPS预处理组肝汞含量显著低于单纯2.5mg kgHgCl2组。尿NAG、ALP、LDH活性和尿蛋白、BUN含量随染汞剂量加大而升高,且2.5mg kgHgCl2组显著高于对照组、0.75和1.5mg kg HgCl2组。BSO预处理组尿NAG、ALP活性和尿蛋白、BUN含量显著高于单纯0.75mg kgHgCl2组和对照组。GSH、VC和DMPS预处理组和单纯2.5mg kgHgCl2组相比,尿NAG、ALP、LDH活性和尿蛋白、BUN含量显著降低。结论随着染汞剂量增加,肝脏、肾皮质和尿汞含量也增加。BSO预处理可增强汞的肾脏毒性作用,而GSH、VC和DMPS预处理则对汞的肾脏毒性具有一定的拮抗作用。     

Mobilization of mercury by DMPS in occupationally exposed workers and in model experiments on rats: evaluation of body burden

The aim of the study was to evaluate the efficacy of DMPS (sodium-2,3-dimercapto-1-propane sulfonate) (Dimaval) administration for mobilizing mercury from the body in occupationally exposed people and experimental animals. Two doses of DMPS were administered at a 24-h interval to: (a) groups of people occupationally exposed to merkury--workers of the chloralkali industry (n = 43), and dentists (n = 12), (b) non-exposed individuals (n = 20), and (c) rats chronically exposed to mercury vapour at the concentration of 0.8 mg/m3 Hg degree (6 h/day, 5 days/week) for 15 weeks. In an out-patient mobilizing test, the urinary excretion of mercury 48 h after the administration of the first dose reached 1513 micrograms in the group of industrial workers, 132.6 micrograms in dentists, and 3.78 micrograms in controls. In rats, two consecutive doses of DMPS decreased kidney content of mercury by about 30% and 50% after oral and intraperitoneal administration, respectively. Kidney mercury burden was calculated on the basis of the data from animal and human studies of the mobilization of mercury via urine after DMPS treatment: 61, 2800 and 28,000 ng/g in controls, dentists and workers, respectively. It was estimated that two doses of DMPS mobilized 17-20% (after oral administration) and 25-30% (after intramuscular administration) of kidney mercury burden, both in the control and exposed subjects.     

Effects of BSO, GSH, Vit-C and DMPS on the nephrotoxicity of mercury

OBJECTIVE: To study the effects of BSO, GSH, Vit-C and DMPS on the nephrotoxicity of mercury. METHODS: The rats in groups 1, 2 and 3 were sc injected with 0.75, 1.5 and 2.5 mg/kg HgCl2, respectively. Fourth group rats were ip injected with 0.5 mmol/kg BSO and 4h later sc administrated with 0.75 mg/kg HgCl2. The rats in groups 5, 6 and 7 were ip injected with 3 mmol/kg GSH, 4 mmol/kg Vit-C, 200 micromol/kg DMPS, respectively, and 2 h later sc administrated with 2.5 mg/kg HgCl2. Eighth group rats were sc injected with saline as a control. Mercury concentrations in the liver, renal cortex and urine, urinary NAG, ALP, LDH activities, protein and BUN contents were determined. RESULTS: Urinary NAG, ALP activities, protein and BUN contents in the rats of BSO pretreatment group were significantly higher than that of 0.75 mg/kg HgCl2 alone group and control group. As compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly. CONCLUSION: BSO pretreatment could enhance the renal toxicity of mercury and GSH, Vit-C and DMPS pretreatment had antagonistic effects on nephrotoxicity of mercury.     

亚急性汞中毒大鼠脊髓及背根神经节TNF-α表达与药物干预研究

目的观察亚急性汞中毒大鼠脊髓和背根神经节(DRG)肿瘤坏死因子-α(TNF-α)的表达。方法雄性SD大鼠40只,体重180～220g,分为7组;对照组(10只)经口灌胃生理盐水(NS),2ml/次,1次/d;A、B、C、D、E、F组(各5只)经口灌胃HgCl2溶液,1次/d。A、B、C组为17mg/kg,D、E、F组为8.5mg/kg。7组均连续灌胃18～22d。染汞组动物出现汞中毒症状后,处死A、D组和对照组各5只大鼠。随后B、E组用二巯丙磺钠注射液(DMPS)按28mg/kg腹腔注射驱汞2个疗程(驱汞3d,休息4d为1个疗程);C组用DMPS+己酮可可碱(按29.22mg/kg经口灌胃,1次/d,共14d);F组腹腔注射NS1ml/次,方法同DMPS。实验结束后处死全部动物,灌注固定后,取出脊髓L5-6节及L5、L6两侧DRG并制成病理切片。用免疫组化SABC法测定DRG和脊髓TNF-α表达水平。结果染毒组大鼠脊髓和DRG内TNF-α平均灰度均显著低于对照组;阳性反应物平均面积均显著高于对照组(P0.05);B、E组用DMPS驱汞2个疗程及F组腹腔注射NS2个周期后均未见TNF-α表达显著减弱,C组(DMPS+已酮可可碱)脊髓和DRG内TNF-α平均灰度显著提高,平均面积减少(P0.05)。结论亚急性HgCl2中毒大鼠脊髓和DRG内TNF-α表达显著增强,SMPS联合已酮可可碱能够有效抵制TNF-α表达。     

口服二巯基丙磺酸钠驱汞试验的研究

使用ＤＭＰＳ（一次口服３００ｍｇ）对龋齿充填者、口腔科技师和医师以及含汞皮肤洗剂生产和使用者共５组不同的汞接触人群以及相应的３个对照组进行了驱汞试验。分别收集投药前６小时和投药后６小时的全部尿样，用冷原子发生器原子吸收分光光度法测定尿汞含量。结果显示５组接汞人群无论投药前或投药后，尿汞均值均明显地高于相应的对照组；自身比较，服药后６小时尿汞排泄量也均显著增加。５组接汞人群用药后尿汞排泄比投药前分别增加了２４、８７、４８、４４和８６倍；相应的３个对照组也分别增加了１８、３４和３７倍。结果提示，口服ＤＭＰＳ是一种很好的驱汞方法，有助于汞中毒的预防、诊断和治疗。     

Evaluation of the protective activity of 2,3-dimercaptopropanol and sodium 2,3-dimercaptopropane-1-sulfonate on methylmercury-induced developmental toxicity in mice

The embryotoxic and teratogenic effects of methylmercury in experimental animals have been established by several investigators. The protective activity of 2,3-dimercaptopropanol (BAL) and sodium 2,3-dimercaptopropane-1-sulfonate (DMPS, a chelator used in the treatment of inorganic and organic mercury) on methylmercury chloride (MMC)-induced maternal and developmental toxicity in mice has been evaluated in the present study. BAL and DMPS were administered subcutaneously or by gavage to pregnant mice immediately after a single oral administration of 30 mg MMC/kg given on day 10 of gestation and at 24, 48, and 72 h thereafter. Amelioration by BAL and DMPS of MMC embryo/fetotoxicity was assessed at 15, 30, and 60 mg/kg/day and at 90, 180, and 350 mg/kg/day, respectively. Treatment with BAL did not ameliorate the maternal toxicity or the developmental toxicity of MMC observed in the mouse. In contrast, DMPS at 90, 180, and 360 mg/kg/day significantly reduced the maternal lethality of MMC, whereas treatment with 180 and 360 mg DMPS/kg/day showed significant protective activity against MMC-induced embryotoxicity and teratogenicity. Based on the present findings, DMPS might be a useful chelator against the maternal and developmental toxicity induced by methylmercury.     

Metabolic alterations in liver and kidney following chronic methyl mercury treatment and withdrawal

Daily intraperitoneal injection of methyl mercury (0.4 and 4 mg/kg) for 45 days to rats decreased liver size without producing any significant change in adrenal, cardiac, renal, testicular, and body weight. Chronic exposure to either dose of this organomercurial augmented the activities of renal and hepatic pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-diphosphatase and glucose 6-phosphatase, elevated the concentration of blood glucose and urea, as well as reduced liver glycogen content. As expected, the degree of alterations in various parameters studied was greater in animals which were injected with the higher dose (4 mg/kg) of methyl mercury. Furthermore, withdrawal of treatment for 28 days in rats that had previously been given the 4 mg/kg daily dose of methyl mercury for 45 days, generally failed to reverse the observed metabolic changes in hepatic and renal carbohydrate metabolism. Our results suggest that the gluconeogenic potential of both liver and kidney is markedly enhanced in animals chronically treated with methyl mercury and that the metabolic alterations persist even after a 28 day period of abstinence from heavy metal treatment.     

Delayed biochemical changes induced by mercury intoxication are prevented by zinc pre-exposure

This work evaluated the delayed effects of mercury and the effectiveness of zinc in preventing such effects. Pups were pre-treated with 1 daily dose of ZnCl₂ (27 mg/kg/day, by subcutaneous injections) from 3rd to 7th postnatal day and received 1 daily dose of 5 mg/kg of HgCl₂, for 5 subsequent days (8-12 days old). Animals were euthanized 21 days after the end of Hg-exposure. Porphobilinogen-synthase activity as well as zinc and mercury contents was determined in the liver and kidneys. Alanine aminotransferase, aspartate aminotransferase and lactic dehydrogenase activities as well as urea, creatinine and glucose levels were analyzed in plasma or serum. Some animals were considered more sensitive to mercury, since they did not recover the body weight gain and presented an increase of renal and hepatic mercury content, urea and creatinine levels; a decrease in renal porphobilinogen-synthase and alanine aminotransferase activities, as well as a decrease in the liver and an increase in kidney weights. Some animals were considered less sensitive to mercury because they recovered the body weight and presented no biochemical alterations in spite of mercury in the tissues. Zinc prevents partially or totally the alterations caused by mercury even those that persisted for a long time after the end of exposure. These findings suggest that there is difference among the animals regarding the sensitivity to mercury.