锌金属硫蛋白对镉致肝肾损伤的修复作用研究

目的：探讨锌金属硫蛋白（Zn-MT）对镉所导致的肝肾毒性的修复作用。方法：以小鼠为研究对象，建立镉中毒动物模型，然后经口给予不同剂量的Zn-MT,测定并分析肝、肾组织中脂质过氧化代谢产物丙二醛（MDA）水平、超氧化物歧化酶（SOD）、谷胱甘肽过氧化酶（GSH－Px）活性及电镜下观察肝肾组织形态学变化。结果：Zn-MT可明显降低肝、肾组织中MDA水平，使肝、肾组织中SOD、GSH－Px活力有一定程度的恢复，且上述作用呈明显的剂量－反应关系；电镜下观察到给予Zn-MT后，肝、肾组织形态学病变得到一定程度的恢复。结论：Zn-MT可对镉所致的肝肾组织脂质过氧化损伤起到一定的修复作用。     

电焊工体内脂质过氧化和血清锰水平调查

对含锰电焊各作业工人血清过氧化脂质代谢物（MDA）和红细胞过氧化物歧化酶（SOD）、谷胱甘肽氧化酶GSH－Px、血清Mn水平进行了检测分析,结果表明：锰焊条作业组MDA和血清Mn显高于对照组;而SOD和GSH－Px显低于对照组,电焊工龄与MDA血清Mn呈一定程度正相关,与SOD、GSH－Px呈一定程度的负相关;O^ 和Ⅰ期的电焊工尘肺MDA、SOD和GSH－Px与对照组有显性差异;血清Mn含量与MDA呈一定程度正相关,与SOD与GSH－Px呈一定程度负相关。提示：长期电焊作业工人体内脂质过氧化反应明显增强,电焊作业对人体的危害与细胞膜损伤可能存在密切的关系。     

氟硒镉致大鼠睾丸脂质过氧化及微量元素变化

目的 探讨氟硒镉对大鼠睾丸脂质过氧化及微量元素变化的影响。方法 将氟硒镉经饮水染毒大鼠，10周后检测睾丸中脂质过氧化物（LPO）和谷胱甘肽过氧化物酶（GSH—Px）及镉硒锌铁的含量。结果 与对照组比较，氟、镉组LPO含量明显增高，GSH—Px显著降低，硒组没有明显改变。任意二联及三联时LPO含量较氟硒镉单独组明显降低，GSH—Px明显增高。各实验组硒无明显变化，氟组的镉硒锌铁也无明显改变，镉组的镉、铁显著增高，硒组、氟硒组的锌、铁显著增高，镉硒、氟镉以及氯硒镉组的镉、铁里明显升高。结论 氟、镉可引起大鼠睾丸脂质过氧化作用增强。抗氧化酶活性降低，硒的影响甚微。当三者任意二联时可降低脂质过氧化作用，三联时作用更强。硒可降低镉在睾丸中的蓄积，同时提高硒、锌水平，氟硒镉均可引起睾丸中铁水平升高，并有协同作用。     

氟硒镉对大鼠体内抗氧化酶及微量元素的影响

目的　探讨氟硒镉对大鼠各组织中脂质过氧化物 (LPO)含量和谷胱甘肽过氧化物酶 (GSH Px)活性以及镉硒锌等微量元素含量的影响。方法　采用SD大鼠经饮水染毒 8周 ,实验结束时处死动物测定各组织中LPO和谷胱甘肽过氧化物酶及镉硒锌的含量。结果　氟、硒、镉实验组均可见大鼠血清、肝、肾组织中GSH Px含量与对照组比呈显著降低 ,LPO含量量呈显著增高。其中任意二元素联合组较氟、硒、镉组GSH Px的含量呈明显回升 ,LPO含量量呈明显降低 ,而氟 +硒 +镉组其升高与降低的作用则更明显 ,以至GSH Px、LPO的水平几乎和对照组相同。过量硒和镉能导致肾硒、肝镉成数倍的增长。氟、镉可引起各组织中硒、锌的缺乏 ,硒则可使肝、肾中锌水平普遍提高。氟 +硒、镉 +硒以及氟 +硒 +镉联合可减少肾硒、肝镉的蓄积 ,同时也可减少氟、镉所致锌的损失。结论　提示过量的氟、硒、镉均可促进动物体内脂质过氧化作用增强 ,并抑制GSH Px的活性 ,使机体抗氧化能力降低。但当其中二或三种化学元素共存时 ,可减轻各自所引起的脂质过氧化作用以及对GSH Px的活性的抑制作用 ,同时减轻镉硒在体内的蓄积和氟镉所致引起体内锌水平的降低。     

茶多酚对镉毒性肾损伤的保护作用

目的：研究茶多酚（TP））对镉（Cd)所致肾毒性作用的保护作用。方法：小鼠随机分为对照组，Cd组，Cd TP组，检测血清中尿素氮（BUN），肌酐（Cr)的含量，过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GSH－Px)活性，及肾脏光镜病理结构的变化。结果：与对照组比较，染镉小鼠血清中BUN，Cr均明显升高，小鼠血清中CAT，GSH－Px活性均明显下降，给PT治疗后，与染镉组比较，血清中的CAT，GSH－Px均上升，血清中的BUN，Cr的含量均有下降，且差异具有显著性，光镜结果表明，Cd TP组肾脏曲管上皮浊肿程度，肾小球间质充血程度均轻于Cd组，结论：TP对镉中毒性肾损伤有一定的拮抗作用。     

泛酸钙对全饥饿大鼠脑组织脂质过氧化的影响

目的：探讨泛酸钙对全饥饿大鼠脑脂质过氧化产物（MDA），还原型谷胱甘肽（GSH），谷胱甘肽过氧化物酶（GSH－Px)，超氧化歧化酶（SOD）的影响及可能的脑保护机制，方法：以饥饿SD大鼠为模型，灌胃补充泛酸钙，观察大鼠饥饿后不同时期脑MDA，GSH，GSH－Px及SOD的变化。结果：饥饿后大鼠脑MDA含量明显升高，泛酸钙补充后大鼠脑MDA量在禁食4与7天较饥饿前无明显升,高，与全饥饿对照组比较差异显，泛酸钙对饥饿大鼠脑SOD，GSH－Px活力无影响，但显提高GSH水平。结论：泛酸钙能抑制饥饿大鼠脑的脂质过氧化损伤，其部分作用可能是通过提高GSH水平来实现的。     

实验性镉中毒大鼠尿钙症及其机理的探讨

经皮一次注射镉金属硫蛋白诱发大鼠急性中毒，作为慢性镉中毒之模型，观察中毒大鼠肾皮质的组织病理学改变和脂质过氧化作用，测定尿液主要生化指标变化。结果显示尿总蛋白、葡萄糖含量，ｒ－谷氨酰转移酶、碱性磷酸酶、Ｎ－乙酰－β－Ｄ－氨基葡萄糖苷酶活性均明显增加，尿钙增加较早。结合光镜和电镜下肾近曲小管病损，以及肾皮质脂质过氧化作用加剧，提示肾脏钙代谢紊乱是镉中毒性肾损害的始动因素；脂质过氧化作用是镉中毒性肾损     

α-硫辛酸和牛磺酸对急性镉氧化损伤影响的实验研究

目的探讨α-硫辛酸（LA）和牛磺酸（Tau）对急性镉氧化损伤的影响。方法实验用Wistar大鼠32只,分为4组,第一组为对照组,第二组为单纯染镉组,两组均先腹腔注射生理盐水,2h后分别皮下注射生理盐水和35μmol／kg CdCl2溶液。第三组和第四组为LA和Tau预处理组,先分别腹腔注射175μmol／kg的LA溶液和4mmol／kg的Tau溶液,2h后皮下注射35μmol／kg CdCl2溶液。染毒24h后腹主动脉取血并取肝肾,测定血清乳酸脱氢酶（LDH）、丙氨酸氨基转移酶（ALT）活性,肝、肾皮质中Cd、丙二醛（MDA）、谷胱甘肽（GSH）含量及谷胱甘肽过氧化物酶（GSH—Px）、超氧化物歧化酶（SOD）活性。结果与对照组比较,单纯染镉组的血清LDH、伽活性及肝、肾皮质镉含量显著升高,SOD活性显著下降。肝GSH、MDA含量显著升高,GSH—Px活性显著下降。与单纯染镉组比较,LA和Tau干预组的血清ALT和LDH活性及肝组织Cd含量显著降低,肝GSH—Px活性显著增高。LA干预组的肝MDA含量显著降低,肝、肾皮质SOD活性显著升高。Tau干预组肝GSH含量、肾皮质镉含量显著降低。结论LA和Tau预处理对镉所致急性肝脏氧化损伤有一定拮抗作用。     

氯丙嗪和异搏定对镉毒性的拮抗作用

目的 探讨氯丙嗪（Chlorpromazine，CPZ）和异搏定（Verapamil，Ver）对镉毒性的影响。方法 32只Wis—tar大鼠随机分成4组：对照组、单纯染镉组、氯丙嗪及异搏定干预组。测定肝和肾皮质镉、丙二醛（MDA）、谷胱甘肽（GSH）含量和谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）活性以及尿N-乙酰-β-D氨基葡萄糖苷酶（NAG）和碱性磷酸酶（ALP）活性。结果 单纯染镉组肝、肾皮质MDA、GSH含量和尿NAG和ALP活性显著高于对照组，而。肾皮质SOD活性显著低于对照组。CPZ干预组肝和。肾皮质MDA含量分别为单纯染镉组的75％，78％；肾皮质GSH含量显著低于单纯染镉组，而GSH-Px和SOD活性显著高于对照组和单纯染镉组。Ver干预组肝、肾皮质MDA和肾皮质GSH含量显著低于单纯染镉组，而肾皮质GSH-Px活性显著高于对照组，肾皮质SOD活性显著高于单纯染镉组。2个干预组尿NAG活性显著低于单纯染镉组。结论 CPZ和Ver对镉毒性具有一定的拮抗作用。     

氧自由基在急性镉中毒性肾损伤中的作用

目的探讨氧自由基在急性镉中毒性肾损伤中的作用。方法给大鼠腹腔注射ＣｄＣｌ２（１５μｍｏｌ／ｋｇ）与巯基乙醇（３００μｍｏｌ／ｋｇ）混合液制备急性镉中毒性肾损伤模型，观察染镉后不同时间肾细胞线粒体、胞浆中一系列脂质过氧化指标的变化，同时测定肾皮质镉含量，检测肾功能和肾脏超微结构的改变。结果染镉后２小时肾皮质镉含量已达峰值；超微结构出现改变；氧自由基生成及丙二醛（ＭＤＡ）含量亦显著高于对照组（Ｐ＜０．０１），超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力下降。至染镉后１２小时，氧自由基产生及脂质过氧化反应达到高峰；肾功能损害亦十分明显；线粒体、溶酶体等细胞器严重受损。结论氧自由基大量生成及由此引起的脂质过氧化反应可能在镉对肾组织的损害中起重要作用。     

含镉粉尘治理前后工人尿镉与血镉水平分析

目的 分析某锌粉加工厂含镉粉尘治理前后作业工人尿镉、血镉和尿β2-微球蛋白的变化.方法 对锌粉加工厂粉尘进行治理,对粉尘治理前后84名镉作业工人尿镉、血镉、β2-微球蛋白水平进行自身对照分析.结果 治理后,作业场所锌尘几何均数由3.38mg/m3降至2.22mg/m3,差异有统计学意义(P＜0.01).治理前调查对象的血镉、尿镉几何均数浓度[血镉(2.19±1.19)μg/L,尿镉(1.96±0.74)μg/gCr]明显高于治理后1年[(1.63±0.83)μg/L,(1.25±0.83)μg/g Cr]和治理后2年[(1.36±0.95)μg/L,(0.94±0.72)μg/g Cr],差异有统计学意义(P＜0.01).治理前及治理后1年、2年接触工人尿镉与血镉浓度作相关分析,r=0.466,差异有统计学意义(P＜0.01).结论 粉尘治理能降低低浓度镉作业工人的血镉、尿镉水平,对防止镉中毒效果明显.     

Carcinogenicity of cadmium

Cadmium has been thought to be carcinogenic for these ten years. The present author reviewed 98 papers on its carcinogenicity. Ten papers describing epidemiological studies on cadmium workers, re-evaluated by the present author, do not derive a solid conclusion that cadmium is carcinogenic. However, there still exists a certain probability that cadmium is a weak carcinogenic substance in the human, because of some data on chromosomal aberrations in cadmium workers, tumorigenesis at the site of cadmium injection in animals, and Leydig cell tumor formation in animals given subcutaneous injections of cadmium.     

Reduction in cadmium teratogenesis by prior cadmium exposure

The administration of cadmium 24–48 hr prior to an optimal teratogenic dose reduces both the number and severity of congenital malformations in hamster embryos. Intraperitoneal administration is more effective in inducing this protective effect than is the subcutaneous route. Oral administration of cadmium at the same pretreatment intervals does not seem to afford any protection. It is suggested that this protection is due to the induction of maternal synthesis of a metal-binding protein, possibly metallothionein. The significance of this protective induction as it relates to the possible role of cadmium in human malformations as well as teratogenic testing is discussed.     

Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan

Long-term exposure to cadmium (Cd) causes renal damage in the general population. The maximum allowable urinary Cd concentration, which was calculated from our previous study performed in a Cd-polluted area, was almost the same as the mean urinary Cd concentration of people living in nonpolluted areas. We assessed whether environmental Cd exposure is related to renal dysfunction of people in nonpolluted areas in Japan. Blood and urine samples were collected from 2753 subjects (1105 men and 1648 women) ages over 50 years old in three nonpolluted areas. Blood was analyzed for Cd and urine was analyzed for Cd, total protein, beta(2)-microglobulin (beta(2)-mg), and N-acetyl-beta-D-glucosaminidase (NAG). Cd in blood or urine was employed as indicators of internal dose; and urinary total protein, beta(2)-mg, and NAG were used as an indicator of renal dysfunction. Multiple regression analysis and logistic regression analysis were performed to clarify the dose-effect and dose-response relationship between blood or urinary Cd concentration and indicators of renal dysfunction. Multiple regression analysis demonstrated a significant dose-effect relationship between Cd in blood and urine and indicators of renal dysfunction. Logistic regression analysis also showed that the probability that individual subjects would have abnormal values of the renal variables was significantly related to Cd in blood and urine.     

Impact of environmental cadmium pollution on cadmium exposure and body burden.

The body burden of cadmium, as estimated from 24-h urine cadmium levels, was determined in 1,523 subjects who were not occupationally exposed and who lived in five areas of Belgium. Urinary cadmium levels differed significantly with place of residence. These differences persisted after standardization for the other significant determinants (i.e., age, body mass index, smoking habits, social class, alcohol consumption, and menopause). The highest 24-h urine cadmium levels were found in subjects who lived in areas that contained cadmium-polluted soils. The body burden overload has been attributed mainly to the consumption of locally grown vegetables and the use of contaminated well water for cooking and drinking. Blood cadmium levels were also dependent on place of residence. However, the geographical differences in blood cadmium did not parallel those of urine cadmium. Blood cadmium is more influenced by recent exposure; therefore, this latter observation might reflect the recent implementation of preventive measures in some areas.     

Effect of Chlorella vulgaris intake on cadmium detoxification in rats fed cadmium

The aim of this study was to investigate if dietary Chlorella vulgaris (chlorella) intake would be effective on cadmium (Cd) detoxification in rats fed dietary Cd. Fourteen-week old male Sprague-Dawley (SD) rats weighing 415.0 ± 1.6 g were randomly divided into two groups and fed slightly modified American Institute of Nutrition-93 Growing (AIN-93G) diet without (n=10) or with (n=40) dietary Cd (200 ppm) for 8 weeks. To confirm alteration by dietary Cd intake, twenty rats fed AIN-93G diet without (n=10) and with (n=10) dietary Cd were sacrificed and compared. Other thirty rats were randomly blocked into three groups and fed slightly modified AIN-93G diets replacing 0 (n=10), 5 (n=10) or 10% (n=10) chlorella of total kg diet for 4 weeks. Daily food intake, body weight change, body weight gain/calorie intake, organ weight (liver, spleen, and kidney), perirenal fat pad and epididymal fat pad weights were measured. To examine Cd detoxification, urinary Cd excretion and metallothonein (MT) concentrations in kidney and intestine were measured. Food intake, calorie intake, body weight change, body weight gain/calorie intake, organ weight and fat pad weights were decreased by dietary Cd intake. Urinary Cd excretion and MT concentrations in kidney and small intestine were increased by dietary Cd. After given Cd containing diet, food intake, calorie intake, body weight change, body weight gain/calorie intake, organ weights and fat pad weights were not influenced by dietary chlorella intake. Renal MT synthesis tended to be higher in a dose-dependent manner, but not significantly. And chlorella intake did not significantly facilitate renal and intestinal MT synthesis and urinary Cd excretion. These findings suggest that, after stopping cadmium supply, chlorella supplementation, regardless of its percentage, might not improve cadmium detoxification from the body in growing rats.