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鎘是一種具有毒性的重金屬，在我們週遭的環境及職業中都可能接觸得到。鎘的主要用途包括：在鐵或銅表面電鍍、合金或電池(Ni－cd)材料等。經由精煉或熔煉的操作，土壤、水和空氣均可能受鎘污染。已被証實的在停經後日本婦女身上發現的痛痛病即由鎘污染所造成。早在1985年，加州ToxicAir Contaminant Program即發現動物經由吸人方式接觸鎘，証實鎘對動物具致癌性，1986年 ，california Department ofHealth services(CDHS)亦發現工人在職業中吸人粉塵中的鎘，証貿鎘具致癌性，直至近幾年來，鎘己被確認無論以吸入或注射方式給予，對人類屬於致癌性金屬。
鎘在體外試驗中，發現鎘對細胞造成脂質過氧化作用(lipid peroxidation，LpO)，雖然LPO不致造成細胞死亡，但卻是細胞早期反應的現象，同時，細胞內對LPO的反應中，亦發現glutathione(GSH)及金屬硫蛋白(metallothionein，MT)參與細胞的保護作用。若以腸胃道以外的給藥途徑(eg.注射)將鎘給予動物，則發現鎘在肝、腎、腦部、肺、心臟及睪丸都有LPO發生。若以經口方式呢？無論是吃或喝到鎘應該是人類接觸鎘的主要途徑，邢麼是否同樣曾造成LPO？
本實驗在以低劑量(0，5及50ppm CdCl2)，口服方式餵予去卵巢大白鼠時間為2週及4週，測量大白鼠肝臟及腎臟中Cytochrome P450與GSH含量，thiobarbituric acid reactiveSubstance(TBARS)及金屬硫蛋白與鎘鍵結含量，另外，還有量血清生化值如：alanine aminotransferase((ALT，aspartateaminotransferase(AST)及blood urea nitrogen(BUN)作為肝、腎功能的指標。
在此研究結果發現，腎臟中GSH含量隨著劑量及時間的增加而降低，TBARS亦在4週時明顯上升，証明了鎘對腎臟造成氧化性傷害，至於MT與鎘鍵結量則於肝、腎皆隨劑量與時間的增加而有上升的情形。無論鎘對肝或腎臟的傷害與否，鎘的給藥途徑、時間長短等皆是主要原因且值得更進一步的探討與研究。
Cadmium is a potent metallic toxicant of continuous environmental and occupational concern. The primary uses of cadmiun includes: metal coating, silver solder, welding electrodes, a hardening agent for copper, and as an electrode component in nickel-cadmium batteries. Through the processing of refinary or smelting, cadmium may contaminate soil, water and air. Cadmium has been implicated as the major cause of Itai-Itai disease in postmenopausal women in Japan. The State of California's Toxic Air Contaminant program (1985) found cadmium to be carcinogenic in animals exposed by the inhalation route and in workers occupatinally exposed to aerosolized cadmium (CaliforniaDepartment of Health Services, 1986). Recently, cadmium has been classified as a human carcinogen.
It has been demonstrated in the in vitro system that lipid peroxidation (LPO) is an early intracellular event following cadmium exposure although it does not seem to be generally critical to cell viability. Glutathione (GSH) and metallothionein (MT) act as protective components against cadmium toxicity in lipid peroxidation. Cadmium stimulated LPO in liver, kidney, brain, lung, heart and testes following parenteral administration. Whether cadmium induced LPO after oral exposure, which is the most likely exposure route in human, has not been fullyelucidated.
In this study, 0, 5 and 50 ppm of cadmium as cadmium chloride was administered to ovariectomized (OX) rats for 2 and 4 weeks. We tested the effects of low dose cadmium oral administration on cytochrome P450 content, GSH concentration, thiobarbituric acid reactive substances (TEARS) and Cd-MT bound concentration in liver and kidney in female Sprague-Dawley rats. We also examined changes in the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and blood urea nitrogen values as functional indicators for liver and kidney toxicity.
The results indicated a dose and time-dependent reduction of GSH content, and increase of TBARS at 4 weeks in kidney, which reflected the formation of oxidative stress. The levels of Cd-MT bound in liver and kidney were increased markedly following cadmium exposure at 2 and 4 weeks. The toxic potential of cadmium in OX rats is worthy of further study.
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