Chmielnicka J, Brzeznicka E A
Bull Environ Contam Toxicol. 1978 Feb;19(2):183-90. doi: 10.1007/BF01685785.
Mercuric chloride, phenylmercuric chloride, ethylmercuric chloride /0,23 mg Hg/kg/ and methylmercurycyan guanidine /0,46 mg Hg/kg/ were orally administered to rats every second day for 14 weeks. The same doses of the above mentioned mercury compounds were administered alternately with sodium selenite /0,18 mg Se/kg/ to parallel groups of rats at the same time. The level of total and inorganic mercury and of metallothionein was determined. All mercury compounds increased the level of metallothionein in rat kidneys. In rats which received only selenium the level of metallothionein was twice lower in the kidneys in relation to the physiological level of this protein. Selenium eliminated the stimulation of biosynthesis of metallothionein by mercury.
每隔一天给大鼠口服氯化汞、苯基氯化汞、乙基氯化汞(0.23毫克汞/千克)和甲基汞氰胍(0.46毫克汞/千克),持续14周。将上述相同剂量的汞化合物与亚硒酸钠(0.18毫克硒/千克)交替给平行组的大鼠同时给药。测定总汞、无机汞和金属硫蛋白的水平。所有汞化合物均提高了大鼠肾脏中金属硫蛋白的水平。仅接受硒的大鼠肾脏中金属硫蛋白的水平相对于该蛋白的生理水平低两倍。硒消除了汞对金属硫蛋白生物合成的刺激作用。