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.
The effect of single (SC) administration of mercuric chloride (1 mg Hg/kg) alone or jointly with (PO) sodium selenite (0.39 mg Se/kg) on kidney disposition of mercury (Hg) and metallothionein (MT) and urinary excretion of Hg, zinc (Zn) and copper (Cu) has been studied in the female rat. The excretion of Hg and essential metals was determined every day following exposure. Daily excretion of endogenous Cu and Zn the Hg-exposed group was about threefold and fourfold, respectively, in comparison with control groups of rats. Sodium selenite prevented the urinary excretion of endogenous Cu and partly of Zn.
Retention, dynamics of 75Se and 65Zn distribution, and elimination were studied in rats after separate or joint single doses of these metals. White female Wistar rats were divided into four groups (fifteen rats each). Group I received Na2(75)SeO3 (0.1 mg Se/kg i.g.), group II received Na2(75)SeO3 + ZnCl2 (5 mg Zn/kg s.c.), group III received 65ZnCl2, and group IV received 65ZnCl2 + Na2SeO3. The zinc and selenium contents in the tissues were estimated during 120 h after administration; excretion in urine and feces of animals was determined throughout the experiment. Combined administration of zinc and selenium resulted in an enhanced selenium retention in the brain, spleen, kidneys, blood, lungs, and heart. A selenium-induced increase in the concentration of zinc was noted in the bowels, blood, liver, kidneys, spleen, brain, and lungs. The effects of the zinc/selenium interaction were visible especially in the lowered level of excretion of these elements. Zinc induced a decrease in the excretion of selenium in urine, with no concomitant changes in the excretion in feces. However, a visible decrease in the excretion of zinc in the feces was observed in the presence of selenium. The present results indicate an occurrence of clear-cut interaction effects between zinc and selenium administered simultaneously in the rat.
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