Effect of rubratoxin B on adenosine triphosphatase activities in the mouse.

Half the animals in groups of selenium-deficient and control rats were given mercury in the drinking water for 6 weeks. The other half of the animals in both groups received tap water ad libitum. Selenium-deficient rats gained significantly less weight when given mercury, but weight gain of controls was unaffected by mercury administration. In another experiment with rats given mercury for 8 weeks, serum creatinine and renal histology were normal in selenium-deficient and control rats. Selenium-deficient rats injected with ²⁰³HgCl₂ 12 days after mercury was added to their drinking water excreted up to 10% of the ²⁰³Hg in the urine in the first 24 hr whereas control animals excreted less than 2%. This trend continued for several days and was shown to be due primarily to a loss of ²⁰³Hg from the kidney in the selenium-deficient rats. The control kidneys contained 4 times as much mercury as the kidneys in selenium-deficient rats at the end of the experiment, and the mercury content appeared to be increasing further. Selenium-deficient kidneys, however, had achieved maximum mercury accumulation by 13 days. Despite the large differences in mercury accumulation due to selenium status, in both groups about 80% of kidney ²⁰³Hg was found in the soluble fraction. Also, regardless of selenium status, about 90% of the soluble fraction ²⁰³Hg was found in a symmetrical peak on gel filtration which probably represents metallothionein. Thus a major effect of selenium status on the metabolism of inorganic mercury seems to be in facilitating the accumulation of mercury by the kidney. Since most of the kidney mercury is bound to metallothionein, selenium may mediate the binding of mercury to this protein or be a permissive factor in the induction of metallothionein by mercury.