Selenium has been shown to alter mercury metabolism and to decrease mercury toxicity. Parizek and his colleagues (1, 2) demonstrated that injection of selenite markedly diminished the toxicity of simultaneously administered mercuric chloride while paradoxically appearing to cause increased retention of the mercury. Ganther el al.( 3 ) reported that chronic methylmercury toxicity was decreased by feeding 0.5 ppm selenium. Recently Potter and Matrone (4) confirmed the findings of Ganther et al. using a dietary selenium concentration of 5 ppm and showed that this amount of selenium also decreases chronic inorganic mercury toxicity.Little is known of the mechanism by which selenium decreases mercury toxicity.

Regulation of the body burden of selenium is important because selenium deficiency and excess both lead to pathologic conditions (1, 2 ) . We showed that after intraperitoneal injection of 75Se032-urinary excretion of ""Se increased as dietary selenium was raised within the range of 0 to 1 ppm (3). Fecal and expired 75Se had no such relationship with dietary selenium under those conditions. Since our previous study showed a marked increase in urinary 75Se when only 0.1 ppm selenium was added to the diet, and since the urine seems to be the major route of selenium excretion, we decided to study even lower dietary selenium levels to determine whether there was a dietary selenium threshold above which urinary selenium began to increase.Methods and Procedures. Five groups of 4 weanling male Holtzman rats each1 were fed a vitamin E-adequate (250 IU dl-a-tocopherol/kg diet) torula yeast diet (3) with 0, 0.030, 0.060, 0.090, and 0.120 ppm selenium added as NazSe03, respectively. The basal diet without selenium supplementation contained 0.024 ppm selenium.2 Rats were weighed weekly and no differences in growth rate were observed among groups. After the rats had consumed the diets for 25 days, each animal was injected intraperitoneally with 2 , NY using the method of Olson, J. Ass. offic.Anal. Chem. 52, 62'1 (1969).pCi of 75Se032-(sp act 119 Ci/g of seleniand placed in a metabolism cage. Urine and feces were collected for 7 days and percentage of administered 75Se in them was determined as before (3). Whole-body counting was performed daily for 17 days. Then the animals were sacrificed and percentage of whole-body '%e in various organs was determined as described previously (3). Figure 1 shows the whole-body retention of 75Se. The 0 and the 0.030 ppm selenium groups retained the same percentage of the %e dose whereas differences among all other groups were highly significant. Urinary excretion accounted for the differences in whole-body retention as shown in Fig. 2. Urinary and fecal excretion accounted for all losses of ?%e as calculated from whole-body retention. Results.In contrast to the identical 75Se total body retention of the 0 and 0.030 ppm groups, tissue distribution in these groups was markedly different as is seen in Fig. 3. Testes ( p < 0.001), adrenals ( p < 0.005), spleen ( p < 0.001), thymus ( p < 0.01), and brain ( p < 0.001) all contained significantly more of the whole-body 75Se per gram in the 0 ppm group, while liver ( p < O.OOS), blood ( p < O.OOS), heart ( p < 0.05) and skeletal muscle ( p < 0.05) contained more in the 0.030 ppm group.Discussion. The whole-body and excretion results indicate the existence of a dietary selenium threshold somewhere between 0.054 ppm (0.024 + 0.030 ppm) and 0.084 ppm (0.024 + 0.060 ppm) for the forms of selenium used in this experiment below which a constant percentage of the administered T5Se is excreted in the urine. Above the threshold

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