Arsenic levels in Oregon waters.

The arsenic content of well water in certain areas of Oregon can range up to 30 to 40 times the U.S.P.H.S. Drinking Water Standard of 1962, where concentrations in excess of 50 ppb are grounds for rejection. The elevated arsenic levels in water are postulated to be due to volcanic deposits. Wells in central Lane County, Oregon, that are known to contain arsenic rich water are in an area underlain by a particular group of sedimentary and volcanic rocks, which geologists have named the Fischer formation. The arsenic levels in water from wells ranged from no detectable amounts to 2,000 ppb. In general the deeper wells contained higher arsenic water. The high arsenic waters are characterized by the small amounts of calcium and magnesium in relation to that of sodium, a high content of boron, and a high pH. Water from some hot springs in other areas of Oregon was found to range as high as 900 ppb arsenic. Arsenic blood levels ranged from 32 ppb for people living in areas where water is low in arsenic to 250 ppb for those living in areas where water is known to contain high levels of arsenic. Some health problems associated with consumption of arsenic-rich water are discussed.

Influence of copper supplementation on blood and liver copper in cattle fed tall fescue or quackgrass.

Copper concentrations were measured in naturally Cu-deficient and Cu-supplemented yearling Hereford heifers fed tall fescue (Festuca arundinacea Schreb.) or quackgrass (Agropyron repens [L] Beauv.) forage. The data were used to establish a relationship between dietary Cu supplementation and accumulation of liver Cu, and to test the influence of diet and Cu supplementation on blood plasma Cu and ceruloplasmin oxidase activity. Dietary Cu supplementation was positively correlated with accumulation of liver Cu; the rate of increase in liver Cu levels diminished at high supplementation rates (liver Cu = 410.43 - 353.47 x e-.00295 x mg Cu supplement; R2 = .740), suggesting an efficient mechanism preventing fast, toxic Cu-overloading in cattle. The linear relationship (R2 = .7878) between blood plasma Cu and ceruloplasmin oxidase activity indicated that similar percentages of blood plasma Cu were present as ceruloplasmin in deficient, normal and Cu-supplemented cattle. However, the portion of plasma Cu occurring as ceruloplasmin changes significantly with type of feed. When compared with quackgrass, tall fescue not only produced rapid Cu depletion in unsupplemented cattle, but affected intermediary Cy metabolism and activity of Cu-enzyme ceruloplasmin differently at all levels of experimental Cu supplementation.

Selenium - induced redistribution of cadmium binding to tissue proteins: a possible mechanism of protection against cadmium toxicity.

The mechanisms involved in the protection by Se against Cd toxicity in the rat were investigated. Se was found to significantly increase the Cd content in the blood and the testis, while decreasing that in the liver and kidney. Se diverted almost all the Cd in the soluble fraction of the testis from low-molecular-weight (MW) proteins to larger ones. Since the soluble fraction was the major subcellular Cd-binding component, the diversion of Cd by Se appears to be a mechanism involved in the protection by this element against the Cd-induced testicular injury. The diversion in binding of the Cd in the soluble fraction to higher MW proteins was also observed in the kidney and liver, and may be a second mechanism involved in the protection of these organs against Cd by Se, in addition to the reductive effect of Se on the tissue Cd concentration. Se was also found in these higher MW Cd-binding proteins. Based on a similarity of MW of about 115,000, the Cd-binding, Se-containing proteins found in these organs appear to be similar. A diversion of Cd from lower MW proteins to larger ones by Se was also found in the plasma, but the Cd-binding, Se-containing proteins in plasma appear to be different from those found in the other organs since they have a larger MW.

Effects of selenium and vitamin E deficiencies in lambs on hepatic microsomal hemoproteins and mitochondrial respiration.

Microsomal hemoprotein levels and delta-amino levulinic acid dehydrase activity were determined in livers and rate of oxygen uptake, ADP:O ratios, and respiration control index were determined on mitochondria from muscle, liver, and heart of normal and white muscle diseased (WMD) lambs. WMD lambs were produced by feeding their dams either low selenium purified or alfalfa hay diets. Vitamin E and/or selenium was injected in a 2 x 2 factorial treatment in the ewes fed purified diets. Hepatic microsomal cytochrome P 450 levels and total heme content were significantly lower in WMD lambs. Cytochrome b5 content was significantly lower in lambs on the -E-Se or -E + Se treatments than those on the +E--Se treatment, but the cytochrome b5 content was not different between WMD and normal lambs from ewes fed the hay diet. No differences were found in hepatic delta-amino levulinic acid dehydrase activity, or in the rate of oxygen uptake, ADP:O ratios or respiratory control index between mitochondria from normal and WMD lamb tissue on any of the treatments.

Cadmium and nickel influence on blood pressure, plasma renin, and tissue mineral concentrations.

Weanling rats were fed a casein-based diet containing either 150 ppm cadmium, 500 ppm nickel, or the combination of these metals for 16 wk. Blood pressure of rats fed the diet with cadmium decreased after 8 wk, but this effect was counteracted by dietary nickel. Cadmium caused a depletion of iron and resulted in an accumulation of zinc in liver and kidney of rats. Nickel partially counteracted the iron loss due to cadmium. In a second experiment, the inclusion of 10 or 20 ppm cadmium in drinking water for 24 mo did not result in elevated blood pressure in normal or genetically hypertensive rats. Cadmium had no effect on the plasma renin levels in either experiment. Low intake of cadmium (10 or 20 ppm) in drinking water resulted in elevated cadmium content in hair. Thus, our data do not indicate that high levels of cadmium contribute to hypertension.

Biological function of metallothionein. V. Its induction in rats by various stresses.

Induction of metallothionein (a Zn-binding protein) was investigated in liver and kidneys of rats under the following stresses: cold environment, hot environment, heat burn, strenuous exercise, and CCl4 intoxication. As markers of metallothionein (MT) synthesis, [14C]cystine and 65Zn were injected parenterally into rats, and MT in liver and kidney supernatants was separated on Sephadex G-75 columns. Among stresses tested, the greatest stimulations of MT synthesis in liver were observed under cold (315%), strenuous exercise (302%), and CCl4 intoxication (543%), as evidenced by increased amount of [14C]cystine and 65Zn incorporation into the MT fraction. In contrast to liver, only small responses were observed in MT synthesis in kidneys. There was a general decline in plasma Zn levels in rats under the stresses employed. However, no great differences were observed in Zn levels in whole liver and kidneys. The present study suggests that various unrelated physiological stresses, which are accompanied with a change in Zn distribution, increase the synthesis of MT in liver of rats.

Biological function of metallothionein-IV. Biosynthesis and degradation of liver and kidney metallothionein in rats fed diets containing zinc or cadmium.

The half-lives of liver and kidney metallothionein of rats fed diets containing either 2,000 ppm Zn or 100 ppm Cd were determined by a single injection of 14C-cystine. This protein was purified by Sephadex G-75 and DEAE cellulose column chromatography. Half-lives of liver metallothionein in rats fed the basal (18 ppm Zn), high Zn (2,000 ppm Zn), high Zn then basal, and high Cd (100 ppm) diet were, respectively, 3.4, 2.7 1.3, and 3.3 days, and that of kidney metallothionein were, respectively, 2.0, 2.2, 1.4, and 3.6 days. Thus, Cd-thionein has a longer half-life than Zn-thionein in both liver and kidney. The major species of metallothionein, which were separated on DEAE cellulose, had similar half-lives. Metallothionein, a protein having high content of metals and relatively short half-life, is possibly involved in cellular regulatory function.

Selenium proteins in ovine tissues: III. Distribution of selenium and glutathione peroxidases in tissue cytosols.

Three 6 week-old lambs were injected with carrier-free selenium-75 as sodium selenite initially and again after 6 days. One lamb received no further injections whereas the other two received injections of either vitamin E or unlabeled Na2SeO3 when the first selenium-75 injection was given. Selected tissues were removed at autopsy 10 days after the first injection. The cytosol from homogenates of these tissues was subjected to gel chromatography, and the elution profiles determined for radioactivity, protein content, and glutathione peroxidase activity using either hydrogen peroxide or cumene hydroperoxide as substrates. The selenium-75 was found to be distributed mainly between 2 different MW peaks. The larger MW seleno-peak (90,000) possessed both glutathione:hydrogen peroxide oxidoreductase, and glutathione:cumene hydroperoxide oxidoreductase activities, but the smaller MW seleno-peak (about 10,000) possessed no glutathione peroxidase activity. A peak of about 60,000 daltons containing only glutathione:cumene hydroperoxide oxidoreductase activity and no selenium-75 was found primarily in the liver and kidney. Vitamin E had no effect on the elution profiles. Selenium status of the animal had only a minor effect on the selenium-75 distribution in the cytosol, but had a marked effect on the absolute amount of the label taken up by tissues.

Effects of selenium and vitamin E deficiencies on reproduction, growth, blood components, and tissue lesions in sheep fed purified diets.

Three 2 X 2 factorial experiments were conducted with sheep fed purified diets to determine the effects of selenium and vitamin E on the incidence of white muscle disease (WMD) and blood components. All lambs reaching 6 weeks of age in the group receiving no vitamin E or selenium developed WMD lesions, whereas only a few lambs in either the +E - Se or -E + Se treatment groups developed these lesions. Plasma activities of creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase were significantly elevated in lambs receiving no vitamin E or selenium, whereas these enzyme activities in those receiving only selenium were non-significantly elevated. The enzyme activities in plasma of those on the +E - Se or +E + Se treatments were maintained at low levels, suggesting vitamin E alone is more effective in preventing WMD than selenium alone. The metabolic interactions of these essentials are discussed.

Effects of selenium and vitamin E on blood selenium levels, tissue glutathione peroxidase activities and white muscle disease in sheep fed purified or hay diets.

The effects of selenium and vitamin E on blood selenium levels and tissue glutathione peroxidase activities were determined in sheep fed purified and hay diets. A significant increase of blood levels of this element and tissue glutathione peroxidase activities was found in sheep given selenium as compared to those not receiving this element. Of the tissues examined, the highest glutathione peroxidase activity was found in the heart. Vitamin E had no influence on either the blood selenium levels or upon the tissue glutathione peroxidase activity. With hydrogen peroxide as the substrate, tissue glutathione peroxidase activity was not correlated with the incidence of white muscle disease. Evidence is presented to suggest that 0.1 ppm dietary selenium is not sufficient under some conditions to meet the physiological requirements for this element.