Intake of nickel and vanadium by humans. A survey of selected diets.

The nickel and vanadium contents of nine institutional diets were determined by atomic absorption spectrometry with background correction. The following values were obtained for nickel: mean concentration, 0.27 +/- 0.02 microgram/g (dry weight); range, 0.19 and 0.41 microgram/g; mean intake, 165 +/- 11 microgram/day or 75 +/- 10 microgram/1000 cal. The respective values for vanadium were: 0.032 +/- 0.004 microgram/g (dry weight); 0.019 to 0.050 microgram/g; 20.4 +/- 2.3 microgram/day or 8.9 +/- 1.0 microgram/1000 cal. Thus, vanadium is present at approximately one order of magnitude less than nickel.

Comparison of the temperature sensitivity of protein synthesis by cell-free systems from liver of rat and skate (Raja ocellata).

Studies were undertaken to determine the component(s) responsible for the temperature optimum characteristic of the protein-synthesizing system from skate and rat. 1. The macromolecular constituents of rat and skate liver ribosomes are compared. The number of ribosomal proteins is similar in the two species, although most proteins display different electrophoretic mobilities on polyacrylamide gels. The RNAs from the small subunit of skate and rat have similar sedimentation coefficients; however, the RNA from the large subunit of skate ribosomes appeared to be slight smaller than the comparable RNA from the rat. 2. Ribosomes from either rat or skate were capable of supporting poly(U)dependent polyphenylalanine synthesis with soluble factors from either species. 3. Maximal leucine incorporation directed by endogenous mRNA occurred at 35--40 degrees C with post-mitochondrial supernatant from the rat liver and at 20--30 degrees C with that from skate liver. 4. The characteristic temperature sensitivity of protein synthesis was dependent upon the source of cell sap and independent of the source of ribosomes. 5. Elongation factor 1 from both the rat and skate exhibited maximum activity at approx. 30 degrees C. 6. Phenylalanyl-tRNA synthetase from skate liver showed maximum activity at 30 degrees C while that from rat was maximally active at 37 degrees C. The rat enzyme, however, was active at 0--10 degrees C, at which temperature protein synthesis in the reconstructed rat system is virtually absent. 7. The protein-synthesizing capacity of the reconstituted system at various temperatures was closely correlated with the activity of Elongation factor 2 (translocase). Elongation factor 2 from rat liver displayed an optimum at 30 degrees C and lost all activity below 10 degrees C, while this same factor from skate liver showed an optimum at 20 degrees C and significant activity below 10 degrees C. At this low temperature the reconstituted skate liver system continued to exhibit the ability to synthesize protein. These studies suggest that Elongation factor 2 is the component responsible for determining the temperature at which the protein-synthesizing system displays its characteristic maximum activity.

Nickel deficiency and nickel-rhodium interaction in chicks.

Nickel deficiency was produced in chicks under near optimal growth conditions. This judgment is based on the finding that chicks fed the experimental diet supplemented with nickel had a very satisfactory growth rate, over 600 g in 4 weeks. To induce nickel deficiency, chicks were raised in plastic cages located inside plastic isolators and were fed diets (containing 2-15 ng of nickel/g) based on dried skim milk, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. In 2 experiments, controls were fed 3 mug of nickel/g as NiCl2-6H2O. In experiment 3, instead of 1 control group 25, 50, 250, and 2,500 ng/g of supplemental dietary nickel as NiCl2-6H2O were each given to separate groups of chicks. Nickel deprivation resulted in: ultrastructural changes in the liver with the most obvious abnormality in the organization of the rough endoplasmic reticulum; altered gross appearance, reduced oxidative ability, and decreased lipid phosphorus in the liver; altered shank skin pigmentation that was associated with a decrease in yellow lipochrome pigments; and lower hematocrits. Deficiency also tended to increase the thickness of the legs and size of the hock; decrease the length:width ratios of the tibias and femurs; and decrease the plasma cholesterol. None of the signs of deficiency were seen in chicks fed diets containing at least 52 ng of nickel/g. In one experiment, a group of birds was fed 50 mug of rhodium/g of diet as (ClRh(NH3)5)SO4 to ascertain whether rhodium is a metabolic antagonist of nickel. Supplemental rhodium increased the hematocrits and liver oxidative ability of both nickel-deficient and -supplemented chicks, and increased total liver lipids, liver lipid phosphorus, and liver cholesterol in the nickel-deficient chicks alone. Rhodium did not increase the signs of nickel deficiency.

Nickel deficiency in rats.

Nickel deficiency was produced in rats fed diet (containing 2-15 ng of mickel/g) based on dried skim mile, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. Controls were fed a supplemental 3 mug of nickel/g of diet as NiCl2-6H2O. The rats were raised in plastic cages located inside laminar flow racks. Nickel deprivation resulted in several consistent pathological findings. These included: (1) increased perinatal mortality, (2) unthriftiness in young rats characterized by a rough coat and/or uneven hair development, (3) altered gross appearance (color) of the liver, (4) increased rate of alpha-glycerophosphate oxidation by liver homogenates, (5) decreased liver cholesterol, and (6) ultrastructural changes in the liver with the most obvious difference in the amount and organization of the rough endoplasmic reticulum. Nickel deficiency in rats tended to decrease growth, hematocrits, and liver total lipids and phospholipids.

The morphology of the swelling process in rat liver mitochondria.

Through the use of combined spectrophotometric and electron microscope techniques, large amplitude swelling of rat liver mitochondria has been described as an ordered sequence of ultrastructural transitions. Prior to the actual swelling, mitochondria undergo two major conformational changes: condensed to twisted form and twisted to orthodox form. This sequence is independent of (a) the nature of swelling agents and (b) the time of onset of swelling. Agents that delay the onset of swelling act to increase the duration of the twisted conformation. Agents that prevent extensive swelling hold mitochondria in intermediate conformations. Gross swelling, immediately preceded by a decrease in electron opacity of the matrix, involves the rupture of the outer membrane and expansion of the inner compartment of the mitochondrion.