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A Schnegg

Publications and source records attributed to A Schnegg.

14 recordsLinked to original sources
PubMed1979

[Activity of proteases, leucine arylamidase and alpha-amylase in pancreatic tissue during nickel deficiency].

In studies on the essentiality of nickel, important differences of enzyme activities and also of substrates were established. The results of the present paper show that these changes cannot be explained by a lowered reduction of dietary proteins, since the activity of the proteases rather increased during Ni deficiency. However, the digestion of the starch by alpha-amylase, being 57% lower, could have been partially responsible for the large differences in the activities of the hepatic enzymes and in the concentrations of the hepatic metabolites and also in the weight gains.

Aminopeptidases↗
PubMed1977

A comparative view on trace elements and growth.

The term 'essentiality' of trace elements is interpreted. The major human diseases due to trace element deficience (Fe, Cu, Zn, Cr) are briefly considered. In growing animals the first clinical deficiency symptom most often is a growth retardation. In order to diagnose a deficient situation before the manifestation of clinical symptoms, model studies with growing animals are presented to show criteria that respond sensitively even to suboptimum intake of trace elements (Zn, Cu, Fe, Ni). Activity measurements of enzymes and hormones are found suitable. During the phase of reproduction, which is closely associated with growth, the trace element concentration in milk may provide an additional diagnostic means. In conclusion, the problems of diagnosing the supply status are discussed. A possibility for determination of the trace element requirement is indicated.

Animals↗
PubMed1977

[Alkaline and acid phosphatase activity in the liver and serum during Ni versus Fe deficiency].

In previous studies on the essentiality of nickel, a reduced iron absorption causing anemia was observed. Since Ni deficiency also affects Zn metabolism, the different phosphatase activities were determined. Ni deficiency, however, resulted in an increased activity of the alkaline phosphatase in liver. On the other hand, the activity of the alkaline phosphatase was deduced by 59% during Fe deficiency. Similarly, the alkaline and acid phosphatases in serum were reduced during Fe deficiency. Consequently, determination of the activity of the alkaline phosphatase in serum, besides that of various liver enzymes, is suited well to differentiate between Fe and Ni deficiency.

Acid Phosphatase↗
PubMed1976

Malate dehydrogenase and glucose-6-phosphate dehydrogenase activity in livers of Ni-deficient rats.

In experiments using rats it was shown that inadequate dietary supply of Ni reduces growth and lowers the erythrocyte count, hematocrit and hemoglobin level in blood, that the Ni supply affects the trace element content of iron, copper and zinc in various body organs, and that the absorption of iron is greatly impaired by Ni deficiency. For further biochemical criteria on the essentiality of nickel, the activities of two dehydrogenases, malate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in liver homogenates from two generations of rats at 30 and 50 days of age. In the 30-day-old rats of both the F1 and F2 generation, the activity of the malate dehydrogenase fell to about two-thirds the level of control animals. In the liver of the 50-day-old rats the activity of this enzyme was about the same in deficient animals as in the controls. The activity of glucose-6-phosphate dehydrogenase of Ni-deficient rats was reduced by 85% in the F1 generation and by 56% in the F2 generation at 30 days of age as compared with control levels. In 50-day-old rats the activity had fallen to half the level of control animals at 30 days of age. At the age of 50 days, there was no significant difference between the deficient and the control groups of either generation.

Animals↗
PubMed1976

[Nickel content in the milk of lactating rats under intake of various amounts of nickel].

Model experiments were carried out with rats showing that the average Ni concentrations in the milk of the experimental animals receiving a Ni deficient diet (40 ppb of dietary Ni), relative to those of the controls (20 ppm), declined from 1088 ng/g to 726 ng/g (33%). This produced a Ni deficiency in the youngs of the rats resulting in retarded growth, reduced Fe absorption and a decline in enzymatic activity. An increase in the Ni content of the milk from both the experimental animals and the controls was observed during lactation. In the Ni deficient group this upward trend was longer noticeable from about the middle of the lactation period onwards. Animals in the Ni deficient group excreted about three times as much Ni through the milk as was ingested with the food. Because of the wide range of deviations of the Ni content in the different animals the Ni content of the milk cannot be used, under practical conditions, as an index of a state of Ni deficiency.

Animal Feed↗
PubMed1976

[Interaction of nickel with iron, copper and zinc].

Studies were carried out investigating the role of nickel as an essential element in the growth of rats. Reduced levels of iron, copper and zinc were found in the liver, spleen and kidneys during Ni deficiency. These findings could be reproduced in 2 generations of 30-day and 50-day-old rats. Reduced rates of Fe storage during Ni deficiency were, in some cases, even noted of the Fe supply was raised to a level of as high as 100 mg Fe per kg of the diet. This accounted for the diminished haemoglobin values, the reduced erythrocyte count and reduced hematocrite found under conditions of Ni deficiency.

Animals↗
PubMed1976

[Absorption and metabolic efficiency of iron in nickel deficiency].

Absorption and Metabolic Efficiency of Iron During Ni Deficiency. Ni deficiency leads to reduced iron contents in organs and to greatly reduced Hb levels and erythrocyte counts. Using models it was studied whether this Ni-dependent Fe anemia can be attributed to an impaired absorption of iron or to its metabolic efficiency. An experiment with seven 30-day-old rats from each of two generations were used for this. In Ni deficiency (0.015 ppm dietary nickel) iron absorption was clearly impaired at both 50 ppm and 100 ppm iron in the diet. Compared to the groups given 20 ppm nickel, the amount of iron absorbed fell two-thirds and one-third, respectively. By comparison, the influence on the metabolic efficiency of the iron was relatively small; at high iron supply, however, it was reduced by 8% in the Ni-deficient animals. Therefore, the reduced levels of hemoglobin, erythrocytes and hematocrit must essentially be caused by the impared absorption.

Animals↗
PubMed1975

[Changes in hemoglobin content, erythrocyte count and hematocrit in nickel deficiency].

In a total of four different studies, two of them involving two generations, the essentiality of nickel could be shown by reduced growth in response to a diet with 15 ppb nickel. In 30-day-old self-reared rats, anemia was induced in the Ni-deficient animals despite a high iron supply of 50 mg iron per kg diet. In the F1 generation of the Ni-deficient animals, the erythrocyte count had fallen by 36%, the hematocrit by 37%, and the Hb content by 44%. In the F2 generation in which the animals were given 100 ppm iron, surpassing their requirement three times, the blood parameters of the deficient animals were reduced by 8-10%. At the age of 50 days of the F1 generation the erythrocyte count had fallen 23% compared to the values of the control group, the hematocrit 14%, and the Hb content (16%) from 12.7 to 10.7 g/100 ml blood. An influence on the protein content of the serum and on the catalase activity of the erythrocytes was not observed and only at times was there an influence on the urea content of serum.

Anemia, Hypochromic↗