Biomedical subjects

G Hunder

Publications and source records attributed to G Hunder.

21 records · Page 2Linked to original sources

PubMed1989

Increase of the intestinal iron absorption in growing rats and mice after 8 days of iron-deficient feeding.

In investigations of intestinal iron absorption the combination of repetitive bleeding and iron-deficient feeding is frequently used. It induces iron deficiency which, in turn, stimulates iron absorption. When this combined procedure was compared with the effect of an 8 d iron-deficient feeding schedule in growing rats, no significant differences were found regarding the stimulating effect on intestinal iron transfer. Body iron stores, however, as represented by the hepatic ferritin and iron content are remarkably less depleted. Contrary to the effect of the combined procedure the animals growth was only marginally retarded and anaemia did not develop. This was also demonstrated in mice. The stimulation of intestinal iron absorption by iron-deficient feeding of growing animals thus seems preferable, as this procedure largely avoids the disturbing side effects observed with repetitive blood sampling.

Anemia, Hypochromic↗

PubMed1987

Investigation on the metabolic degradation of the side chain of furazolidone.

The investigation was aimed at providing insight into the side chain metabolism of furazolidone in mice. The agents used in the experiments were furazolidone, 3-amino-2-oxazolidinone, oxazolidinone, nitrofurantoin, 3-aminohydantoin and hydantoin, administered intraperitoneally at five equimolar doses ranging from 0.178 to 0.888 mmol/kg. The parameters investigated included ethane and ethylene expiration, formation of malondialdehyde and total glutathione content in the liver. Ethylene expiration was found to be strongly enhanced by aminooxazolidinone and slightly increased by furazolidone. Ethane expiration was increased after aminooxazolidinone administration. Malondialdehyde formation was not affected by any of the agents used. Total glutathione was decreased by furazolidone and nitrofurantoin. The above findings indicate that, in vivo, the azomethine linkage of the side chain of furazolidone hydrolyses to form 3-amino-2-oxazolidinone, subsequently cleaved to ethylene.

Animals↗

PubMed1987

Role of lipid peroxidation in the toxicity of T-2 toxin.

Recent reports suggest that lipid peroxidation may be involved in the toxicity of T-2 toxin. In the present study the influence of T-2 toxin on two parameters of lipid peroxidation was examined: the formation of thiobarbituric acid reactive material in isolated hepatocytes and liver homogenates from rats and ethane exhalation in vivo. In isolated hepatocytes there was no significant increase in thiobarbituric acid reactive material, neither after addition of T-2 toxin in vitro nor when the toxin had been applied to the rats 15 hr before preparation of hepatocytes. In liver homogenates the amount of thiobarbituric acid reactive material was increased up to 50% over the controls, depending on the dose of T-2 toxin. The increased values are difficult to interpret, because the extent of the increase depends on the method used for determination of thiobarbituric acid reactive material. Measuring another parameter of lipid peroxidation, i.e. ethane exhalation, there was no difference between the T-2 toxin treated rats and the controls whereas carbon tetrachloride treated rats exhaled high amounts of ethane. These results suggest that lipid peroxidation does not play a major role in T-2 toxin toxicity.

Animals↗