European Journal of Nutrition (v.19, #3)

R.B.C.'s amino acid pattern was investigated in control and PEM subjects. The effect of oral dosing with cysteine, tryptophan and lysine on total amino acid nitrogen level of R.B.C.s was also studied. Results revealed that in moderate and severe kwashiorkor the total essential and non-essential R.B.C.'s amino acids were decreased. In 2nd grade marasmus the total R.B.C.'s amino acids in general showed lower values than normal. After oral administration of the tested amino acids, the transport index calculated as the level of maximum value of the total R.B.C.'s amino acids reached to the fasting level was lower in malnourished cases relative to controls except in 2nd grade marasmic cases given tryptophan or lysine. This criteria was considered to indicate lower rate of amino acid transport to R.B.C.s due to lower concentration in plasma or shift of transport mechanism from active transport to exchange diffusion.

The role of pH on tissue alkaline phosphatases have been investigated in different human tissues. Different isoenzymes have been observed in different organs. Bone and liver were similar in having the isoenzymes optimally active at 9.4 and pH 9.9. The kidney has a single alkaline phosphatase optimally active at pH 9.2, while the adrenal gland has two isoenzymes of optimum pH 9.2 and 10.1. Intestinal alkaline phosphatase was optimally active at pH 9.7.

Boulti fish (Tilapia nilotica Linn.) from Naser's lake in Aswan was converted to a ready marketable product (paste) in aluminium tubes. The quality of the product was ascertained by chemical indices. The product has a good flavour and can be kept for 5 weeks without undesirable changes. It is concluded that the production of fish paste in aluminium tubes is one of the possibilities of converting fish to precooked product.

Total viable bacterial count reached 109 per gram of raw fish. It was decreased to 107 in fish paste and increased to 108–109 after storage at 2–4 °C for 5 weeks. It was observed that fish paste showed higher counts when preserved in polyethylene bags than in alimunium tubes.

Effect of calories restriction and protein deficiency on protein metabolism in rats by Abd El Halim A. Moustafa; I. H. Borai; S. Shoukry (166-172).
The changes induced by the deficiency of calories or nitrogen on the protein metabolism in rats were investigated. Animals were fed either a restricted normal diet, a protein-deficient diet or control dietad libitum. Rats receiving protein-free diet failed to grow, while the growth of animals given restricted diet was less than those fedad libitum. Despite that, the dietary deficiency of either calories or proteins caused the loss of protein and increased the incorporation of 1−C14 glycine into liver proteins. The contents of liver-free amino acids and urea were significantly increased only in the protein-deficient rats.

The effect of vitamin B12 on tetracycline-induced fatty liver by Tahani H. Mikhail; Kh. M. Ibrahim; R. Awadallah; E. Mona (173-178).
The effect of vitamin B12 on the metabolic alterations due to tetracycline toxicity was studied experimentally on laboratory animals.Treatment of Sprague-Dawley rats with 120 or 250 mg tetracycline (i.p.) per kg per day for two or three days caused an accumulation of lipids, mainly triglycerides in the liver of 75% of animals studied, while phospholipid level tend to decrease.These doses are approximately twice and four times the recommended maximum dose for man.In the present work no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride, although livers of rats treated with 250 mg tetracycline/kg appeared uniformly pale yellow.Elevated serum triglyceride was found predominantly in rats treated with 120 mg/kg, while there was no obvious difference between serum triglyceride of rats treated with 250 mg tetracycline and control rats, indicating a block in the release of hepatic triglycerides.Where protection by vitamin B12 was studied, the vitamin was given i.m. (50 μg/ animal) 3 hours before the injection of 120 mg tetracycline per kg.There was a good evidence that lipid abnormalities caused by tetracycline improved by vitamin B12.Thus both hepatic and serum total lipid and triglycerides were significantly lower than those of rats treated with tetracycline, although hepatic total cholesterol was significantly increased as in case of tetracycline only.

Der Einfluß von Äthanol, Aminophenazon und Phenobarbital auf den Coffeinstoffwechsel wurde an Mäuseleberschnitten unter Verwendung von 1-Methyl-14C-Coffein als Markersubstanz untersucht.Der Coffeinstoffwechsel erhöhte sich bei Verlängerung der Inkubationsdauer. Während 60 min nahm der Coffeinumsatz annähernd linear zu, und in dieser Zeit wurden 109,5 nM Coffein pro Gramm Leber Feuchtgewicht umgesetzt.Äthanol verminderte den Coffeinstoffwechsel von Mäuseleberschnitten. Nach Äthanolkonzentrationen von 23,36, 46,72 und 93,44 mM war eine deutliche und dosisabhängige Hemmung des Coffeinumsatzes festzustellen, wobei ein maximaler Hemmeffekt von 67,1% auftrat.Aminophenazon verminderte ebenfalls den Stoffwechsel von Coffein. Dieser Effekt wurde durch steigende Aminophenazonkonzentrationen (10,4, 20,8, 41,6 und 104,0 μM) verstärkt, und ein maximaler Hemmeffekt von 63.8% ergab sich nach der höchsten Konzentration von Aminophenazon.Vorbehandlung von Mäusen mit Phenobarbital bewirkte über die dadurch ausgelöste Enzyminduktion in der Leber eine deutliche Erhöhung des Coffeinumsatzes von Mäuseleberschnitten. Unter diesen Bedingungen wurde der Coffeinumsatz um mehr als 300% gesteigert.Im Gegensatz zu Leberschnitten war in Nieren- oder Gehirnschnitten der Maus kein nennenswerter Coffeinumsatz nachzuweisen.Mäuseleberschnitte metabolisierten Coffein wesentlich schneller als Leberschnitte von Ratten. Der Coffeinumsatz pro Gramm Leber Feuchtgewicht und 60 min war bei Mäusen etwa doppelt so groß wie bei der Ratte. The influence of ethanol, aminophenazon, and phenobarbital on the caffeine metabolism of mice liver slices was tested using 1-methyl-14C-caffeine as the marker substance.Caffeine metabolism was increased by the extension of the incubation time. The caffeine metabolism increased almost linearly up to 60 min, and during this time 109.5 nmol caffeine were metabolized per gram liver wet weight.Ethanol decreased the caffeine metabolism of mice liver slices. Ethanol concentrations of 23.36, 46.72 and 93.44 mM showed a clear and dose-dependent inhibition of caffeine metabolism, reaching a maximal value of 67.1%.Aminophenazon also decreased the metabolism of caffeine. This effect was augmented by increasing the concentrations of aminophenazon (10.4, 20.8, 41.6, 104.0 M) and an inhibition of 63.8% was observed after giving the highest concentration.Pretreatment of mice with phenobarbital, producing an enzyme induction of the liver, clearly increased the metabolism of caffeine of mice liver slices. Under these conditions, the caffeine metabolism was increased by more than 300%.In contrast to liver slices no important caffeine metabolism could be detected in kidney or brain slices of mice.Mice liver slices were able to metabolize caffeine more quickly than liver slices of the rat. Within 60 min the metabolized caffeine per gram liver wet weight was more than twice higher for mice as compared to rats.

Nutritional evaluation of sunflower-seed protein products by F. S. Taha; M. Abbassy; A. S. El-Nockrashy; Z. E. Shoeb (191-202).
Defatted sunflower-seed meal, sunflower-seed protein concentrate and protein isolate were fed to protein-depleted chicks. The effect of the enrichment of meal and of protein isolate with lysine, methionine, or a mixture of both on the nutritional value was investigated. Sunflower-seed protein products are primarily limited in lysine. Food consumption, weight gain and protein/efficiency ratio reveal superior performance of lysine- or lysine- and methionine-enriched meal or protein isolate, as compared to the correponding non-enriched products. Methionine enrichment does not improve the nutritional quality and even result in inferior performance. Non-enriched protein isolate supports better growth than non-enriched meal specially at later stages of chick growth.

Histologische Untersuchungen über die Auswirkung eines chronischen Vitamin-A-Mangels auf die Strukturen des Innenohres hatten widersprüchliche Ergebnisse gebracht. Neuere mikrofluorometrische Messungen zeigten, daß Vitamin A in hoher Konzentration im Innenohr von Meerschweinchen vorkommt.Nach einem sechswöchigen Vitamin-A-Mangel bei jungen Ratten fanden wir in den äußeren Haarzellen ein Fehlen der Cuticula. Auch in den inneren Haarzellen kam es zu Veränderungen der cuticularen Zone. Weiter fand sich eine Fragmentation und Verminderung des retikulären Systems der Intermediärzone. Die Ergebnisse weisen auf eine spezielle Bedeutung des Vitamin A für die Funktionsfähigkeit der Sinneszellen hin.Histologic studies of the inner ear in rats with chronic vitamin A deficiency have produced contradicting results. In our own electronmicroscope investigations of the inner ear of young rats after a six week vitamin A deficit diet we found a lacking of the cuticle in the outer hair cells and a subtotally lacking of the cuticle in the inner hair cells. Furthermore, we found changes in the reticular system of the intermediate zone. These morphologic changes together with the recent findings of high concentrations of vitamin A in the corti organ support the hypothesis that the acoustic sensory receptors contain or functionally depend upon vitamin A.

Coffein wurde sehr schnell vom Gastrointestinaltrakt der Maus resorbiert. Eine Zugabe von Äthanol hatte keinen nennenswerten Einfluß auf die Resorption von Coffein.Die Elimination von Coffein aus dem Serum und den untersuchten Geweben (Leber, Niere, Gehirn, Muskel) zeigte einen exponentiellen Verlauf mit einer Halbwertszeit von 40 bis 60 Minuten und war nach 4 bis 5 Stunden beendet.Durch Alkoholgabe wurde die Elimination von Coffein signifikant vermindert, und seine Halbwertszeit stieg auf 160 bis 240 Minuten.Die Coffeinmetaboliten erreichten ihre Maximalkonzentration im Serum und den untersuchten Geweben im Verlauf von 2 Stunden. In der Leber und der Niere war die Konzentration der Coffeinmetaboliten größer als im Serum, in Gehirn und Muskel dagegen niedriger. Bei Versuchsende erreichten die Coffeinmetaboliten nur noch eine sehr geringe Konzentration.Nach Verabreichung von Äthanol waren die Coffeinmetaboliten von der 30. bis 180. Minute in der Leber und der Niere signifikant vermindert, im Serum dagegen nur sehr leicht herabgesetzt und im Muskel und Gehirn nahezu unverändert. Aufgrund der Ergebnisse dieser Untersuchungen wird vermutet, daß Äthanol den Stoffwechsel von Coffein in der Leber zu hemmen vermag, und zwar durch Beeinflussung hauptsächlich seiner Demethylierung zu anderen Dimethyl- und Monomethylxanthinen und möglicherweise auch seiner weiteren Oxidation zu Methylharnsäuren.Caffeine was very quickly absorbed from the gastro-intestinal tract of mice. Addition of ethanol had no noticeable influence on the absorption of caffeine.The elimination of caffeine from the serum and tissues examined (liver, kidney, brain, muscle) showed an exponential course with a half life of 40–60 minutes and was completed after 4 to 5 hours.By giving ethanol the elimination of caffeine was significantly decreased and its half life increased to 160–240 minutes.The caffeine metabolites reached their maximal concentration in serum and tissues examined within two hours. In the liver and kidney the concentration of caffeine metabolites was greater than in the serum, whereas they were lower in the brain and muscle. At the end of the experiment the concentration of caffeine metabolites reached only very low values.After administration of ethanol the caffeine metabolites were significantly decreased from the 30th to 180th minute in the liver and kidney; they were only slightly lowered in the serum and almost unchanged in the muscle and brain. The results of these experiments suggest that ethanol inhibits the metabolism of caffeine in the liver, especially by influencing its demethylation to other dimethyl- and monomethylxanthines and probably also its oxidation to methyluric acids.

Buchbesprechungen by K. Lang; H. Glatzel; H. Kraut; D. Senczek; K. H. Bäßler (228-232).