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Biomedical subjects

P Budowski

Publications and source records attributed to P Budowski.

At least 37 records · Page 2Linked to original sources
PubMed1980

Lysosomal acid phosphatase decrease in nutritional encephalopathy in chicks.

Encephalopathy was induced in 14-day-old chicks by a vitamin E-deficient diet containing 15% thermally oxidized safflower oil. Bound acid phosphatase activity in the cerebellum was markedly lower in affected chicks than in vitamin E-supplied control chicks. Free activity also tended to be lower in the deficient group. There were no differences in enzyme activities of cerebrum and liver between deficient and control chicks.

Acid Phosphatase↗
PubMed1980

[Protective effect of alpha-linolenic acid in encephalomalacia in chickens].

Encephalomacia is a vitamin E deficiency syndrome which affects the cerebellum of young chicks. The lesion includes degenerative alterations of cellular and fibrillar elements, apparently as the result of the ischaemia caused by thrombotic events in the microvascular system. A supply of linoleic acid, as fatty acid methyl esters prepared from safflower oil (Carthamus tinctorius), caused a high incidence of encephalomalacia. On the other hand, linseed oil esters, rich in alpha-linolenic acid, did not induce any symptoms and protected the chicks to a large extend against the development of signs produced by linoleic acid. Fatty acid esters of cod liver oil, rich in long-chain derivatives of alpha-linolenic acid, exerted a relatively weak protective effect. The analytical results show that a supply of alpha-linolenic acid led to an accumulation of eicosapentaenoic acid, 20:5 omega 3, and a reduced concentration of arachidonic acid in the phospholipds of liver and plasma. The results suggest that, under the conditions leading to encephalomalacia, the prostacyclin-thromboxane balance is shifted in direction of an excessive production of TXA2, causing thrombus formation in the capillaries of the cerebellum, alpha-linolenic acid, by modifying the PUFA profile, exerts a multiple action the main result of which appears to be an antithrombotic effect at the level of the microvascular system of the cerebellum.

Animals↗
PubMed1979

Cholesterol metabolism in the liver and intestine of the chick: effect of dietary cholesterol, taurocholic acid and cholestyramine.

The effect of feeding cholesterol, taurocholic acid, or cholestyramine to chicks on cholesterogenesis from [1-14C] acetate in liver and intestine was determined in vitro using tissue slices, and in vivo by i.v. injection of [14C] acetate. The conversion of cholesterol to bile acids in liver in vivo was measured in the same treatments after i.v. injection of [3H] cholesterol. Hepatic cholesterogenesis in vitro and in vivo was depressed by dietary cholesterol and taurocholate and enhanced by cholestyramine. Intestinal cholesterogenesis in vivo was depressed only by taurocholate whereas ileal cholesterogenesis in vitro was reduced by dietary cholesterol. Conversion of cholesterol to bile acids was enhanced by dietary cholesterol and cholestyramine and depressed by taurocholate. Hepatic cholesterol metabolism in the chick appears to be regulated by mechanisms similar to those reported for other species.

Acetates↗
PubMed1979

Lipid oxidation products and chick nutritional encephalopathy.

Safflower oil and its distilled methyl esters were thermally oxidized and fed to young chicks in a vitamin E deficient diet. At a dietary level of 10%, the oxidized lipids caused more severe nutritional encephalopathy (NE) than the unoxidized methyl esters, indicating that factors other than dietary linoleic acid and vitamin E affect the development of NE. A polar lipid extract from oxidized methyl esters accelerated the induction of NE, as did the synthetic methyl esters of keto-octadecenoic and keto-octadecadienoic acids. Dicumarol exerted a protective action against NE. The possibility is discussed that conjugated keto-polyenoic fatty acids, provided by oxidized oils or formed endogenously in vitamin E deficiency, may play a role in causing NE.

Aging↗
PubMed1979

Protective effect of nicarbazin on nutritional encephalopathy in chicks.

Nutritional encephalopathy was induced in young chicks by vitamin E-deficient diets containing either 4% methyl esters of safflower oil or 10% thermally oxidized safflower oil. The coccidiostat nicarbazin (an equimolecular complex of 4,4'-dinitrocarbanilide and 2-hydroxy 4,6-dimethylpyrimidine) reduced the incidence of encephalopathy, but zoalene (3,5-dinitro-o-toluamide) and amprolium [1-(4-amino-2-n-propyl-5-pyrimidinylmethyl)-2-picolinium chloride hydrochloride] did not. Neither of the two components of nicarbazin affected the rate of development of encephalopathy when fed separately, but when included together in the diet, they reduced the incidence of the disease.

Animals↗
PubMed1978

Mineralized cells: neurons, glia or macrophages? Ultrastructure of cerebellum in chick nutritional encephalopathy.

Mineralized dead cells were found in infarcted areas in the cerebella of three chicks killed in the healing stage of nutritional encephalopathy. The mineral depostis were found in vacuoles and consisted of radially packed threads and spicules, concentric laminated structures and centrally located amorphous masses. The cells in which these deposits were found were positively identified as astrocytes and macrophages. The presence of such deposits in neurons was suspected but not proven.

Animals↗
PubMed1978

Hydrolysis of biliary phospholipids in the upper small intestine of the chick.

Chick endogenous phospholipids were doubly labeled by an intravenous injection of [32P] phosphate and [1-14C] oleic acid, and the free fatty acid and phospholipid fraction of gall bladder bile and in contents of upper small intestine were analyzed 4 days later. There was evidence of hydrolysis of biliary phosphatidylcholine to lysophosphatidylcholine in the duodenum and jejunum, but this did not account for the pronounced increase in the 14C radioactivity of the free fatty acids relative to the 32P phospholipid radioactivity between bile and upper intestinal segments. It is suggested that phosphatidylcholine is largely absorbed in the duodenum of the chick while the remainder is progressively hydrolyzed and absorbed.

Animals↗
PubMed1977

The effect of lipids on taurocholate absorption from intestinal loops in the rat.

The rates of uptake and serosal transfer of [14C]-labelled taurocholate (7.77 mM in bicarbonate buffer, pH 6.5) were determined in situ in ligated segments of rat intestine in the presence of lipids. Oleic acid, monoolein, lecithin, and lysolecithin enhanced taurocholate uptake and transfer in the jejunum, each lipid exhibiting an optimal concentration at which the bile acid fluxes were maximal. The maximal rates of bile acid uptake observed with the various lipids were close to four times the uptake rates found with the lipid-free taurocholate medium, whereas serosal transfer rates under optimal conditions were enhanced about six-fold. The optimal concentrations differed widely among the various lipids, being inversely related to the lipids' polarity. Simultaneous measurement of taurocholate and [3H]-labelled oleic acid showed that under optimal conditions, when the molar concentration of oleic acid was about equal to that of the bile acid, the fatty acid and bile acid also exhibited closely similar rates of absorption. At other fatty acid concentrations, the fractional rate of absorption of the bile acid was much lower than that of the fatty acid. The rates of uptake and serosal transfer of pure taurocholate by the ileum exceeded those of the jejunum by factors of about 7 and 15, respectively, but in the presence of lipids this difference in absorptive capacity for bile acid between the distal and proximal segment largely disappeared.

Animals↗
PubMed1977

Utilization of choline from crude soybean lecithin by chicks. 1. Growth and prevention of perosis.

Data obtained with growing chicks fed a semi-purified diet indicate that choline from crude soybean lecithin is as well utilized as synthetic choline chloride, on the basis of growth, relative liver weight and prevention of perosis. Extrapolation of the results on growth and perosis prevention, obtained between 1 and 3 weeks of age, to performance on practical-type diets yields choline requirements for broiler-type chicks ranging from 800 to 1000 mg./kg. diet (as choline chloride). The requirement seems to decrease with age.

Animals↗