Acid In Chickens Research Articles

Conversion of 1, 3-Butanediol or Acetaldol to β-Hydroxybutyric Acid in Chicks

Enzymic oxidizing system of 1,3-butanediol in chicks was studied in comparison with that in rats. 1,3-Butanediol was oxidized with NAD+ as a cofactor in the cytosol fraction of chick liver, kidney, and rat liver. NADP+ was about 40% as effective as NAD+ in chick liver, kidney, whereas the former was ineffective in rat liver. Inhibitory effect of pyrazole on 1,3-butanediol dehydrogenase activity was recognized distinctly both in chicks and rats, but the effect was much higher in rat liver than that in chick liver and kidney. Both in chicks and rats, the conversion of 1,3-butanediol to β-hydroxybutyric acid was detected clearly, and the rate of β-hydroxybutyrate production increased remarkably by employing NAD+-regenerating system, i.e., lactic dehydrogenase and pyruvic acid. β-Hydroxybutyric acid was also formed from acetaldol, the most probable intermediate of 1,3-butanediol, with NAD+ both in chicks and rats. From the observations for coenzyme specificity, inhibitory effect of pyrazole, and so on, it is ...

1758. Complexities of amino-acid toxicity: Nutrition Reviews (1968). Imbalance and toxicity of amino acids. ibid26, 115. Smith, R. E. (1968). Effect of arginine upon the toxicity of excesses of single amino acids in chicks. J. Nutr.95, 547

1758. Complexities of amino-acid toxicity: Nutrition Reviews (1968). Imbalance and toxicity of amino acids. ibid26, 115. Smith, R. E. (1968). Effect of arginine upon the toxicity of excesses of single amino acids in chicks. J. Nutr.95, 547

Dietary Antibiotics and the Absorption of Zinc-65 and 131I-Labeled Oleic Acid ,

THE addition of antibiotics to the diet has been repeatedly shown to increase growth rates. This area has been extensively reviewed by Branion et al. (1953) who have also discussed, in the same review, several suggestions as to the mechanism responsible for the observed increase in growth rates. Anderson et al. (1952) and Byerly (1964) and many others have suggested that the inclusion of the antibiotics in the ration of growing animals may improve the absorption of the nutrients in that ration. A recent paper by Lotenkov and Podluzknaya (1967) indicates that chlortetracycline at 20 mg./kg. stimulated intestinal absorption of amino acids in chicks. To further investigate the hypothesis that the growth stimulation obtained by feeding antibiotics was due to increased nutrient absorption, the following study was initiated, using a mineral, zinc, and a fatty acid, oleic acid.PROCEDUREIn each of the three trials to be reported, day-old broiler .

Effect of Arginine upon the Toxicity of Excesses of Single Amino Acids in Chicks

A series of experiments was conducted to elucidate the mechanism through which arginine relieves the imbalance caused by the addition of excessive levels of amino acids in chick diets. Excess quantities of the L-isomer amino acids, lysine, tyrosine, histidine, glycine, methionine, cystine, valine, threonine, isoleucine, phenylalanine, tryptophan, glutamic acid and leucine were added singly to a balanced low protein casein diet and fed to week-old chicks for 2 weeks’ duration. Each of the amino acids fed at super-optional levels resulted in some manifestation of imbalance, i.e., reduction in growth or feed intake, or both, on the part of the chicks. Amounts of these amino acids required to bring about an imbalance, ranged from 10% (L-glutamic acid) to 0.4% (L-lysine·HCl). The aforementioned conditions of imbalance were, with the exception of those caused by tryptophan, leucine and glutamic acid, all alleviated to some extent by the addition of arginine. The level of arginine required to bring about this relief ranged from 0.3% to 2.0% but did not appear to be dependent upon the severity of the imbalance. Attempts to define the unique role of arginine in the detoxification of amino acid excesses were not successful. It appears that supplemental arginine in imbalanced diets does not exert its benefit because of a deficiency of this amino acid due to a reduced feed intake, does not mediate its influence through competitive inhibition at absorption or reabsorption sites, nor does it appear to act as a cycle intermediate in a possible latent urea cycle.

DIETARY BILE ACIDS AND LIPID METABOLISM. V. REVERSIBILITY OF THE EFFECTS OF LITHOCHOLIC ACID IN CHICKS.

DIETARY BILE ACIDS AND LIPID METABOLISM. V. REVERSIBILITY OF THE EFFECTS OF LITHOCHOLIC ACID IN CHICKS.

DIETARY BILE ACIDS AND LIPID METABOLISM. I. INFLUENCE ON LIPIDS AND LIVER SIZE OF CHICKS.

SummaryDietary lithocholic acid elevated plasma cholesterol and lipid phosphorus levels, and increased liver size of growing chicks. In cholesterol-fed chicks, lithocholic acid depressed liver lipid and cholesterol levels. The effects of lithocholic acid were partially reversed by cholic acid in chicks fed a cholesterol-free diet and almost completely reversed in chicks fed cholesterol. The plasma cholesterol level of cholesterol-fed chicks was increased by cholic acid feeding.

Effect of pyridoxine deficiency on cholesterol and polyenoic fatty acids in chicks.

Summary.The influence of pyridoxine deficiency on chicks fed fat‐free and 10% peanut oil‐diets with and without 1 % cholesterol was studied.Cholesterol: The pyridoxine‐deficient diets caused significantly higher plasma cholesterol than the diets with added pyridoxine.The aorta vliolcsterol showed changes in the same direction. Liver chiolesterol was not, significantly affectd.The pyridoxine‐deficient diets caused lower cholesterol content in the heart than did the supplemented diets.Polyevie fatty acids: With a fat‐free, pyrudixine‐deficient diet a marked content of tetraenoic acid was found in heart and liver, whereas the tritenoic acid was proportionally decreased.Feeding of 10% peanut oil without pyridoxine caused less deposition of tetraenoic in heart and especially in the liver than feeding of 10 % peanut oil with pyridoxine.Addition of 1% cholesterol to the diets resulted in a decrease in the amount of tetraenoic acid in heart and liver.

Thioctic Acid in Complete and Deficient Diets for Chicks

ABSTRACT THIOCTIC acid (6,8-dithiooctanoic acid, lipoic acid, protogen) is known to be an important growth factor for protozoa and bacteria, as well as a component of certain enzyme systems in microorganisms and animal tissues (see reviews by Gunsalus, 1954; and Reed and DeBusk, 1954). Despite little evidence for its growth promoting activity in higher animals, thioctic acid has been called a vitamin (Seaman, 1952; Anonymous, 1953; Fischer, 1955) and has been included as a B vitamin in recent reviews on the vitamin B complex (Cheldelin, 1954; Johnson, 1955; Plaut and Betheil, 1956). DeBusk and Williams (1955) reported that thioctic acid added to a purified diet stimulated the growth of White Leghorn chicks and of Wistar rats. However, Stokstad, Broquist and Patterson (1953) had reported earlier that they could not produce a growth response with thioctic acid in chicks or rats fed a purified diet. Recently, Stokstad et al. (1956) and workers . . .

Variations in the total amounts of polyenoic fatty acids in chicks and rats reared on a nearly fat-free diet.

Summary.Chicks reared on a nearly fat‐free diet for 4 weeks and rats reared on a fat‐free diet for 18 weeks showed a considerable decrease of total dienoic fatty acid in the body. At the same time trienoic fatty acid increased markedly. The increase in trienoic fatty acid must have originated from dienoic since the changes of the other polyenoic fatty acids could not account for it.

Failure to obtain growth responses with thioctic acid in chicks from different sources

dl-Thioctic acid was added to two different purified and one practical chick ration and fed to chicks of three different genetic sources and from dams fed different diets without effect as measured by growth and feed efficiency.

Experiments on Selection for Resistance to Riboflavin Deficiency in Single Comb White Leghorns

IN THE summer of 1939 the senior author in collaboration with Dr. Samuel Lepkovsky undertook a series of experiments on selection for resistance to different nutritional deficiencies in rats and in chicks. Preliminary trials with several substances (pantothenic acid and fatty acids in rats; riboflavin and pantothenic acid in chicks) did not produce particularly encouraging results, and the project on an originally planned comprehensive scale was abandoned. Certain indications that positive results may be obtained with riboflavin deficiency in chicks prompted the present writers to continue tests on a modest scale. The publication of an abstract by Lamoreux and Hutt in 1943 (Genetics 28: 79–80) wherein they reported establishment of strains of White Leghorns differing in resistance to riboflavin deficiency suggested an extension of these tests.Continually inconclusive results indicated that little information is to be gained from limited experiments of the nature conducted by us, and the series .