@article{tyczkowski_hamilton_ruff_1991, title={ALTERED METABOLISM OF CAROTENOIDS DURING PALE-BIRD SYNDROME IN CHICKENS INFECTED WITH EIMERIA-ACERVULINA}, volume={70}, ISSN={["0032-5791"]}, DOI={10.3382/ps.0702074}, abstractNote={The progression of changes in carotenoid metabolism during pale-bird syndrome caused by a coccidial infection was investigated. Male broiler chickens 15 days of age on a yellow corn and soybean meal-based diet were infected with Eimeria acervulina oocysts and their serum, liver, and toe webs were sampled at 0, 4, 6, and 10 days postinfection for HPLC analysis of carotenoids. At 4 days postinfection a drastic reduction (71%) in serum lutein, the main body carotenoid, and smaller reductions in liver (58%) and toe webs (38%) occurred. Derivative forms of lutein, mainly esters, continued to be lost from tissues for 10 days postinfection. These carotenoids were apparently lost via the intestinal tract because birds placed on a white corn and soybean meal-based diet at time of infection had lutein in their jejunal contents even at 7 days postinfection. The loss of carotenoids from the body was accompanied by a decreasing ability to absorb canthaxanthin, a red carotenoid, from the intestinal contents. The absorption of canthaxanthin measured at 0, 3, 4, 5, 6, and 7 days reached its low point of 1% of preinfection ability on Day 5 before a slow recovery commenced. Thus, the pale-bird syndrome caused by E. acervulina appeared to be the result of a loss of previously absorbed carotenoids coupled with drastic malabsorption of dietary carotenoids.}, number={10}, journal={POULTRY SCIENCE}, author={TYCZKOWSKI, JK and HAMILTON, PB and RUFF, MD}, year={1991}, month={Oct}, pages={2074–2081} }
 @article{tyczkowski_schaeffer_hamilton_1991, title={MEASUREMENT OF MALABSORPTION OF CAROTENOIDS IN CHICKENS WITH PALE-BIRD SYNDROME}, volume={70}, ISSN={["0032-5791"]}, DOI={10.3382/ps.0702275}, abstractNote={Because pale-bird syndrome (PBS), defined as the failure of birds to realize the color potential of their diet, has been demonstrated to be caused by malabsorption or by hyperexcretion of carotenoids, a method for measuring malabsorption of carotenoids would be useful. The absorption of dietary canthaxanthin, a red diketocarotenoid, into serum during aflatoxicosis was measured in an experiment with a 2 x 9 factorial arrangement of treatments (0 and 5 micrograms of aflatoxin/g of diet; serum collected at 0, 2, 4, 6, 8, 10, 12, 14, and 24 h after a standard meal fed to four groups of 10 3-wk-old birds). Serum canthaxanthin levels determined by HPLC attained plateau values between 8 and 14 h after the meal. The absorption of canthaxanthin was depressed significantly (P less than .05) in birds with aflatoxicosis from 4 to 24 h after feeding the standard meal. Four field flocks diagnosed as having PBS were tested for malabsorption by intubating 10 birds with a standard amount of canthaxanthin and measuring serum canthaxanthin 12 h later. One flock had about 85% normally pigmented birds and 15% extremely pale birds, the second flock had a coccidiosis history, the third had a Newcastle disease history, and the fourth had a history of both coccidiosis and Newcastle disease. The flocks were 5- to 6-wk-old, received feed of the same manufacture, and their disease outbreaks had occurred 2 wk earlier.(ABSTRACT TRUNCATED AT 250 WORDS)}, number={11}, journal={POULTRY SCIENCE}, author={TYCZKOWSKI, JK and SCHAEFFER, JL and HAMILTON, PB}, year={1991}, month={Nov}, pages={2275–2279} }
 @article{tyczkowski_hamilton_1991, title={PREPARATION OF PURIFIED LUTEIN AND ITS DIESTERS FROM EXTRACTS OF MARIGOLD (TAGETES-ERECTA)}, volume={70}, ISSN={["0032-5791"]}, DOI={10.3382/ps.0700651}, abstractNote={Abstract The unavailability of low-priced lutein, the major carotenoid in typical poultry diets and tissues, in purity good enough for analytical standards has hindered research on carotenoids and the production of efficiently pigmented chickens by the poultry industry. Simple extraction and crystallization procedures were developed that gave lutein of 96.0 to 99.2% purity in 57 to 68% yield depending on the batch of commercially available saponified extracts of marigold (Tagetes erecta) petals, which were the source of impure lutein. Reaction of the purified (99.2%) lutein with fatty acyl chlorides gave the diesters of lutein in >99% purity and yield as judged by HPLC. The purity of the products was equal or superior to commercial standards, which are very expensive and not always available.}, number={3}, journal={POULTRY SCIENCE}, author={TYCZKOWSKI, JK and HAMILTON, PB}, year={1991}, month={Mar}, pages={651–654} }
 @article{tyczkowski_schaeffer_hamilton_1989, title={INFLUENCE OF DIETARY LIPIDS ON PIGMENTATION OF YOUNG CHICKENS}, volume={68}, ISSN={["0032-5791"]}, DOI={10.3382/ps.0681246}, abstractNote={Abstract Supplementation of a basal casein-dextrose diet (40 μg added lutein/g) with 2% coconut or olive oil increased serum lutein significantly (P Coconut oil, which contains primarily short chain, saturated fatty acids, gave higher (P}, number={9}, journal={POULTRY SCIENCE}, author={TYCZKOWSKI, JK and SCHAEFFER, JL and HAMILTON, PB}, year={1989}, month={Sep}, pages={1246–1254} }
 @article{schaeffer_tyczkowski_riviere_hamilton_1988, title={Aflatoxin-Impaired Ability to Accumulate Oxycarotenoid Pigments During Restoration in Young Chickens}, volume={67}, ISSN={0032-5791}, url={http://dx.doi.org/10.3382/ps.0670619}, DOI={10.3382/ps.0670619}, abstractNote={The mechanism by which aflatoxin causes paling in chickens was investigated by measuring its effect on the restoration of pigments in 3-wk-old birds made pale by feeding a white corn-soy diet. Pigment restoration was accomplished by feeding the same diet supplemented with lutein (70 micrograms/g of diet), which is the major oxycarotenoid pigment in chicken diets and tissues. The oxycarotenoids (free, monoester, and diester forms of lutein) in the toe web, liver, serum, and jejunal mucosa of control and aflatoxin-fed (2 micrograms/g of diet) birds were measured by HPLC at 0, 1, 2, 3, 6, and 9 days of repletion. Aflatoxin caused a significant (P less than .05) depression of all forms of lutein in the toe web. In the liver, aflatoxin decreased lutein significantly (P less than .05) but increased lutein monoester and lutein diester. Lutein accumulation in serum and mucosa were inhibited significantly (P less than .05) starting on Days 2 and 3, respectively. These data imply that the normal accumulation of lutein from the diet proceeded into and through the mucosa to the serum to depot sites in the liver and integument, where lutein was acylated to its monoester, which was acylated to its diester. Further, aflatoxin inhibited, apparently independently, the accumulation of lutein by the mucosa, serum, liver, and integument. Pharmacokinetic analysis of the data indicated that both acylation steps in the integument were sensitive to aflatoxin, but the passage of lutein from serum into the integument was not affected.}, number={4}, journal={Poultry Science}, publisher={Elsevier BV}, author={Schaeffer, Jonathan L. and Tyczkowski, Juliusz K. and Riviere, J. Edmond and Hamilton, Pat B.}, year={1988}, month={Apr}, pages={619–625} }