Depletion of oxycarotenoid pigments in chickens and the failure of aflatoxin to alter it.

Aflatoxin, a demonstrated cause of pale bird syndrome in chickens, was investigated for its effects on the depigmentation of chickens placed on a diet low in carotenoids. Chickens were pigmented by feeding for 3 wk a white corn-soy diet supplemented with 50 micrograms free lutein and 0 or 4 micrograms aflatoxin/g diet. Then birds were switched to the same diets unsupplemented with lutein. At 0, 1, 2, 3, 6, and 9 days after switching, jejunal contents and mucosa, serum, liver, and toe web of 4 groups of 10 birds were removed for analysis of their carotenoids by high performance liquid chromatography. In control birds the order of decrease in total lutein was jejunal contents greater than jejunal mucosa greater than serum greater than liver greater than toe web. Aflatoxin did not alter the depletion process, except for minor retardation of lutein depletion in the mucosa and liver. Pharmacokinetic analysis of the data indicated that lutein depletion in the integument was accomplished through three sequential reactions (lutein diester----lutein monoester----lutein----serum lutein) and that aflatoxin had no effect on the reactions. These results imply that aflatoxin induces pale bird syndrome by interfering with the accumulation of pigment by chickens rather than by enhancing the depletion of pigment.

Aflatoxin-impaired ability to accumulate oxycarotenoid pigments during restoration in young chickens.

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.

Focal loss of pigment in the Belgian Tervuren dog.

Hypopigmentation most commonly affecting the face and mouth of the Belgian Tervuren dog was characterized by an absence of melanocytes in the epidermis. Pigment loss usually occurred during young adulthood, and although there was partial repigmentation in some dogs, complete repigmentation did not occur. Treatment with vitamin and mineral supplements was unrewarding. The condition appeared to have some degree of heritability and to be similar to vitiligo in man.