Hematological toxicology following embryonic exposure to aflatoxin-B1.

The influence of embryonic exposure to aflatoxin-B1 (AF-B1) upon the erythroid system of the maturing chicken was examined using a variety of assays. Since the chick embryo is known to possess mixed-function oxidase activity, this animal serves as an excellent model system for studies of human fetal toxicology. AF-B1 (0.1 microgram) was administered to either 6- or 12-day embryos by the air sac method. This level of AF-B1 was highly mutagenic and was found to induce an average of 10.6 sister chromatid exchanges (SCEs) per cell compared with 1.8 SCEs per cell for the acetone control solvent. Despite selection against treated embryos through acute and chronic embryonic toxicity, hatched chicks from AF-B1 treatment groups exhibited erythroid anemia when compared to the acetone controls. Cell count, hematocrit, and hemoglobin concentration were all significantly reduced in the 12-day AF-B1 treatment groups compared with controls. Both sexes were equally affected. While the number of peripheral erythrocytes was reduced following exposure to AF-B1, the differentiation status of erythrocytes was apparently unaltered. Mean cell volume, percentage of circulating reticulocytes, and incidence of an erythroid differentiation marker, chicken fetal antigen, were parameters in which no treatment effects were observed. An apparent maturation effect was noted since adult hematocrits were similar between control and treatment groups. Possible explanations for this age effect are discussed. The ability to detect significant posthatch erythroid toxicity following embryonic exposure to mutagenic levels of AF-B1 suggests the importance of this general approach to perinatal carcinogenic evaluation.