Abstract #405

# 405
Aflatoxin compromises development of the preimplantation bovine embryo through mechanisms independent of reactive oxygen production.
Y. Jiang*1, P. J. Hansen1, I. M. Ogunade2, X. Yao1, T. Amaral1, K. G. Arriola1, D. Vyas1, A. T. Adesogan1, 1Department of Animal Sciences, University of Florida, Gainesville, FL, 2Division of Food and Animal Science, Kentucky State University, Frankfort, KY.

Aflatoxin is a potent carcinogen often detected in animal feedstuffs. Aflatoxin has been reported to impair fetal development in humans and mice but its actions on development of the preimplantation bovine embryo are not known. The objective was to study the effects of different concentrations of aflatoxin on development of the preimplantation bovine embryo and understand mechanisms underlying these effects. Experiments were conducted with embryos produced in vitro and cultured, beginning after fertilization with various concentrations of aflatoxin. For Experiment 1, embryos were treated with control, AF40 (40 µg/L, aflatoxin B1, AFB1); or AF400 (400 µg/L AFB1, 4) or AF4000 (4000 µg/L AFB1). Proc Glimmix of SAS was used to analyze the data. The statistcal model includes fixed effect of treatment and random effect of replicate. Applying AFB1 at 40, 400, and 4000 µg/L tended to reduce (P < 0.10) cleavage rate. As compared with control, AF40 reduced the percent of oocytes becoming blastocysts and the percent of cleaved embryos becoming blastocysts (19.7 vs 8.1% and 30.3 vs 14.3%, respectively, P < 0.05). Complete inhibition of blastocyst formation occurred for AF400 and AF4000. Experiments 2 and 3 involved a 2 × 2 factorial design with effects of AFB1 (0 and 40 µg/L) and the antioxidant Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) (0 and 5 µM) and their interaction on production of reactive oxygen species (ROS) in putative zygotes (Experiment 2) and development (Experiment 3). The statistical model included fixed effects of AFB1 and Trolox and their interaction as well as the random effect of replicate. ROS was increased by AF40 (P < 0.05) and this effect was reversed by Trolox (AF40 x Trolox; P < 0.05). However, Trolox did not prevent the reduction in blastocyst rate caused by AF40 in Experiment 3. Thus, the antidevelopmental effects of AFB1 are not caused solely by increased ROS production. Rather, other underlying mechanisms exist for the adverse effects of aflatoxin on embryonic development.

Key Words: aflatoxin, antioxidant, embryonic development