Embryonic exposure to aflatoxin‐B₁: Mutagenicity and influence on development and immunity

Abstract

Chick embryos were mutagenized in ovo in order to study developmentally related alterations in immune functions in survivors of this prenatal toxicant insult. In this experimental system, a single exposure of 6-day chick embryos to 0.1 microgram aflatoxin-B1 (AF-B1) in 10 microliters of acetone was employed, and the control embryos received 10 microliters of solvent alone. This dosage of AF-B1 administered to 6-day embryos was found to increase the incidence of sister chromatid exchanges in blood cells approximately fivefold above the baseline observed in solvent controls. A second sham control, where no solvent was administered, was included in some experiments. The cell cycle times in blood increased slightly during the initial exposure to AF-B1. However, a majority of the AF-B1 and acetone exposed embryos survived and hatched without incident. Losses occurred mainly in the latter part of embryogenesis. After hatching, no significant differences were observed in body weight between different treatment groups up to 26 weeks of age and no change in primary humoral immunity was detected. In contrast, two parameters of cell-mediated immunity, graft vs host (GvH), and cutaneous basophil hypersensitivity (CBH) reactions were both depressed as a result of exposure to AF-B1. The AF-B1 treatment group was significantly reduced in the GvH reaction compared with sham-treated controls. In the CBH assay, AF-B1-exposed chicks showed reduced immunity compared with acetone controls. These results suggest that long-term selective immune depression can occur following embryonic exposure to AF-B1.

Determination of the effects of aflatoxin B1givenin ovoon the proximal tibial growth plate of broiler chickens: histological, histometric and immunohistochemical findings

“…The higher mortality of fertilized eggs occurred with increasing toxin doses in a positive doseÁresponse manner (Table 1). These results are similar to the results of previous studies (Dietert et al, 1985;Prelusky et al, 1987;Celik et al, 2000;Sur & Celik, 2003).…”

“…In the present study, relatively higher doses (5, 15 and 40 ng AFB 1 /egg) were used since the limits are frequently exceeded. In poultry food and foodstuffs, contamination and residues may cause a serious poultry production problem in fertilized eggs (Dietert et al, 1985). The carry-over of AF from the feed to the fertilized egg causes serious economic loss because the residual AF can affect embryo viability and hatchability (Qureshi et al, 1998;Sur et al, 2011) and causes organ malformations (Cilievici et al, 1980).…”

“…In developing and fast-growing bones, such as the tibia, growth plate cartilage determines the rate of longitudinal growth as well as the ultimate length of bones (Orth, 1999). Previously, Fusarium roseum-contaminated corn was found to induce a high Fusarium-induced osteochondrosis incidence of leg lesions in broiler chicks (Walser et al, 1982;Haynes et al, 1985;Farquharson, 1999). Chicks fed 2% F. roseum culture had a 90% incidence of tibial dyschondroplasia, which was well advanced by 4 to 6 weeks of age (Walser et al, 1982;Haynes et al, 1985).…”

“…Although in Turkey the legal upper limits in food for laying hens are 10 mg/kg for AFB 1 and 20 mg/kg for AF (Ministry of Agriculture of Turkey, 1997), surveys have shown that these limits were frequently exceeded (Nizamlioglu, 1996;Oguz et al, 2011). In poultry food and foodstuffs, AF contamination and residues may be a serious problem in the poultry industry because of the residues in fertilized eggs (Dietert et al, 1985). Moreover, the carry-over of AF from the feed to the fertilized egg might result in economic losses by decreasing embryo viability and hatchability (Qureshi et al, 1998), and by causing several organ malformations (Cilievici et al, 1980).…”

“…The growth plate comprises chondrocytes and their extracellular matrix where proteoglycans and collagen type II predominate (Farquharson et al, 1992;Farquharson & Jefferies, 2000). During the longitudinal bone growth, progressive changes occur in the proliferation rate, shape and size of the chondrocytes, and in the synthesis and deposition of extracellular matrix components of the growth plate cartilage (Farquharson et al, 1995;Farquharson & Jefferies, 2000). These gradual changes result in formation of the resting, proliferating, maturing/transitional, hypertrophic and degenerating chondrocyte zones in the epiphyseal growth plate (Loveridge et al, 1993;Germiller & Goldstein, 1997).…”