Mycotoxicity and embryonic development: I- Aflatoxin B1 reduces quality and birth rate during mice embryonic development

Abstract

Mycotoxins are fungal products often found in food, formed during growth, harvesting, drying or storage of fruits, seeds, or grains, leading to a variety of toxic effects in humans and animals. Aflatoxins are a family of polyketide secondary metabolite produced by the food-contaminating moulds Aspergillus parasiticus and Aspergillus flavus. Aflatoxin B1 (AFB1) is a carcinogenic, teratogenic, mutagenic and growth inhibitory mycotoxin. To explore the negative morphological effects of AFB1 on the developing mice embryo, 50 adult females albino mice (CD1) were divided into five groups (10 females for each group): Control, positive control and three groups treated with a daily oral dose of 5, 10 or 20 μg/kg bw of AFB1 extract. Fifteen days after treatments, females were caged with males. Pregnancy, mortality, embryos number rates and body weight of female mice and infants were recorded. At 21 days old, crown rump, head, ear, tail, fore and hind-limb lengths of mice infants were investigated. Current data showed a decrease in pregnancy and embryo number rate among females in the animals treated with 10 & 20 μg AFB1, while treatment with 5 μg showed an increase in pregnancy and embryo number rate compared to control one, while mortality rate among fetuses increased in the three experimental animals treated with AFB1. Some cases of abortion were observed in 10 & 20 μg groups, while ulcers were observed in 20 μg groups. Weight and all morphometric parameters showed significant decrease except tail length that showed insignificant increase in the treated groups compared to the control one, while ear length showed significant increase. Different congenital malformations were observed in infants such as tail loss, delayed hair and teeth development and poor ossification in treated groups. The present study demonstrated that AFB1 induced developmental anomalies and reduced quality and birth rate. Data clarified that minimum concentration of AFB1 required to induce teratogenicity is far beyond the minimum concentrations estimated in earlier literatures. It is suggested that AFB1 might change genetic elements and consequently interfere with bone mineralization and induce teratogenicity and anomalies during mice embryonic development. Further studies are required to explore the mechanism of action.

Keywords

• aflatoxicosis
• teratogenicity
• congenital anomalies
• birth rate
• abortion.