# Prenatal Aflatoxin B1 Exposure: A Review of Pathogenesis and Impact on Fetal Skeletal Development and Ossification

## TL;DR

This paper reviews how prenatal exposure to aflatoxin B1 can harm fetal bone development and suggests further research is needed to understand and prevent these effects.

## Contribution

The paper systematically reviews the pathogenesis of aflatoxin B1's impact on fetal skeletal development.

## Key findings

- AFB1 exposure is linked to skeletal malformations and ossification defects in fetuses.
- AFB1 affects bone development through vitamin D, calcium metabolism, and inflammatory pathways.
- Oxidative stress and parathyroid hormone alterations are key mechanisms in AFB1-induced skeletal issues.

## Abstract

Prenatal exposure to aflatoxin B1 (AFB1) poses a significant risk to fetal development and is associated with reduced birth weight in humans. Experimental studies consistently show that AFB1 induces fetal abnormalities, with skeletal malformations and ossification defects being the most common. However, the specific impact of AFB1 on fetal osteogenesis remains unclear. Given this knowledge gap, this study aimed to review the existing literature concerning the pathogenesis of AFB1 and its potential influence on bone development. The primary mechanisms implicated in AFB1’s impact on bone include dysfunction in vitamin D and calcium metabolism, alterations in parathyroid hormone production and function, induction of inflammatory responses, and oxidative stress. Collectively, these mechanisms have the potential to impair osteoblast and osteoclast function and, consequently, compromise ossification. Based on these findings, studies should explore and elucidate the effects of AFB1. Elucidating these mechanisms is crucial for mitigating the deleterious impacts of AFB1 on fetal skeletal development.