Pathological mecha
Pathological
mechanisms of liver injury caused by oral administration of bisphenol A
Rehab M. Hussein and
Jehane I. Eid
Department of Zoology,
Faculty of Science, Cairo University, Egypt
Abstract: Bisphenol
A (BPA) is a widely produced, endocrine disrupting compound that is
pervasive in the environment. BPA is a contaminant with increasing exposure to
it and exerts both toxic and estrogenic effects on mammalian cells. Due to
variability in study design, the disruptive effects of BPA have been proven
difficult to experimentally replicate. BPA exposure
causes oxidative stress leading to inflammation in the liver.
However, its precise mechanisms are not fully elucidated. This study
was designed to assess the molecular, biochemical and histological alterations
behind inflammation and hepatic injury caused by BPA. We investigated the
disruptive hepatotoxic actions of oral exposure to BPA by measuring changes in oxidative stress,
cytokine expression and histopathology in the liver tissue of mice. Swiss
albino mice were exposed to BPA via drinking water at doses of 1/50, 1/40,
1/30, 1/20 and 1/10 LD50 (48, 60, 80, 120 and 240 mg/kg b.w. respectively) for
three weeks. Oral exposure to BPA caused dose-related hepatotoxic effects,
including oxidative stress in terms of increase lipid peroxidation and
decrease catalase antioxidant enzyme. The mRNA levels of liver
pro-inflammatory cytokines IL-6, and IL-1β were up-regulated in a dose
dependant manner by BPA. Our data demonstrated that BPA exposure causes liver
injury, which is associated with remarkable inflammatory
response, oxidative stress, and histopathological alterations.
[Rehab M. Hussein and Jehane I. Eid. Pathological
mechanisms of liver injury caused by oral administration of bisphenol A. Life Sci J 2013;10(1):663-673]. (ISSN:
1097-8135). http://www.lifesciencesite.com.
Keywords: Bisphenol A – hepatotoxicity - inflammatory cytokines – kupffer cells – oxidative stress
