Journal: |
Anatomical records
Wiley online library
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Abstract: |
Bisphenol A (BPA) is an environmental contaminant that might be harmful. Human exposure to
BPA can occur during the fetal and postnatal periods and extends throughout life. This study aimed
to estimate the effects of oral administration of BPA on rat liver and assess the possibility of
recovery after cessation. Adult male albino rats were orally administered with BPA (50 mg/kg
body weight) for 8 weeks, and then one group was left to recover for 4 weeks. Histological,
immunohistochemical, biochemical, and quantitative real-time polymerase chain reaction (RTqPCR) assessments were performed. Loss of hepatic architecture, vascular dilatation congestion,
and exudation, as well as cellular vacuolation, fat accumulation, and pyknotic nuclei were detected.
Furthermore, inflammatory infiltration, localized metaplasia, and excessive collagen deposition in
the portal triad were observed. Expression of Bcl-2-associated X protein (Bax) and transforming
growth factor beta 1 (TGFβ1) was prominent, denoting apoptosis and fibrosis. After the
administration of BPA, serum levels of alanine aminotransferase (ALT), aspartate
aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, cholesterol, triglycerides, and
low-density lipoproteins (LDL) were enhanced. Additionally, total protein, albumin, and highdensity lipoproteins (HDL) decreased. After a recovery for 4 weeks, hepatic cellular and vascular
pathologies returned to normal, except for some inflammatory infiltration. Regarding biochemical
affection, most of the parameters were directed toward normal during recovery. However, most of
them were still significantly different from controls. This explored BPA hepatotoxicity from
structural and functional aspects, and the possible spontaneous reversibility was confirmed.
However, the precise mechanisms underlying hepatotoxicity or recovery need more in-depth
investigations
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