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Related Experiment Video

Updated: May 7, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

Polychlorinated biphenyls increase apoptosis in the developing rat brain.

Dongren Yang1, Pamela J Lein

  • 1Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, 95616, USA.

Current Neurobiology
|September 21, 2013
PubMed
Summary

Perinatal exposure to polychlorinated biphenyls (PCBs) causes neurotoxicity in developing rats. This study shows PCBs increase oxidative stress and neuronal apoptosis in newborn rat brains, particularly the cerebellum.

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Area of Science:

  • Environmental toxicology
  • Neuroscience
  • Developmental biology

Background:

  • Epidemiological and animal studies link perinatal polychlorinated biphenyls (PCBs) exposure to cognitive deficits.
  • In vitro studies suggest PCBs induce neuronal apoptosis via reactive oxygen species (ROS).
  • In vivo evidence for PCB-induced neurotoxicity mechanisms in the developing brain is lacking.

Purpose of the Study:

  • To investigate the in vivo effects of perinatal PCB exposure on apoptosis and oxidative damage in the developing rat brain.
  • To determine if PCB-induced neurotoxicity involves oxidative stress and altered neuronal cell death.

Main Methods:

  • Rat pups were exposed to Aroclor 1254 (A1254) via maternal diet during gestation and lactation.
  • Apoptosis (caspase-3 activity, TUNEL) and oxidative damage markers (3-nitrotyrosine, 4-hydroxynonenal) were quantified in brain regions.
Keywords:
Apoptosisdevelopmental neurotoxicityneurodevelopmentoxidative stresspolychlorinated biphenyls

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  • Analyses were performed in newborn and weanling rats.

    • Main Results:

    • A1254 exposure significantly increased caspase-3 activity in newborn rat cortex, hippocampus, and cerebellum, with the cerebellum most affected.
    • PCB-induced apoptosis was confirmed in the cerebellum using TUNEL.
    • Elevated levels of 3-nitrotyrosine and 4-hydroxynonenal in the cerebellum indicated increased protein and lipid oxidative damage.

    Conclusions:

    • Perinatal PCB exposure induces oxidative stress and alters apoptosis in the developing rat brain in vivo.
    • These findings support oxidative stress as a key mechanism in PCB developmental neurotoxicity.
    • The cerebellum is particularly vulnerable to PCB-induced neurotoxic effects during development.