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Published on: April 26, 2018
Effects of polychlorinated biphenyls on the development of neuronal cells in growth period; structure-activity
1Department of Neurology, Catholic University of Daegu School of Medicine, Daegu 705-718, Korea.
Insights
Non-coplanar polychlorinated biphenyls (PCBs) are more potent neurotoxins than coplanar PCBs, increasing protein kinase C activity and reactive oxygen species. These findings suggest non-coplanar PCBs should be included in future risk assessments.
Area of Science:
- Environmental Toxicology
- Neuroscience
- Biochemistry
Background:
- Polychlorinated biphenyls (PCBs) accumulate in the body, causing adverse health effects, particularly neurotoxicity in neonates.
- Understanding the structure-activity relationship of PCB congeners is crucial for assessing their neurotoxic potential.
Purpose of the Study:
- To analyze the structure-activity relationship among PCB congeners.
- To investigate the mechanism of PCB-induced neurotoxicity in neonatal rat cerebellar granule cells.
- To identify potential biomarkers for differentiating PCB congener toxicity.
Main Methods:
- Exposure of neonatal rat cerebellar granule cells to different structural PCBs.
- Measurement of total protein kinase C (PKC) activities and isoforms using [(3)H]PDBu binding assay.
- Assessment of reactive oxygen species (ROS) levels and mRNA induction of neurogranin (RC-3) and growth associated protein-43 (GAP-43) via Western blot and RT-PCR.
Main Results:
- Non-coplanar PCBs significantly increased total PKC-α and βII activity compared to coplanar PCBs.
- Non-coplanar PCBs induced higher levels of ROS and mRNA for RC-3 and GAP-43.
- RC-3 and GAP-43 mRNA induction may serve as biomarkers differentiating non-coplanar from coplanar PCBs.
Conclusions:
- Non-coplanar PCBs are more potent neurotoxic congeners than coplanar PCBs.
- The study provides evidence for including non-coplanar PCBs in future risk assessments for neuroendocrinal adverse effects.
- This research enhances the accuracy of PCB exposure risk assessment by considering structural congener differences.
Abstract:
Polychlorinated biphenyls (PCBs) are accumulated in our body through food chain and cause a variety of adverse health effects including neurotoxicities such as cognitive deficits and motor dysfunction. In particular, neonates are considered as a high risk group for the neurotoxicity of PCBs exposure. The present study attempted to analyze the structure-activity relationship among PCB congeners and the mechanism of PCBs-induced neurotoxicity. We measured total protein kinase C (PKC) activities, PKC isoforms, reactive oxygen species (ROS), and induction of neurogranin (RC-3) and growth associated protein-43 (GAP-43) mRNA in cerebellar granule cells of neonatal rats with phorbol 12, 13-dibutyrate ([(3)H]PDBu) binding assay, western blot, ROS assay, and reverse transcription PCR (RT-PCR) analysis respectively following the different structural PCBs exposure. Only non-coplanar PCBs showed a significant increase of total PKC-α and βII activity as measured with [(3)H]PDBu binding assay. ROS were more increased with non-coplanar PCBs than coplanar PCBs. The mRNA levels of RC-3 and GAP-43 were more induced with non-coplanar PCBs than coplanar PCBs, indicating that these factors may be useful biomarkers for differentiating non-coplanar PCBs from coplanar PCBs. Non-coplanar PCBs may be more potent neurotoxic congeners than coplanar PCBs. This study provides evidences that non-coplanar PCBs, which have been neglected in the risk assessment processes, should be added in the future to improve the quality and accuracy of risk assessment on the neuroendocrinal adverse effects of PCBs exposures.
