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686 SECTION | IX Gases, Solvents and Other Industrial Toxicants
VetBooks.ir neurostructural disruption of the CA1 dendritic arbor fol- perturbations, and neurotransmitter imbalance. While cer-
tain congeners and isomers can pose a very serious threat
lowing PCB exposure; however, the branching area of the
to the health of animals and humans, environmental expo-
Purkinje cells returned to normal level. Developmental
exposure to PCBs also resulted in a significantly smaller sure situations are generally such that risks of health
spine density in hippocampus, but not in cerebellum. This effects are generally low. The most significant problem
dysmorphic cytoarchitecture could be the structural basis from these compounds involve accidental poisoning via
for long-lasting neurocognitive deficits in PCB-exposed food supply and consumption of contaminated food indi-
rats (Lein et al., 2007; Yang et al., 2009). Previously, cating that oral ingestion was a major route of exposure.
Pruitt et al. (1999) reported a reduced growth of intra- and Additionally, there are areas of the environment that are
infrapyramidal mossy fibers following developmental heavily contaminated by these chemicals because of past
exposure to PCBs. These studies indicate that developmen- industrial activities. Animals and humans residing in or
tal exposure to a PCB mixture resulted in altered cellular near contaminated locations certainly are at risk of serious
distribution of PKC isoforms, which can subsequently dis- health effects. Efforts must continue to reduce exposure
rupt the normal maintenance of signal transduction in to protect wildlife and humans. The best way to accom-
developing neurons. The perturbations in intracellular sig- plish this is to modernize technological processes to pre-
naling events could lead to structural changes in the brain. vent the release of these chemicals into the environment.
These findings suggest that altered subcellular distribution
of PKC isoforms may be a possible mode of action for ACKNOWLEDGMENTS
PCB-induced neurotoxicity. Fig. 51.1 illustrates the intra-
cellular signaling events, transcription factors, and brain The authors thank Drs. Steven Bursian, John Newsted, and Matthew
morphometry affected by these chemicals. Zwiernik for the material provided in the previous edition of this
PCBs have been shown to induce oxidative stress (Lee book chapter. Also, Dr. Michael F. Hughes of USEPA, Research
Triangle Park, NC and Dr. Ramesh Gupta of Murray State
and Opanashuk, 2004), and this could potentially repre-
University, Hopkinsville, KY are acknowledged for the constructive
sent one mechanism of the deleterious effects of PCBs.
review of this book chapter. The contents of this chapter have been
Recently it has been shown that exposure to PCB 126,
reviewed by the National Health and Environmental Effects
PCB 153, or binary mixtures can increase the occurrence Research Laboratory of the US Environmental Protection Agency,
of DNA oxidative adducts in Sprague Dawley rat hepato- and approved for publication. Approval does not signify that the
cytes which, in turn, can influence the prevalence of liver contents necessarily reflect the views and policies of the Institute or
cancer (Mutlu et al., 2016) Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
CONCLUDING REMARKS AND FUTURE REFERENCES
DIRECTIONS
Abbott, B.D., Birnbaum, L.S., 1991. TCDD exposure of human embry-
PCBs, PBBs, PCDDs, and PCDFs belong to a group of onic palatal shelves in organ culture alters the differentiation of
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Abbott, B.D., Harris, M.W., Birnbaum, L.S., 1992. Comparisons of the
tally and biologically persistent. These chemicals have a
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chain. Residues of these chemicals have been detected in
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developmental exposures are particularly sensitive, and Angus, W.G., Contreras, M.L., 1995. Aroclor 1254 alters the binding of
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depressed circulating TH levels and abnormal thyroid Aragon, A.C., Kopf, P.G., Campen, M.J., et al., 2008. In utero and lac-
cytology; developmental effects on the heart, palate and tational 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin exposure: effects on
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Baldridge, M.G., Marks, G.T., Rawlins, R.G., et al., 2015. Very low-
compromised neural function. Although AhR activation
dose (femtomolar) 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD)
has been attributed to several dioxin-like coplanar com- disrupts steroidogenic enzyme mRNAs and steroid secretion by
pounds, some PCBs that are noncoplanar in nature seem human luteinizing granulosa cells. Reprod. Toxicol. 52, 57 61.
to exert their toxic effects through different mechanisms, Bansal, R., Zoeller, R.T., 2008. Polychlorinated biphenyls (Aroclor
including calcium signaling, oxidative stress, TH 1254) do not uniformly produce agonist actions on thyroid hormone