Page 721 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
P. 721

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
                                                                  medial epithelial cells. Teratology. 43 (2), 119 132.
             compounds that are structurally related and environmen-
                                                                Abbott, B.D., Harris, M.W., Birnbaum, L.S., 1992. Comparisons of the
             tally and biologically persistent. These chemicals have a
                                                                  effects of TCDD and hydrocortisone on growth factor expression
             tendency to bioaccumulate and biomagnify in the food
                                                                  provide insight into their interaction in the embryonic mouse palate.
             chain. Residues of these chemicals have been detected in
                                                                  Teratology. 45 (1), 35 53.
             remote areas of the world and in a variety of animal spe-
                                                                Ahmed, R.G., 2013. Early weaning PCB 95 exposure alters the neonatal
             cies, including humans. Exposure to these chemicals has  endocrine system: thyroid adipokine dysfunction. J. Endocrinol. 219
             been linked to a broad spectrum of effects. Fetal and early  (3), 205 215.
             developmental exposures are particularly sensitive, and  Angus, W.G., Contreras, M.L., 1995. Aroclor 1254 alters the binding of
             can have different outcomes from adult exposure. Latent  125 I-labeled nerve growth factor in PC12 cells. NeurosciLetter. 191
             effects of early exposures include, but are not limited to,  (1), 23 26.
             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
                                                                  fetal and adult cardiac gene expression and adult cardiac and renal
             kidney; delayed cognitive development; altered sensory
                                                                  morphology. Toxicol. Sci. 101 (2), 321 330.
             and motor abilities; and reproductive impairment and
                                                                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
   716   717   718   719   720   721   722   723   724   725   726