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Assessment of the Mitigative Capacity of Dietary Zinc on PCB126 Hepatotoxicity and the Contribution of Zinc to Toxicity
Journal article   Open access   Peer reviewed

Assessment of the Mitigative Capacity of Dietary Zinc on PCB126 Hepatotoxicity and the Contribution of Zinc to Toxicity

William D Klaren, Katherine N Gibson-Corley, Brian Wels, Donald L Simmons, Michael L McCormick, Douglas R Spitz and Larry W Robertson
Chemical research in toxicology, Vol.29(5), pp.851-859
05/16/2016
DOI: 10.1021/acs.chemrestox.6b00022
PMCID: PMC5100827
PMID: 26967026
url
https://doi.org/10.1021/acs.chemrestox.6b00022View
Published (Version of record) Open Access

Abstract

Hepatic levels of the essential micronutrient, zinc, are diminished by several hepatotoxicants, and the dietary supplementation of zinc has proven protective in those cases. 3,3',4,4',5-Pentachlorobiphenyl (PCB126), a liver toxicant, alters hepatic nutrient homeostasis and lowers hepatic zinc levels. The current study was designed to determine the mitigative potential of dietary zinc in the toxicity associated with PCB126 and the role of zinc in that toxicity. Male Sprague-Dawley rats were divided into three dietary groups and fed diets deficient in zinc (7 ppm Zn), adequate in zinc (30 ppm Zn), and supplemented in zinc (300 ppm). The animals were maintained for 3 weeks on these diets, then given a single IP injection of vehicle or 1 or 5 μmol/kg PCB126. After 2 weeks, the animals were euthanized. Dietary zinc increased the level of ROS, the activity of CuZnSOD, and the expression of metallothionein but decreased the levels of hepatic manganese. PCB126 exposed rats exhibited classic signs of exposure, including hepatomegaly, increased hepatic lipids, increased ROS and CYP induction. Liver histology suggests some mild ameliorative properties of both zinc deficiency and zinc supplementation. Other metrics of toxicity (relative liver and thymus weights, hepatic lipids, and hepatic ROS) did not support this trend. Interestingly, the zinc supplemented high dose PCB126 group had mildly improved histology and less efficacious induction of investigated genes than did the low dose PCB126 group. Overall, decreases in zinc caused by PCB126 likely contribute little to the ongoing toxicity, and the mitigative/preventive capacity of zinc against PCB126 exposure seems limited.
Zinc - administration & dosage Gene Expression Oxidative Stress Rats Feeding Behavior Male Animals Metallothionein - genetics Diet Liver - drug effects Polychlorinated Biphenyls - toxicity Receptors, Aryl Hydrocarbon - metabolism Zinc - pharmacology Superoxide Dismutase - metabolism ISRP Project 1 2015-2020 Synthesis Core

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