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Title: Immunogenicity of Structurally Perturbed Hen Egg Lysozyme Adsorbed to Silicone Oil Microdroplets in Wild-Type and Transgenic Mouse Models

Authors:
; ; ; ; ; ; ;
Publication Date:
Sponsoring Org.:
USDOE
OSTI Identifier:
1413387
Resource Type:
Journal Article: Publisher's Accepted Manuscript
Journal Name:
Journal of Pharmaceutical Sciences
Additional Journal Information:
Journal Volume: 106; Journal Issue: 6; Related Information: CHORUS Timestamp: 2017-12-14 19:00:52; Journal ID: ISSN 0022-3549
Publisher:
Elsevier
Country of Publication:
United States
Language:
English

Citation Formats

Chisholm, Carly F., Soucie, Kaitlin R., Song, Jane S., Strauch, Pamela, Torres, Raul M., Carpenter, John F., Ragheb, Jack A., and Randolph, Theodore W.. Immunogenicity of Structurally Perturbed Hen Egg Lysozyme Adsorbed to Silicone Oil Microdroplets in Wild-Type and Transgenic Mouse Models. United States: N. p., 2017. Web. doi:10.1016/j.xphs.2017.02.008.
Chisholm, Carly F., Soucie, Kaitlin R., Song, Jane S., Strauch, Pamela, Torres, Raul M., Carpenter, John F., Ragheb, Jack A., & Randolph, Theodore W.. Immunogenicity of Structurally Perturbed Hen Egg Lysozyme Adsorbed to Silicone Oil Microdroplets in Wild-Type and Transgenic Mouse Models. United States. doi:10.1016/j.xphs.2017.02.008.
Chisholm, Carly F., Soucie, Kaitlin R., Song, Jane S., Strauch, Pamela, Torres, Raul M., Carpenter, John F., Ragheb, Jack A., and Randolph, Theodore W.. 2017. "Immunogenicity of Structurally Perturbed Hen Egg Lysozyme Adsorbed to Silicone Oil Microdroplets in Wild-Type and Transgenic Mouse Models". United States. doi:10.1016/j.xphs.2017.02.008.
@article{osti_1413387,
title = {Immunogenicity of Structurally Perturbed Hen Egg Lysozyme Adsorbed to Silicone Oil Microdroplets in Wild-Type and Transgenic Mouse Models},
author = {Chisholm, Carly F. and Soucie, Kaitlin R. and Song, Jane S. and Strauch, Pamela and Torres, Raul M. and Carpenter, John F. and Ragheb, Jack A. and Randolph, Theodore W.},
abstractNote = {},
doi = {10.1016/j.xphs.2017.02.008},
journal = {Journal of Pharmaceutical Sciences},
number = 6,
volume = 106,
place = {United States},
year = 2017,
month = 6
}

Journal Article:
Free Publicly Available Full Text
This content will become publicly available on May 13, 2018
Publisher's Accepted Manuscript

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  • Alcohol consumption increases reactive oxygen species formation and lipid peroxidation, whose products can damage mitochondrial DNA (mtDNA) and alter mitochondrial function. A possible role of manganese superoxide dismutase (MnSOD) on these effects has not been investigated. To test whether MnSOD overexpression modulates alcohol-induced mitochondrial alterations, we added ethanol to the drinking water of transgenic MnSOD-overexpressing (TgMnSOD) mice and their wild type (WT) littermates for 7 weeks. In TgMnSOD mice, alcohol administration further increased the activity of MnSOD, but decreased cytosolic glutathione as well as cytosolic glutathione peroxidase activity and peroxisomal catalase activity. Whereas ethanol increased cytochrome P-450 2E1 and mitochondrialmore » ROS generation in both WT and TgMnSOD mice, hepatic iron, lipid peroxidation products and respiratory complex I protein carbonyls were only increased in ethanol-treated TgMnSOD mice but not in WT mice. In ethanol-fed TgMnSOD mice, but not ethanol-fed WT mice, mtDNA was depleted, and mtDNA lesions blocked the progress of polymerases. The iron chelator, DFO prevented hepatic iron accumulation, lipid peroxidation, protein carbonyl formation and mtDNA depletion in alcohol-treated TgMnSOD mice. Alcohol markedly decreased the activities of complexes I, IV and V of the respiratory chain in TgMnSOD, with absent or lesser effects in WT mice. There was no inflammation, apoptosis or necrosis, and steatosis was similar in ethanol-treated WT and TgMnSOD mice. In conclusion, prolonged alcohol administration selectively triggers iron accumulation, lipid peroxidation, respiratory complex I protein carbonylation, mtDNA lesions blocking the progress of polymerases, mtDNA depletion and respiratory complex dysfunction in TgMnSOD mice but not in WT mice.« less
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