Dual behavior of N-acetylcysteine during ethanol-induced oxidative stress in embryonic chick brains

Objectives: Ethanol (EtOH) causes oxidative stress in embryos. Because N-acetylcysteine (NAC) failures and successes in ameliorating EtOH-induced oxidative stress have been reported, the objective was to determine if exogenous NAC ameliorated EtOH-induced oxidative stress within embryonic chick brai...

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Published in:	Nutritional neuroscience Vol. 20; no. 8; pp. 478 - 488
Main Authors:	Bauer, Alison K., Fitzgerald, Mary, Ladzinski, Adam T., Lenhart Sherman, Sydney, Maddock, Benjamin H., Norr, Zoe M., Miller, Robert R.
Format:	Journal Article
Language:	English
Published:	England Taylor & Francis 14-09-2017
Subjects:	Acetylcysteine - administration & dosage Acetylcysteine - pharmacology Animals Brain - drug effects Brain - embryology Brain - physiopathology Brain Chemistry - drug effects Cell Membrane - chemistry Chick Embryo Dose-Response Relationship, Drug Ethanol Ethanol - pharmacology Fatty acids Fatty Acids - analysis Fatty Acids, Unsaturated - analysis Glutathione - analysis Glutathione peroxidase Glutathione Peroxidase - analysis Lipid hydroperoxides Lipid Peroxides - analysis N-acetylcysteine Oxidative Stress - drug effects Time Factors Glutathione peroxidase Ethanol Lipid hydroperoxides Fatty acids N-acetylcysteine
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Summary:	Objectives: Ethanol (EtOH) causes oxidative stress in embryos. Because N-acetylcysteine (NAC) failures and successes in ameliorating EtOH-induced oxidative stress have been reported, the objective was to determine if exogenous NAC ameliorated EtOH-induced oxidative stress within embryonic chick brains. Methods: Control eggs were injected with approximately 25 µl of water on day 0, 1, and 2 of development (E 0-2 ). Experimental eggs were injected with dosages of either 3.0 mmol EtOH/kg egg; 747 µmol NAC/kg egg; 3.0 mmol EtOH and 747 µmol NAC/kg egg; 1000 µmol NAC/kg egg; or 3.0 mmol EtOH and 1000 µmol NAC/kg during the first 3 days of development (E 0-2 ). At 11 days of development (E 11 ; late embryogenesis), brains were harvested and subsequently assayed for oxidative stress markers including the loss of long-chain membrane polyunsaturated fatty acids (PUFAs); the accumulation of lipid hydroperoxides (LPO); decreased glutathione (GSH) and glutathione/glutathione disulfide (GSSG) levels; and decreased glutathione peroxidase (GPx) activities. Results: EtOH (3 mmol/kg egg), medium NAC (747 µmol/kg egg), and EtOH and medium NAC promoted oxidative stress. These treatments caused decreased brain membrane long-chain PUFAs; increased LPO levels; decreased GSH levels and GSH/GSSG levels; and decreased Se-dependent GPx activities. High NAC dosages (1000 µmol/kg egg) attenuated EtOH-induced oxidative stress within EtOH and high NAC-treated chick brains. Discussion: Exogenous EtOH and/or medium NAC propagated oxidative stress. Meanwhile, high NAC ameliorated EtOH-induced oxidative stress.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1028-415X 1476-8305
DOI:	10.1080/1028415X.2016.1185261