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

• 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
• ISSN: 1028-415X; 1476-8305
• DOI: 10.1080/1028415X.2016.1185261

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.