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Intermittent Hypoxia Protects Brain from Ethanol Withdrawal: Role of Free Radicals
Author(s) -
Jung Marianna E,
Mallet Robert T,
Downey H Fred,
Simpkins James W
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.716.9
Subject(s) - neuroprotection , chemistry , intermittent hypoxia , hypoxia (environmental) , ethanol , medicine , endocrinology , anesthesia , pharmacology , biochemistry , oxygen , organic chemistry , obstructive sleep apnea
We have reported that intermittent hypoxia (IH) conditioning protected against behavioral signs of ethanol withdrawal (EW) in rats. Here, we tested the hypothesis that IH‐induced free radicals evoke neuroprotective adaptations against EW. Male rats consumed a 6.5% ethanol diet for 5 weeks, and then the diet was abruptly withdrawn to create EW stress (EW group). During the last 20 d of ethanol consumption, subsets of these rats received IH [repetitive (5–8 cycles/d), brief (5–10 min) periods of hypoxia (9.5–10% O 2 )] with (EW/IH + NAC) or without (EW/IH) daily ip injections (100 mg/kg) of the antioxidant N ‐acetyl cysteine (NAC) to test whether blockade of IH‐induced free radical generation would blunt IH‐induced protection against EW insults. Table (means ± SEM, n = 5–6): EW rats showed severe EW signs, including tremor and rigidity, and excess cerebellar superoxide content vs. sham rats fed an isocaloric dextrin diet (*P < 0.05 vs. sham). IH mitigated EW signs and superoxide formation ( † P < 0.05 vs. EW), but NAC treatment during the IH program abrogated neuroprotection during subsequent EW. These results suggest that IH‐induced free radicals activate endogenous defenses against EW insults. (Support: NIAAA/AA013864, NIAAA/AA015982, NCCAM/AT003598)