Abstract
Cyclic bouts of intermittent, normobaric hypoxia (IH) have been found to protect the central nervous system from ischemic and excitotoxic injury. We investigated whether IH mitigates oxidative brain injury in male rats subjected to ethanol intoxication and abrupt ethanol withdrawal (EW). We assessed the effects of IH on superoxide generation, protein oxidation, and mitochondrial membrane swelling and rupture as a marker of mitochondrial permeability transition pore (PTP) opening. Male rats consumed dextrin control diet or 6.5% ethanol diet for 5 weeks. During the last 20 days of the diet, rats were treated with repetitive (5‐8/day), brief (5‐10 min) periods of hypoxia (9.5‐10% inspired O2) separated by 4 min exposures to room air. Cerebellum, cortex and hippocampus were biopsied at the end of the ethanol diet or at 24 hours of EW. Superoxide and protein carbonyl contents in tissue homogenates and rate of absorbance decline at 540 nm in mitochondrial suspensions were measured as indicators of oxidative stress, protein oxidation and PTP opening, respectively. EW increased superoxide and protein carbonyl contents and accelerated PTP opening in all three brain areas in a manner that was ameliorated by IH. These results suggest that antecedent IH conditioning during chronic ethanol consumption attenuates subsequent oxidative damage to the brain in ethanol withdrawn rats. (supported by NIAAA/AA013864, NIAAA/AA015982, NCCAM/AT003598).
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