This study examined whether 17β-estradiol (E2) administration protects against ethanol withdrawal (EW)-associated oxidative insults by assessing oxidative markers thiobarbituric-acid-reacting-substances (TBARS). Ovariectomized rats implanted with E2 (EW/E2) or oil pellets (EW/Oil) received chronic ethanol (7.5% wt./vol., 5 weeks) or control dextrin diet (Dextrin/Oil). At 24 or 48 h of EW, rats were tested for overt EW signs and the cerebellum, hippocampus, and cortex were prepared for TBARS assessment in the presence and absence of FeCl 3. For control experiments, we assessed E2 effects on blood ethanol concentrations and TBARS levels during ethanol exposure prior to EW. The EW/Oil group showed enhanced endogenous- and FeCl 3-stimulated membrane TBARS levels in the cerebellum and hippocampus in a manner inhibited by E2 treatment. There was a relationship between the severity of EW and elevation of TBARS levels, particularly in the cerebellum. The enhanced TBARS levels at 24 h of EW appeared to diminish at 48 h in the hippocampus, but persisted in the cerebellum. E2 treatment did not alter blood ethanol concentrations and ethanol exposure alone did not enhance TBARS levels. These data suggest that EW rather than ethanol enhances brain lipid peroxidation that is transient and brain-region specific. Estrogens protect against the brain lipid peroxidation in a manner independent of blood ethanol concentrations (Supported by NIH/NIAAA 013864).
- 17β-estradiol (E2)
- Ethanol withdrawal (EW)
- Thiobarbituric-acid-reacting-substances (TBARS)