Zinc supplementation does not attenuate alcohol-induced cerebellar Purkinje cell loss during the brain growth spurt period

Background: Alcohol-induced zinc deficiency is one of the mechanisms propos ed as a cause of developmental brain damage associated with fetal alcohol s yndrome. It is known that alcohol exposure during the brain growth spurt pe riod leads to cerebellar Purkinje cell loss. Therefore, this study examined whether zinc supplementation was capable of preventing alcohol-induced Pur kinje cell loss in the cerebellar vermis in a neonatal rat model system. Methods: Sprague-Dawley rat pups were given alcohol (EtOH; 45 g/kg/day), zi nc (Zn; 0.54 mg/ml diet; [10 times the regular diet Zn concentration]), or both from postnatal days (PD) 4 through 9 using the artificial-rearing para digm. A gastrostomy control (GC) and a suckle control group (SC) also were included. Ah pups were killed on PD 10. Following perfusion, the cerebellar vermis was dissected and processed for stereological cell counting. The to tal number of Purkinje cells and the volume BE the cerebellar vermis were d etermined. Results: Alcohol produced a significant loss of Purkinje tells compared wit h that in the GC group (no EtOH and no Zn supplement). The zinc supplementa tion had no effect in attenuating alcohol-induced Purkinje cell loss in the cerebellar vermis. In fact, the serum zinc concentration data indicated hi gher zinc concentrations following either EtOH or Zn treatment. Interesting ly, the GC group showed a significantly lower zinc concentration compared w ith the SC group, even though no significant difference in Purkinje cell nu mbers was observed between these two control groups. Conclusion: These findings indicate that alcohol exposure during the third trimester equivalent did not result in zinc deficiency in this neonatal rat model system, nor did zinc supplementation rescue the alcohol-induced Purk inje cell loss in the cerebellar vermis. These findings showed clearly that the serum zinc concentration was not correlated with Purkinje cell loss, s uggesting that alcohol-induced loss of cerebellar Purkinje cells in this ne onatal rat model system is independent of the availability of serum zinc.