Literature DB >> 12170110

Melatonin (an antioxidant) does not ameliorate alcohol-induced Purkinje cell loss in the developing cerebellum.

Russell B Edwards1, Ehrine J P Manzana, Wei-Jung A Chen.   

Abstract

BACKGROUND: One popular mechanism proposed to account for alcohol-induced brain damage is the generation of free radicals after alcohol exposure. Therefore, it is reasonable to hypothesize that administration of an antioxidant should reduce the severity of alcohol-induced brain damage. Recently, melatonin has been shown to be an effective free-radical scavenger. In this study, the ability of melatonin to attenuate alcohol-induced cerebellar Purkinje cell loss in the cerebellar vermis and lobule I was assessed.
METHODS: Sprague-Dawley rat pups were used in this study. These neonatal pups were exposed to alcohol (4.5 g/kg), melatonin (10 mg/kg), both alcohol and melatonin, or control vehicle via artificial-rearing methods from postnatal day (PD) 4 to PD 9. Alcohol, melatonin, or control vehicle was mixed with milk formula in 2 of the daily 12 feedings. Pups were killed 90 min after the beginning of the second alcohol feeding on PD 9.
RESULTS: Alcohol significantly reduced the Purkinje cell numbers in the vermis and lobule I, with a higher percentage of cell loss in lobule I compared with the vermis. However, melatonin, per se, neither affected the Purkinje cell number nor diminished alcohol-induced Purkinje cell loss.
CONCLUSIONS: Melatonin was not effective in attenuating alcohol-induced loss of Purkinje cells in our neonatal rat model system, even though such a dosage of melatonin is capable of reversing free radical-induced damage in other tissues.

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Year:  2002        PMID: 12170110     DOI: 10.1097/01.ALC.0000021148.70836.75

Source DB:  PubMed          Journal:  Alcohol Clin Exp Res        ISSN: 0145-6008            Impact factor:   3.455


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  9 in total

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