Alcohol
Volume 29, Issue 2 , Pages 91-100, February 2003

Interaction of aging and intermittent ethanol exposure on brain cytochrome c oxidase activity levels

  • Pia Jaatinen

      Affiliations

    • University of Tampere, Medical School, FIN-33014 University of Tampere, Finland
    • Department of Internal Medicine, Tampere University Hospital, FIN-33521 Tampere, Finland
    • Corresponding Author InformationCorresponding author. Tampere University Hospital, Department of Internal Medicine, P.O. Box 2000, FIN-33521 Tampere, Finland. Tel.: +358-3-247-7560; fax: +358-3-215-6164
    • ,
  • Jarno Riikonen

      Affiliations

    • School of Public Health, FIN-33014 University of Tampere, Finland
    • ,
  • Päivi Riihioja

      Affiliations

    • School of Public Health, FIN-33014 University of Tampere, Finland
    • ,
  • Olli Kajander

      Affiliations

    • Institute of Medical Technology, FIN-33014 University of Tampere, Finland
    • ,
  • Antti Hervonen

      Affiliations

    • School of Public Health, FIN-33014 University of Tampere, Finland

Received 22 October 2001; received in revised form 11 November 2002; accepted 10 December 2002.

Editor: S. Borg

Abstract 

The effects of chronic, intermittent ethanol exposure on brain cytochrome c oxidase (CO) activity levels were studied in young (3- to 4-month-old) and aged (29- to 30-month-old) male Wistar rats. The rats were given highly intoxicating doses of ethanol three times a day by intragastric intubation for four successive days, followed by a 3-day ethanol-withdrawal period. This 4-day ethanol-exposure with 3-day ethanol-withdrawal cycle was repeated five times to simulate the binge drinking of human alcoholics. The histochemical demonstration of CO showed a markedly decreased activity level in the medial prefrontal cortex (especially layer V pyramids and neuropil) of the ethanol-exposed rats of both age groups compared with findings for the respective controls. In the cerebellar vermis, CO activity level was decreased in the Purkinje neurons of the aged ethanol-exposed rats and in the granule cells of both young and aged ethanol-exposed rats. The CO activity level in the locus coeruleus was decreased in both young and old ethanol-exposed rats, but the decrease was more pronounced in the young ethanol-exposed group. Aging per se did not markedly change CO histochemical findings in either prefrontal or cerebellar cortex, but CO activity levels were increased in the locus coeruleus. In summary, results of the current study support our conclusion that CO activity levels were decreased in the cerebral and cerebellar cortices as well as in the locus coeruleus—CNS regions known to be negatively affected by chronic ethanol exposure. Defective energy metabolism due to decreased CO activity levels might compromise neuronal energy stores and thereby contribute to ethanol-induced brain dysfunction and irreversible CNS degeneration.

Keywords:  Aging, Ethanol, Cerebellum, Prefrontal cortex, Locus coeruleus, Rat

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PII: S0741-8329(03)00002-8

doi:10.1016/S0741-8329(03)00002-8

Alcohol
Volume 29, Issue 2 , Pages 91-100, February 2003

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