Changes in brain MAO activity and glycogen levels upon chronic alcoholization of three successive generations of rats

Abstract

Changes in neurobiological parameters were examined from early life (10 days post-natal) until late adulthood (8 months post-natal) in three successive generations of alcoholized rats. The mean daily consumption of alcohol by the 2nd and 3rd generation rats (7.40 +/- 0.22 and 7.70 +/- 0.20 g ethanol/kg body weight, respectively) was significantly greater than that of the 1st generation alcoholized group (4.26 +/- 0.33 g/kg). Brain/body weight ratios of alcoholized rats, 10 days post-natal, were significantly greater than controls, with 1st generation alcoholized rats presenting significantly greater brain/body weight ratios than those of the 2nd or 3rd generation, which tended toward control weights and ratios. This difference between alcoholized rats and controls persisted, although to a lesser extent, at 8 months post-natal. Glycogen content in the brains of rats of all alcoholized generations was significantly lower than in controls at 10 days post-natal, with a reversal of this situation in later life for 2nd and 3rd generation rats, which presented significantly greater cerebral glycogen levels than control or 1st generation alcoholized rats (which had an equivalent cerebral glycogen content). In 10-day-old rat pups, monoamine oxidase (MAO) activity in brain tissues had a tendency (mostly non-significant) to be greater in alcoholized rats than in controls, with a reversal of this situation, ie a statistically significant decrease in MAO activity in the 2nd and 3rd alcoholized generations with respect to controls, in 8-month-old rats. MAO activity in adrenal glands of alcoholized rats was greater than in controls at 10 days post-natal, and this difference persisted at 8 months.

Monoamine oxidase gene transcription in human cell lines: Treatment with psychoactive drugs and ethanol

“…The effects of ethanol treatment were assayed since several reports indicate that chronic alcohol intake might result in quantitative changes ill MAO catalytic activity (Aliyu and Upahi, 1988;Anokhina et al, 1990;Nevo and Parvez, 1994;Tabakoff et al, 1985). Two concentrations of ethanol were used in these transfection experiments, 50 and 100 mM, respectively.…”

“…For example, MAO-B activity in platelets is significantly altered in psychiatric patients as a consequence of treatment with neuroleptics (Baron et al, 1982;Chojnacki et al, 1981) and lithium salts (Bockar et al, 1974;Chojnacki et al, 1981;Huang et al, 1984). Moreover, an association between MAO activity and ethanol consumption has been proposed by several investigators (Aliyu and Upahi, 1988;Anokhina et al, 1990;Nevo and Parvez, 1994;Tabakoff et al, 1985). Presently, nothing is known about the mechanism for these changes in enzyme activity.…”