Chronic ethanol increases ganglioside sialidase activity in rat leukocytes, erythrocytes, and brain synaptosomes

In view of the chronic alcohol-mediated pathological changes in various sia lic acid-deficient glycoconjugates and the potential importance of sialidas e in the generation of these glycoconjugates in the blood compartment and i n the brain, we have investigated the effects of chronic ethanol feeding fo r 8 weeks on ganglioside sialidase activities in rat blood end brain, Gangl ioside sialidase activity in erythrocytes (whether expressed as units/mg of protein or units/ml of blood) was 1.37- to 1.40-fold higher (p < 0.01) in the ethanol-fed group than in the control group, On the other hand, the sam e ethanol treatment increased sialidase activity in the leukocyte soluble f raction by 2.50- to 2.60-fold (p < 0.01) and by 1.61- to 1.63-fold (p < 0.0 1) in the leukocyte particulate fraction, compared with the control group. More importantly, most of the blood compartment sialidase activity was loca lized in the leukocytes particulate fraction (80 to 86% of total blood acti vity). Similarly, chronic ethanol treatment increased brain synaptosomal si alidase activity (whether expressed as units/gram of brain or units/mg of p rotein) 2.16- to 2.43-fold (p < 0.01). In contrast, brain lysosomal sialida se was not significantly altered by ethanol treatment, even though the majo r proportion of the brain sialidase activity was localized in the lysosomes . The proportion of synaptosomal sialidase activity as the percentage of to tal brain sialidase activity increased markedly from 13% in the control gro up to 24% in the ethanol group. Thus, chronic ethanol-mediated increases in sialidase activity in the leukocytes and brain synaptosomes could account for alterations in the ganglioside status of the animal and consequent adve rse effects of chronic ethanol on behavioral and pathological changes.