Alcohol Reduces GM1 Ganglioside Content in the Serum of Inbred Mouse Strains

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Abstract

Background:

Endogenous and exogenous gangliosides in the plasma affect physiologic and pathologic processes such as angiogenesis and atherogenesis. However, the genetic and environmental factors that regulate the expression of plasma gangliosides are not well known. As shown in the liver and the brain, profiles of gangliosides in the plasma may be strain-specific and can be altered by intake of alcohol. Therefore, we analyzed serum gangliosides derived from inbred mouse strains with and without alcohol treatment.

Methods:

C57BL/6ByJ (B6By) and BALB/cJ mice (60–70 days old) were injected with 20% alcohol (1–6 g/kg) or saline intraperitoneally, and the ganglioside content of the serum, liver, and cerebellum was measured 4 hr after the injection. Also, the effect of oral alcohol self-administration for 18 days with escalating (3–12%) concentrations of alcohol on the serum GM1 content was studied in B6By mice. The quantification of GM1 was performed with a thin-layer chromatography-staining procedure using a cholera toxin B subunit, and the content of other gangliosides was measured after staining with resorcinol reagent.

Results:

We found that basal GM1 (containing N-glycolylneuraminic acid) content in the serum of BALB/cJ mice (4.8 ± 0.26 ng/μl) was 25 times higher than that of B6By mice (0.19 ± 0.01 ng/μl); the major ganglioside in both strains was GM2. The ganglioside profile in the liver was similar to that of the serum, and the GM1 content in BALB/cJ was nine times higher than that of B6By. Both injection and oral self-administration of alcohol lowered GM1 levels in the serum.

Conclusions:

Endogenous ganglioside profiles in the serum are under genetic control among inbred mouse strains, and they can be altered by acute and chronic alcohol administration. These genetic and alcohol-induced differences in the plasma gangliosides, which appear to reflect ganglioside metabolism in the liver, may affect alcohol-related behaviors and pathologic processes.

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