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Updated: Jul 19, 2026
Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
Published on: December 14, 2014
Ethanol decreases rat hepatic arylsulfatase A activity levels
Smith Jean1, Chinnaswamy Kasinathan, Steven Buyske
1Department of Psychiatry, University of Medicine and Dentistry of New Jersey (UMDNJ)-Robert Wood Johnson Medical School, 671 Hoes Lane, Piscataway, NJ 08854, USA.
Background:
Arylsulfatase A (ASA) is an enzyme that catalyzes the degradation of sulfatides, a glycosphingolipid found in many tissues, but predominantly in myelin and kidney. Arylsulfatase A is 1 member of a family of sulfatases that is activated by a required co- or posttranslational modification with the oxidation of cysteine to formylglycine. This conversion requires a novel oxygenase mechanism that can be inhibited by reactive oxygen species. Ethanol is known to cause an increase in reactive oxygen species in the liver. Because of its effect on the levels of hepatic reactive oxygen species, we hypothesized that ethanol would cause a specific decrease of rat hepatic ASA activity levels.
Methods:
Male Sprague-Dawley rats received ethanol-containing, Lieber-DeCarli liquid diets for 15 days, and control rats were pair-fed a liquid diet in which dextrose was isocalorically substituted for ethanol.
Results:
Arylsulfatase A activity levels decreased in livers of animals receiving alcohol compared with control animals. No significant changes in ASA activity levels were observed in the cerebral cortex and kidney. Furthermore, ethanol did not have any significant effect on hexosaminidase activity in any of the tissues examined.
Conclusion:
Ethanol caused a tissue-specific decrease in hepatic ASA activity levels, but not hexosaminidase activity levels.
