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Transglutaminase activity in rat brain after ethanol exposure
A Sessa1, P Tunici, E Rabellotti
1Centro di Studio sulla Patologia Cellulare, CNR, Milan, Italy.
Alcoholism, Clinical and Experimental Research
|November 5, 1997
Summary
Ethanol exposure increases tissue transglutaminase activity in rat brains, potentially lowering protective polyamine spermine levels. This effect was observed in both acute and chronic ethanol treatments.
Area of Science:
- Biochemistry
- Neuroscience
- Pharmacology
Background:
- Tissue transglutaminase is a calcium-dependent enzyme involved in protein cross-linking.
- Ethanol's effects on brain enzyme activity and polyamine metabolism are not fully understood.
- Spermine is a crucial polyamine with known cellular protective functions.
Purpose of the Study:
- To investigate the impact of acute and chronic ethanol administration on rat brain tissue transglutaminase activity.
- To determine if ethanol itself or its metabolites are responsible for changes in enzyme activity.
- To explore the relationship between altered transglutaminase activity and spermine levels in the brain.
Main Methods:
- Enzyme activity assays were performed on homogenates and cytosolic fractions of rat brain (telencephalon and diencephalon).
- Acute ethanol treatment involved a single oral dose (5 g/kg).
- Chronic ethanol exposure was achieved through a 4-month ethanol-containing diet.
Main Results:
- A single ethanol dose significantly increased transglutaminase activity by 6 hours post-administration.
- In vitro studies confirmed ethanol, not its metabolite acetaldehyde, enhanced enzyme activity.
- Both acute and chronic ethanol treatments correlated with decreased spermine levels in the brain.
Conclusions:
- Ethanol exposure, both acute and chronic, enhances tissue transglutaminase activity in the rat brain.
- The observed increase in enzyme activity may contribute to a reduction in cellular spermine levels.
- This decline in spermine could impair its protective functions within brain cells, potentially contributing to ethanol-induced neurotoxicity.