Publication | Open Access
Acetaldehyde alone may initiate hepatocellular damage in acute alcoholic liver disease.
59
Citations
13
References
1985
Year
ImmunologyCirrhosisOxidative StressInflammationToxicologyHepatotoxicityAcetaldehyde BoundBiochemistryLiver PhysiologyHepatology InflammationNmol AcetaldehydeAlcohol-related Liver DiseasePharmacologyDrug-induced Liver InjuryHepatocellular DamageHepatologyNatural SciencesComplement SequenceLiver DiseaseLiverMedicine
Acetaldehyde may be the injurious agent in acute alcoholic liver disease. It has been suggested that the mechanism of liver injury in this situation may be immunologically mediated. In the present study acetaldehyde has been bound to human liver plasma membranes. The activation of C3 by the acetaldehyde/membrane product was measured by immunofixation of the separated C3 components. Activation of C3 by acetaldehyde exposed liver plasma membranes was increased to 16.4% compared with 6% by non-exposed membranes (p = 0.004). Human liver plasma membranes bound 212 +/- 18 nmol acetaldehyde per mg membrane protein. The binding constant was 439 +/- 81 microM. It is concluded that acetaldehyde bound to human liver plasma membranes activates the complement sequence and this may be the initial stage in the pathogenesis of acute alcoholic liver disease.
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