Beneficial Effects of S-Adenosyl- l-Methionine on Aminolevulinic Acid Dehydratase, Glutathione, and Lipid Peroxidation During Acute Lead–Ethanol Administration in Mice

Abstract

Beneficial effects of S-adenosyl- l-methionine (SAM) in preventing inhibition of blood delta-aminolevulinic acid dehydratase (ALAD), alterations in blood and hepatic glutathione (GSH), hepatic and brain malondialdehyde (MDA) formation, and uptake of lead following acute lead plus ethanol coexposure were investigated in mice. Whereas exposure to both lead or ethanol individually produced a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity, ethanol administration alone produced only a marginal depletion of hepatic glutathione (GSH). A significant elevation of hepatic MDA concentration was observed following lead or ethanol ingestion. An appreciable increase in brain GSH following ethanol administration whereas a moderate elevation in MDA level following lead plus ethanol administration was observed. Combined lead plus ethanol exposure produced a more pronounced depletion of blood ALAD activity and an increase in hepatic MDA level compared to lead- or ethanol-alone administration. Brain GSH concentration showed an increase compared to untreated control animals or lead-alone-exposed mice. Concomitant administration of SAM partially reversed the inhibition of blood ALAD activity in all three exposed groups (i.e., lead, ethanol, or lead plus ethanol). Lead concentration in blood, liver, and brain was significantly reduced by SAM in lead-alone or lead plus ethanol coexposed groups. The results suggest that supplementation of SAM may have beneficial effects in preventing alterations in some biochemical variables and accumulation of lead in blood, liver, and brain during acute lead plus ethanol exposure in animals.