Elisa Dicker

TL;DR: Results suggest that NADH acting via the outer membrane NADH reductase can catalyze an iron-dependent production of oxygen radicals by rat liver mitochondria, which may play an important role in the development of a state of oxidative stress in the liver by ethanol.

TL;DR: Evidence of heterogeneity within JME is shown and a marker associated with the linked form of HLA is proposed, suggesting that JME may be predominantly maternally inherited and that the HLA-linked form is more likely to occur in families of European origin.

TL;DR: The results suggest that ethanol oxidation by microsomes can be dissociated from drug metabolism and that the mechanism of ethanol oxidation may involve, in part, the interaction of ethanol with hydroxyl radicals that are generated bymicrosomes during the oxidation of NADPH.

TL;DR: The results suggest that GABA synthesis disruption predisposes to common IGE and that clinical seizures are triggered when mutations at other genes, or perhaps other insults, are present.

TL;DR: Rat liver microsomes catalyse the oxidation of straight-chain aliphatic alcohols and of hydroxyl-radical-scavenging agents during NADPH-dependent electron transfer and suggest that primary alcohols may be oxidized by two pathways in microsome, one dependent on the interaction of the alcohols withhydroxyl radicals (desferrioxamine-sensitive), the other which appears to be independent of these radicals.