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ALCAT1 controls mitochondrial etiology of fatty liver diseases, linking defective mitophagy to steatosis

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moreover, treatment with alpha-tocopherol and n-acetylcysteine, which have recognised anti-oxidant properties, provided a partial rescue of these cells, thus suggesting the involvement of reactive oxygen species in this pathological cascade.80 The potential interference with thrombosis and inflammation mechanisms was suggested by another study showing that exposing platelets to electronic cigarette vapour extracts induced a significant upregulation of the pro-inflammatory complementary elements C1 and C3b, even higher than traditional tobacco smoke extracts, and was accompanied with a concomitant boost in platelet activation, aggregation and adhesion capacity

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