122 research outputs found
Glycosylation defects underlying fetal alcohol spectrum disorder: a novel pathogenetic model: “When the wine goes in, strange things come out” – S.T. Coleridge, The Piccolomini
Fetal alcohol spectrum disorder (FASD) is an umbrella term used to describe the craniofacial dysmorphic features, malformations, and disturbances in growth, neurodevelopment and behavior occurring in individuals prenatally exposed to alcohol. Fetal alcohol syndrome (FAS) represents the severe end of this spectrum. Many pathophysiological mechanisms have hitherto been proposed to account for the disrupted growth and morphogenesis seen in FAS. These include impaired cholesterol-modification of the Sonic hedgehog morphogen, retinoic acid deficiency, lipoperoxidative damage due to alcohol-induced reactive oxygen species combined with reduced antioxidant defences, and malfunctioning cell adhesion molecules. In this report, we propose a completely novel concept regarding the pathogenesis of FAS. Based on our observation that transferrin isoelectric focusing (TIEF) – the most widely used screening tool for congenital disorders of glycosylation (CDG) – was transiently abnormal in a newborn with FAS and a confirmed maternal history of gestational alcohol abuse, we came to believe that FAS exemplifies a congenital disorder of glycosylation secondary to alcohol-inflicted disruption of (N-linked) protein glycosylation. Various pieces of evidence were found in the literature to substantiate this hypothesis. This observation implies, among others, that one might need to consider the possibility of maternal alcohol consumption in newborns with transient glycosylation abnormalities. We also present an integrated pathophysiological model of FAS, which incorporates all existing theories mentioned above as well as our novel concept. This model highlights the pivotal role of disrupted isoprenoid metabolism in the origination of FAS
Quantification of ubiquinone output in bile after interruption of enterohepatic recirculation.
Effect of ethanol intoxication on the levels of dolichols in rat liver Golgi apparatus
none4D. COTTALASSO;M. A. PRONZATO;U. M. MARINARI;G. NANNICottalasso, Damiano; Pronzato, MARIA ADELAIDE; Marinari, Umberto; Nanni, Giorgi
Phospholipids, vitamin A and ubiquinone of the Golgi apparatus subfractions from rat liver after acute ethanol intoxication.
1,1,2,2-tetrachloroethane-induced early decrease of dolichol levels in rat liver microsomes and Golgi apparatus.
Intensive insulin treatment reduces the accumulation of oxidation and glycation end-products in diabetic rat collagen.
[Effect of acute ethanol intoxication on the Golgi apparatus, isolated from the hepatocyte. II. Incorporation of 3H palmitic acid].
Influence of chronic ethanol consumption on toxic effects of 1,2-dichloroethane: glycoprotein retention and impairment of dolichol concentration in rat liver microsomes and Golgi apparatus
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