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The main pathway of ethanol metabolism involves its conversion to acetaldehyde by alcohol dehydrogenase (ADH; Figure 1).Acetaldehyde is oxidized to acetate by aldehyde dehydrogenase (ALDH).
Human genetic studies on alcohol-related phenotypes have used family-based linkage and population-based association analyses to identify quantitative trait loci (QTLs).
Linkage studies are based on co-segregation between genetic markers and alcohol dependence in families with several affected members.
This can be done by considering the effects of molecular polymorphisms on phenotypes mediated via complex networks of transcriptional, protein, metabolic and neurogenetic endophenotypes.
Here, we review genetic risk factors and transcriptional correlates for alcohol consumption in humans, with insights from studies on model genetic organisms.
Finally, alcohol consumption during pregnancy can result in birth defects that comprise fetal alcohol syndrome .
Alcoholism Thesis Paper
The diversity of pathologic effects of alcohol indicates that this drug exerts toxicity through multiple mechanisms, each of which can be modulated by different genetic variants.
In addition, a small fraction of ethanol is metabolized by cytochrome P450 2E1 (CYP2E1) and in the brain by catalase.
The diagram presents only those members of the ADH and ALDH families referred to in the text.
Accumulation of acetaldehyde is responsible for the physiological malaise commonly known as 'hangover'.
The positive reinforcing effects of alcohol are mediated through the corticomesolimbic dopaminergic reward pathway, which extends from the ventral tegmental area to the nucleus accumbens and is modulated by a wide range of neurotransmitters.