Advanced glycation end products (AGEs) are potentially harmful and heterogeneous
molecules derived from nonenzymatic glycation. The pathological implications of AGEs are …

Anxiety disorders, depression, and alcohol use disorder are common neuropsychiatric
diseases that often occur together. Oxidative stress has been suggested to contribute to their …

In this review first we evaluate evidence on the role of the neurobiological alterations
induced by chronic ethanol consumption in the development of ethanol tolerance …

There are multiple mechanisms by which alcohol can damage the developing brain, but the
type of damage induced will depend on the amount and developmental timing of exposure …

The oxidative status of liver and kidney of rats co-exposed to cadmium (50 mg Cd/l in
drinking water) and ethanol (5 g EtOH/kg body weight/24 h, intragastrically) for 12 weeks …

Inflammatory processes and cytokine expression have been implicated in the pathogenesis
of several neurodegenerative disorders. Chronic ethanol intake induces brain damage …

A major pathogenic mechanism of chronic alcoholism involves oxidative burden to liver and
other cell types. We show that adult neurogenesis within the dentate gyrus of the …

CYP2B6 metabolizes drugs such as nicotine and bupropion, and many toxins and
carcinogens. Nicotine induces CYP2B1 in rat brain and in humans polymorphic variation in …

Background: Binge ethanol administration causes corticolimbic brain damage that models
alcoholic neurodegeneration. The mechanism of binge ethanol‐induced degeneration is …

Acetaldehyde, the first product of ethanol metabolism, has been speculated to be involved in
many pharmacological and behavioral effects of ethanol. In particular, acetaldehyde has …