Liver cell injury and cell death is a prominent feature in all liver disease processes. During
the last 5–10 years, most research activities focused almost exclusively on evaluating …

Susceptibility to drug toxicity is influenced by a variety of factors, both genetic and
environmental. The focus of this article is the evidence addressing the hypothesis that …

Acetaminophen overdose causes massive hepatic failure via mechanisms involving
glutathione depletion, oxidative stress, and mitochondrial dysfunction. The ultimate target of …

The increase in cellular and mitochondrial glutathione disulfide (GSSG) levels and the
GSSG: GSH ratio after acetaminophen (AAP) overdose suggest the involvement of an …

The transcription factor NF‐E2‐related factor 2 (Nrf2) plays an essential role in the
mammalian response to chemical and oxidative stress through induction of hepatic phase II …

Abstract ROS, RNS, BRIs and ROS-RNS hybrids are produced during drug or chemical
metabolism in vivo. These reactive species are instrumental to the culmination of cellular …

An unprecedented interest in biomarker development has arisen from the increasing use of
genomic information and high-throughput technologies in the field of drug development …

To study the biochemical and toxicological properties of cytochrome P450 2E1 (CYP2E1),
an adenovirus containing human CYP2E1 cDNA (Ad-CYP2E1) was constructed and was …

Acute liver injury can develop as a consequence of viral hepatitis, drug-or toxin-induced
toxicity or rejection after liver transplantation, whereas chronic liver injury can be due to long …

Objective: Chronic alcoholism has been considered to be a risk for acetaminophen (APAP)
hepatotoxicity, but little is known about the effect of binge alcohol drinking on APAP-induced …