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Different Contribution of Redox-Sensitive Transient Receptor Potential Channels to Acetaminophen-Induced Death of Human Hepatoma Cell Line
Introduction
Acetaminophen (N-acetyl-para-aminophenol, APAP) is a widely used and safe over-the-counter analgesic antipyretic drug (Rumack, 2004). However, an accidental APAP overdose can result in potentially lethal hepatotoxicity in both humans and experimental animals (Thomas, 1993; Hinson et al., 2010). Adverse reactions of APAP account for a substantial number of acute liver failure cases necessitating liver transplantation (Larson et al., 2005; Myers et al., 2007; Chun et al., 2009). Determining the exact pathways underlying APAP-induced hepatocellular death should provide important cues for preventing its lethal side effects.
It has been established that APAP overdose causes a constellation of co-related cellular events (Hinson et al., 2010). APAP is largely converted by hepatic cytochrome P450-dependent oxidases to a reactive intermediate metabolite, which depletes glutathione (GSH) and covalently binds to cellular proteins and lipids. Research on its mechanisms of toxicity has recently focused on oxidative stress exerted through accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), due to the depleti
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Highlights
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A large proportion of analgesics fail to translate from rodents to humans.
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Large animals share anatomical and behavioral similarities to humans.
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Studying large animals can provide novel insights for arthritic pain.
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In vitro techniques developed in rodents can be adopted in large animals.
Keywords: Arthritis, Large animals, Sensory neurons, In vitro, Pain models
Abstract
Pain arising from musculoskeletal disorders such as arthritis is one of the leading causes of disability. Whereas the past 20-years has seen an increase in targeted therapies for rheumatoid arthritis (RA), other arthritis conditions, especially osteoarthritis, remain poorly treated. Although modulation of central pain pathways occurs in chronic arthritis, multiple lines of evidence indicate that peripherally driven pain is important in arthritic pain. To understand the peripheral mechanisms of arthritic pain, various in vitro and in vivo models have been developed, largely in rodents. Although rodent models provide numerous advantages for studying arthritis pathogenesis and treatment, the anatomy and biomechanics of rodent joints differ considerably to those of humans. By contrast, the anatomy and biomechanics of joints in larger animals, such as dogs, show greater simi
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