Abstract
Approximately 4 years ago, Mates, Alonso and Marquez published their famous review on the implications of oxidative stress on cell functions (Mates et al. 2008). Meanwhile, their review is one of the most cited articles in our journal. Mates and colleagues defined oxidative stress as the imbalance between cellular oxidant species production and antioxidant capacity. They systematically reviewed how reactive oxygen species influence intracellular processes, such as proliferation and apoptosis. The editors are pleased that the same authors have now contributed a comprehensive update of their 2008 article. Oxidative stress still represents one of the cutting-edge topics in toxicology (Wang et al. 2011a, b; Stewart et al. 2011a, b; Schumann et al. 2009; Baird and DinkovaKostova 2011; Zimmermann et al. 2012; Bolt and Hengstler 2010). A particularly large number of articles analyses the role of reactive oxygen species as a mechanism of metal toxicity (Nogueira and Rocha 2011; Yen et al. 2011; Barcelos et al. 2011; Bolt and Marchan 2010; Brozmanova et al. 2010; Hengstler et al. 2003), neurotoxicity (Takahashi et al. 2011; Li et al. 2011; Wang et al. 2011a, b; Frimat et al. 2010; Hardelauf et al. 2011), compromised lipid integrity (Bauer et al. 2009; Stewart et al. 2012; Schober et al. 2009; Cadenas et al. 2012) and carcinogenesis (Morita et al. 2011; Cadenas et al. 2010; Nishimura et al. 2010). In their present review (Mates et al. 2012; this issue), Mates and colleagues revisit the role of reactive oxygen species and the gradient of O 2 generated by mitochondrial respiration as key regulatory signals for apoptosis. Moreover, they focus on the research field of ROS-scavenging strategies, which has been massively expanding in recent years, including small molecules mimicking antioxidant enzymes, spin trap like SOD mimetics, and porhyrins. The article is highly recommended to anyone interested in oxidative stress and its impact on cell function.
Published Version
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