Mechanisms of cell death in oxidative stress. Review uri icon

Overview

MeSH

  • Animals
  • Carbon Monoxide
  • Heme Oxygenase-1
  • Humans
  • Photochemotherapy
  • Radiation
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Reperfusion Injury

MeSH Major

  • Apoptosis
  • Cell Death
  • Models, Biological
  • Oxidative Stress

abstract

  • Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress have long been implicated in tissue injury in the context of a variety of disease states. ROS/RNS can cause cell death by nonphysiological (necrotic) or regulated pathways (apoptotic). The mechanisms by which ROS/RNS cause or regulate apoptosis typically include receptor activation, caspase activation, Bcl-2 family proteins, and mitochondrial dysfunction. Various protein kinase activities, including mitogen-activated protein kinases, protein kinases-B/C, inhibitor-of-I-kappaB kinases, and their corresponding phosphatases modulate the apoptotic program depending on cellular context. Recently, lipid-derived mediators have emerged as potential intermediates in the apoptosis pathway triggered by oxidants. Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke. Additionally ROS generated in the lung and other organs as the result of high oxygen therapy or ischemia/reperfusion can stimulate cell death pathways associated with tissue damage. Cells have evolved numerous survival pathways to counter proapoptotic stimuli, which include activation of stress-related protein responses. Among these, the heme oxygenase-1/carbon monoxide system has emerged as a major intracellular antiapoptotic mechanism.

publication date

  • January 2007

has subject area

  • Animals
  • Apoptosis
  • Carbon Monoxide
  • Cell Death
  • Heme Oxygenase-1
  • Humans
  • Models, Biological
  • Oxidative Stress
  • Photochemotherapy
  • Radiation
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Reperfusion Injury

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1089/ars.2007.9.49

PubMed ID

  • 17115887

Additional Document Info

start page

  • 49

end page

  • 89

volume

  • 9

number

  • 1