An update on oxidative stress-mediated organ pathophysiology

Food Chem Toxicol. 2013 Dec;62:584-600. doi: 10.1016/j.fct.2013.09.026. Epub 2013 Sep 29.


Exposure to environmental pollutants and drugs can result in pathophysiological situations in the body. Research in this area is essential as the knowledge on cellular survival and death would help in designing effective therapeutic strategies that are needed for the maintenance of the normal physiological functions of the body. In this regard, naturally occurring bio-molecules can be considered as potential therapeutic targets as they are normally available in commonly consumed foodstuffs and are thought to have minimum side effects. This review article describes the detailed mechanisms of oxidative stress-mediated organ pathophysiology and the ultimate fate of the cells either to survive or to undergo necrotic or apoptotic death. The mechanisms underlying the beneficial role of a number of naturally occurring bioactive molecules in oxidative stress-mediated organ pathophysiology have also been included in the review. The review provides useful information about the recent progress in understanding the mechanism(s) of various types of organ pathophysiology, the complex cross-talk between these pathways, as well as their modulation in stressed conditions. Additionally, it suggests possible therapeutic applications of a number of naturally occurring bioactive molecules in conditions involving oxidative stress.

Keywords: AA; ADG; ALX; APAP; AZT; Antioxidant; As; CAT; CCl(4); CRF; Cd; Cell death; DM; DN; DOX; DSL; F(−); GABA; GPx; GR; GSH; GSSG; GST; HIV; Hg; IR; KT; N-acetyl-parabenzoquinone imine; NAPQI; Organ pathophysiology; Oxidative stress; Pb; SOD; STZ; TBHP; acetaminophen; advanced glycation end product; alloxan; arjunolic acid; arsenic; azidothymidine; cadmium; carbon tetrachloride; catalase; chronic renal failure; d-saccharic acid-1,4-lactone; diabetes mellitus; diabetic nephropathy; doxorubicin; fluoride; gamma amino butyric acid; glutathione S-transferase; glutathione peroxidases; glutathione reductase; human immunodeficiency virus; insulin receptor; kombucha tea; lead; mercury; mitochondrial DNA; mtDNA; oxidized glutathione; reduced glutathione; streptozotocin; superoxide dismutase; tertiary butyl hydroperoxide.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acetaminophen / adverse effects
  • Acetaminophen / toxicity
  • Animals
  • Antioxidants / metabolism
  • Arsenic / toxicity
  • Cadmium / toxicity
  • Carbon Tetrachloride / toxicity
  • Cisplatin / adverse effects
  • Cisplatin / toxicity
  • Diabetes Mellitus / metabolism
  • Diabetes Mellitus / physiopathology*
  • Doxorubicin / adverse effects
  • Doxorubicin / toxicity
  • Drug-Related Side Effects and Adverse Reactions / metabolism
  • Drug-Related Side Effects and Adverse Reactions / physiopathology*
  • Humans
  • Lead / toxicity
  • Mercury / toxicity
  • Oxidative Stress / physiology*
  • Sulfonamides / adverse effects
  • Sulfonamides / toxicity


  • Antioxidants
  • Sulfonamides
  • Cadmium
  • Lead
  • Acetaminophen
  • Doxorubicin
  • Carbon Tetrachloride
  • Mercury
  • Arsenic
  • Cisplatin
  • nimesulide