Reactive oxygen molecules, oxidant injury and renal disease

Research output: Contribution to journalReview article

97 Scopus citations


Oxidant injury has been implicated in the pathogenesis of inflammotory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likeky to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.

Original languageEnglish (US)
Pages (from-to)733-742
Number of pages10
JournalPediatric Nephrology
Issue number6
StatePublished - Nov 1 1991


  • Free radicals
  • Oxidant injury
  • Reactive oxygen molecules
  • Renal disease

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

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