Tight junction proteins and oxidative stress in heavy metals-induced nephrotoxicity

Biomed Res Int. 2013:2013:730789. doi: 10.1155/2013/730789. Epub 2013 Apr 22.

Abstract

Kidney is a target organ for heavy metals. They accumulate in several segments of the nephron and cause profound alterations in morphology and function. Acute intoxication frequently causes acute renal failure. The effects of chronic exposure have not been fully disclosed. In recent years increasing awareness of the consequences of their presence in the kidney has evolved. In this review we focus on the alterations induced by heavy metals on the intercellular junctions of the kidney. We describe that in addition to the proximal tubule, which has been recognized as the main site of accumulation and injury, other segments of the nephron, such as glomeruli, vessels, and distal nephron, show also deleterious effects. We also emphasize the participation of oxidative stress as a relevant component of the renal damage induced by heavy metals and the beneficial effect that some antioxidant drugs, such as vitamin A (all-trans-retinoic acid) and vitamin E ( α -tocopherol), depict on the morphological and functional alterations induced by heavy metals.

Publication types

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

MeSH terms

  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / pathology*
  • Antioxidants / metabolism
  • Humans
  • Kidney / drug effects*
  • Kidney / physiopathology
  • Kidney Glomerulus / drug effects
  • Kidney Glomerulus / pathology
  • Kidney Tubules, Proximal / drug effects
  • Kidney Tubules, Proximal / pathology*
  • Metals, Heavy / toxicity*
  • Nephrons / drug effects
  • Nephrons / pathology
  • Oxidative Stress*
  • Tight Junction Proteins / metabolism
  • Tretinoin / administration & dosage

Substances

  • Antioxidants
  • Metals, Heavy
  • Tight Junction Proteins
  • Tretinoin