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10.1155/2013/730789

http://scihub22266oqcxt.onion/10.1155/2013/730789
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23710457!3654622!23710457
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suck abstract from ncbi

pmid23710457      Biomed+Res+Int 2013 ; 2013 (?): 730789
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  • Tight junction proteins and oxidative stress in heavy metals-induced nephrotoxicity #MMPMID23710457
  • Reyes JL; Molina-Jijon E; Rodriguez-Munoz R; Bautista-Garcia P; Debray-Garcia Y; Namorado Mdel C
  • Biomed Res Int 2013[]; 2013 (?): 730789 PMID23710457show ga
  • 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 ( alpha -tocopherol), depict on the morphological and functional alterations induced by heavy metals.
  • |*Oxidative Stress[MESH]
  • |Acute Kidney Injury/chemically induced/*pathology[MESH]
  • |Antioxidants/metabolism[MESH]
  • |Humans[MESH]
  • |Kidney Glomerulus/drug effects/pathology[MESH]
  • |Kidney Tubules, Proximal/drug effects/*pathology[MESH]
  • |Kidney/*drug effects/physiopathology[MESH]
  • |Metals, Heavy/*toxicity[MESH]
  • |Nephrons/drug effects/pathology[MESH]
  • |Tight Junction Proteins/metabolism[MESH]


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