Intraperitoneal injection of the iron chelate ferric-nitrilotriacetate (Fe-NTA) induces in rodents renal and hepatic suffering, associated with oxidative damage. We investigated the oxidation pattern in plasma of treated rats in relation to liver and kidney, monitoring the variation of the lipid components more susceptible to oxidation, unsaturated fatty acids (UFA) and alpha-tocopherol, as biomarkers of the oxidative damage. A sublethal dose of Fe-NTA induced a strong and extremely significant decrease of UFA levels at 1 h after injection in the plasma compartment and at 3 h in the kidney, with reductions up to 40-50% of the control values, together with an increase of conjugated dienes fatty acids hydroperoxides and a consumption of alpha-tocopherol. The same modifications were observed in the liver, but to a lesser extent. Histological observation proved that biochemical changes in the lipid fraction were a direct consequence of an ongoing membrane lipid peroxidation process. Our data show that oxidative damage to the lipid fraction is initially evident in the plasma compartment, where Fe-NTA toxicity is assumed to be caused by the elevation of serum free iron concentration, and proceeds with different speed and severity in the kidney and liver.

Lipid peroxidation in plasma of rats treated with ferric-nitrilotriacetate, in relation to kidney and liver modifications

DEIANA, MONICA;ROSA, ANTONELLA;ENNAS, MARIA GRAZIA;
2005-01-01

Abstract

Intraperitoneal injection of the iron chelate ferric-nitrilotriacetate (Fe-NTA) induces in rodents renal and hepatic suffering, associated with oxidative damage. We investigated the oxidation pattern in plasma of treated rats in relation to liver and kidney, monitoring the variation of the lipid components more susceptible to oxidation, unsaturated fatty acids (UFA) and alpha-tocopherol, as biomarkers of the oxidative damage. A sublethal dose of Fe-NTA induced a strong and extremely significant decrease of UFA levels at 1 h after injection in the plasma compartment and at 3 h in the kidney, with reductions up to 40-50% of the control values, together with an increase of conjugated dienes fatty acids hydroperoxides and a consumption of alpha-tocopherol. The same modifications were observed in the liver, but to a lesser extent. Histological observation proved that biochemical changes in the lipid fraction were a direct consequence of an ongoing membrane lipid peroxidation process. Our data show that oxidative damage to the lipid fraction is initially evident in the plasma compartment, where Fe-NTA toxicity is assumed to be caused by the elevation of serum free iron concentration, and proceeds with different speed and severity in the kidney and liver.
2005
lipid peroxidation, kidney, liver
File in questo prodotto:
File Dimensione Formato  
deiana 2005 BIOF.pdf

Solo gestori archivio

Tipologia: versione editoriale
Dimensione 145.29 kB
Formato Adobe PDF
145.29 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/16037
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus 6
  • ???jsp.display-item.citation.isi??? 7
social impact