Ochratoxin A (OTA) is a natural mycotoxin, involved in the development of important human and animal diseases. In this work we have studied the role of oxidative stress in the development of OTA nephrotoxicity and the effect of a new recombinant mitochondrial manganese containing superoxide dismutase (rMnSOD) to prevent kidney damage induced by OTA. Blood pressure, glomerular filtration rate and renal histology were analyzed in control rats and in OTA treated rats. In addition, lipid peroxidation, catalase and superoxide dismutase productions were measured. Our data showed that animals treated with OTA presented hypertension and reduction of glomerular filtration rate (GFR). These effects are most probably related to an increase in the reactive oxygen species (ROS) productions. In fact, we have shown that treatment with rMnSOD restored the levels of blood pressure and GFR simultaneously. Moreover, we have noted that OTA induced alteration on glomerular and tubular degeneration and interstitial infiltrates and that use of rMnSOD combined with OTA prevent this renal histological damage confirming the potential therapeutic role in the treatment of rMnSOD OTA nephrotoxicity. This article is protected by copyright. All rights reserved.

Recombinant mitochondrial manganese containing superoxide dismutase protects against Ochratoxin A-induced nephrotoxicity / Ciarcia, Roberto; Damiano, Sara; Squillacioti, Caterina; Mirabella, Nicola; Pagnini, Ugo; Florio, Alessia; Severino, Lorella; Capasso, Giovambattista; Borrelli, Antonella; Mancini, Aldo; Boffo, Silvia; Romano, Gaetano; Giordano, Antonio; Florio, Salvatore. - In: JOURNAL OF CELLULAR BIOCHEMISTRY. - ISSN 0730-2312. - (2016), pp. N/A1352-N/A 1358. [10.1002/jcb.25425]

Recombinant mitochondrial manganese containing superoxide dismutase protects against Ochratoxin A-induced nephrotoxicity

CIARCIA, ROBERTO;Damiano, Sara;SQUILLACIOTI, CATERINA;MIRABELLA, NICOLA;PAGNINI, UGO;SEVERINO, LORELLA;CAPASSO, GIOVAMBATTISTA;FLORIO, SALVATORE
2016

Abstract

Ochratoxin A (OTA) is a natural mycotoxin, involved in the development of important human and animal diseases. In this work we have studied the role of oxidative stress in the development of OTA nephrotoxicity and the effect of a new recombinant mitochondrial manganese containing superoxide dismutase (rMnSOD) to prevent kidney damage induced by OTA. Blood pressure, glomerular filtration rate and renal histology were analyzed in control rats and in OTA treated rats. In addition, lipid peroxidation, catalase and superoxide dismutase productions were measured. Our data showed that animals treated with OTA presented hypertension and reduction of glomerular filtration rate (GFR). These effects are most probably related to an increase in the reactive oxygen species (ROS) productions. In fact, we have shown that treatment with rMnSOD restored the levels of blood pressure and GFR simultaneously. Moreover, we have noted that OTA induced alteration on glomerular and tubular degeneration and interstitial infiltrates and that use of rMnSOD combined with OTA prevent this renal histological damage confirming the potential therapeutic role in the treatment of rMnSOD OTA nephrotoxicity. This article is protected by copyright. All rights reserved.
2016
Recombinant mitochondrial manganese containing superoxide dismutase protects against Ochratoxin A-induced nephrotoxicity / Ciarcia, Roberto; Damiano, Sara; Squillacioti, Caterina; Mirabella, Nicola; Pagnini, Ugo; Florio, Alessia; Severino, Lorella; Capasso, Giovambattista; Borrelli, Antonella; Mancini, Aldo; Boffo, Silvia; Romano, Gaetano; Giordano, Antonio; Florio, Salvatore. - In: JOURNAL OF CELLULAR BIOCHEMISTRY. - ISSN 0730-2312. - (2016), pp. N/A1352-N/A 1358. [10.1002/jcb.25425]
File in questo prodotto:
File Dimensione Formato  
Reco.pdf

accesso aperto

Tipologia: Documento in Post-print
Licenza: Dominio pubblico
Dimensione 874.01 kB
Formato Adobe PDF
874.01 kB Adobe PDF Visualizza/Apri

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/11588/614052
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 27
  • ???jsp.display-item.citation.isi??? 27
social impact