Clinical and Experimental Nephrology

, Volume 18, Issue 3, pp 424–431

Effect of a recombinant manganese superoxide dismutase on prevention of contrast-induced acute kidney injury

Authors

  • Antonio Pisani
    • Department of NephrologyUniversity Federico II of Naples
  • Massimo Sabbatini
    • Department of NephrologyUniversity Federico II of Naples
    • Department of NephrologyUniversity Federico II of Naples
  • Roberta Rossano
    • Department of NephrologyUniversity Federico II of Naples
  • Michele Andreucci
    • Department of NephrologyMagna Graecia University
  • Clemente Capasso
    • CNR. Institute of Protein Biochemistry (IBP)
  • Viviana De Luca
    • CNR. Institute of Protein Biochemistry (IBP)
  • Vincenzo Carginale
    • CNR. Institute of Protein Biochemistry (IBP)
  • Mariano Bizzarri
    • Italian Space Agency, La Sapienza University
  • Antonella Borrelli
    • National Cancer Institute G. Pascale
  • Antonella Schiattarella
    • National Cancer Institute G. Pascale
  • Michele Santangelo
    • Department of SurgeryUniversity Federico II of Naples
  • Aldo Mancini
    • National Cancer Institute G. Pascale
Original Article

DOI: 10.1007/s10157-013-0828-2

Cite this article as:
Pisani, A., Sabbatini, M., Riccio, E. et al. Clin Exp Nephrol (2014) 18: 424. doi:10.1007/s10157-013-0828-2

Abstract

Background

Contrast media (CM)-induced nephropathy (CIN) is an acute deterioration of renal function following administration of CM mediated to a large extent by the increased production of ROS within the kidney. Aim of this study was to evaluate whether a novel isoform of a recombinant Manganese SOD (rMnSOD) could provide an effective protection against CIN; this molecule shares the same ability of physiological SODs in scavenging reactive oxygen species (ROS) but, due to its peculiar properties, enters inside the cells after its administration.

Methods

We studied the effects rMnSOD on oxidative damage in a rat model of CIN in uninephrectomized rats, that were randomly assigned to 3 experimental Groups: Group CON, control rats treated with the vehicle of CM, Group HCM, rats treated with CM and Group SOD, rats treated with CM and rMnSOD.

Results

In normal rats, pretreatment with rMnSOD, reduced renal superoxide anion production, induced by the activation of NAPDH oxidase, by 84 % (p < 0.001). In rats of Group HCM, ROS production was almost doubled compared to rat of Group CON (p < 0.01) but returned to normal values in rats of Group SOD, where a significant increase of SOD activity was detected (+16 % vs HCM, p < 0.05). Administration of CM determined a striking fall of GFR in rats of Group HCM (−70 %, p < 0.001 vs CON), greatly blunted in Group SOD (−28 % vs CON, p < 0.01); this was associated with a lower presence of both tubular necrosis and intratubular casts in SOD-treated rats (both p < 0.01 vs Group HCM).

Conclusions

Our data indicate that rMnSOD is able to reduce renal oxidative stress, thus preventing the reduction of GFR and the renal histologic damage that follows CM administration.

Keywords

Contrast-induced nephropathy Superoxide dismutase Oxygen radicals

Abbreviations

b.w.

Body weight

CIN

Contrast media-induced nephropathy

CM

Contrast media

DCF

Dichlorofluorescein

DCFH-DA

2′,7′-Dichlorofluorescin diacetate

GFR

Glomerular filtration rate

IF

Intensity Fluorescence

i.p.

Intraperitoneal

i.v.

Intravenous

LSA

Liposarcoma cell line

rMnSOD

Recombinant manganese superoxide dismutase

ROS

Reactive oxygen species

SOD

Superoxide dismutase

WST

Water-soluble tetrazolium salt

Copyright information

© Japanese Society of Nephrology 2013