Contrast media (CM)-induced nephropathy(CIN) is an acute deterioration of renal function following administration of CM mediated, to large extent, by an increased production of ROS within the kidney. Aim of this study was to evaluate whether a novel isoform of a recombinant Manganese SOD (rMnSOD), which shares the same ability of physiological SODs in transforming free radicals into hydrogen peroxide, but show peculiar properties that allow the molecule to enter inside the cells after its administration, could provide an effective protection against CIN.
We studied the effects rMnSOD on oxidative damage in a rat model of CIN:uninephrectomized rats 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.
In comparison to rats pre-treated with vehicle, the rats of SOD group showed significantly reduced intrarenal O2- levels (-84%; p<0.0001) and a significant increase in SOD activity in kidneys (+16%; p=0.05). ROS production in rats of Group HCM was almost doubled compared to rat of Group CON (p<0.01). Conversely, in rats of Group SOD ROS production overlapped those of Group CON. Pre-treatment with rMnSOD determined a consistent preservation of renal function after the toxic insult (p < 0.05 vs HCM). rMnSOD attenuated the tubular necrosis, proteinaceous casts and medullary congestion, although significant protective effects, were observed in tubular necrosis (P = 0.001) and proteinaceous cast (P < 0.001).
Our data indicate that rMnSOD is able to reduce renal oxidative stress, and its improving the reduction of GFR following CM administration ant to prevent the associated histopathologic damage.
