| Abstrakt: |
Ischemia-reperfusion (I-R) injury causes a reduction in the viability of donor organs during long-term conservation. In the present study, an antioxidant enzyme peroxiredoxin 6 was used to increase the resistance of donor kidneys to I-R injury. To find the efficiency of using peroxiredoxin 6, we evaluated the morphological and functional parameters of the isolated kidney, the expression level of kidney injury molecule-1 (KIM-1) as a marker of kidney damage, and the level of malonic dialdehyde in the tissue. Cold storage of the kidney in DMEM solution, which was not customized, was shown to result in organ death during perfusion. In contrast, the use of Custodiol solution allowed the kidney to survive an episode of prolonged ischemia and perfusion. The combination of peroxiredoxin 6 with Custodiol solution led to a better outcome. In addition to a decreased damage to nephron structures, a 2.3-fold reduction of the malonic dialdehyde level was registered, thus indicating neutralization of hyperproduction of reactive oxygen species. The urinary flow rate, glomerular filtration rate, and the amount of urea in the urine increased fourfold, thereby indicating that tubular structures were preserved, as confirmed by a 1.5-fold decrease in the level of KIM-1. Thus, the use of peroxiredoxin 6, an exogenous antioxidant protein, during perfusion increases the resistance of the donor kidney to ischemia-reperfusion injury after prolonged cold storage in Custodiol solution. [ABSTRACT FROM AUTHOR] |
Full text from SpringerLink