engleski

Antioxidant defence and tissue injury in prolonged cold ischemia

Introduction Cold storage of kidneys during transplantation is used as a preservation technique to slow down damaging effect of normothermic ischemia and to reduce metabolic and enzymatic activity. Although cold ischemia reduces the oxygen demand it is known that shortened graft survival and posttransplant morbidity are associated with cold storage organ injury. The causative role of reactive oxygen species (ROS) in cold storage induced injury is not well recognized. Oxidative stress and resulting lipid peroxidation and protein oxidation are responsible for altered kidney function. Aim of this study was to determine the effects of cold ischemia on antioxidant enzyme activities and examine protein oxidation and lipid peroxidation in rat kidney tissue. Materials and methods Kidneys of male Wistar rats (3 months old) were harvested and flushed via intraaortic cannula with cold saline. Organs were placed in a small container with 50 ml of saline and stored at 4ºC for 6, 12 or 24 hours. In control group kidney were flushed and immediately frozen. Lipid peroxidation (LPO) was measured via the thiobarbituric acid color reaction for malondialdehyde (MDA). Protein carbonyl content (PCC) was determined spectrophotometrically after labeling with 2, 4- dinitrophenylhydrazine (DNPH). Superoxide dismutase (SOD) and glutathione peroxidase (GSH- Px) activity were determined using comercialy available kit. Results Cold storage caused a time dependant increase of lipid peroxidation (LPO) and protein carbonyl content (PCC). SOD activity was markedly and time dependantly increased with cold storage and positively correlated with levels of LPO and PCC. Same result was observed with GSH-Px activity. Conclusions Results of this study demonstated that cold storage causes time dependant increase in antioxidant activity and tissue injury.

cold ischemia ; kidney ; oxidative stress

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