Abstract
Glutathione peroxidase (GPx) is a seleno-enzyme with an antioxidant function that counteracts reactive oxygen species generated during irrigation-reperfusion injury in transplant organs. GPx activity increased post mortem by seleno-methionine (SeMet) administration in vivo. GPx degradation was studied in the organs of rats supplemented with SeMet to obtain insights into organ thanatochemistry and improve its survival. Studies were performed in the liver, kidneys, and heart of rats. After death, organs were ablated at different post mortem intervals (PMI). GPx1 was extracted and determined by size exclusion chromatography (SEC) and affinity chromatography (AC) coupled to inductively coupled plasma mass spectrometry (ICP-MS). Degradation products were studied by analyzing low molecular weight selenium fractions (< 10 kDa). GPx1 degradation velocity (VGPx1) in the different organs was evaluated by data analysis of GPx1 concentration variations according to PMI. GPx1 was determined in concentrations ranging from 0.19–0.76 mg kg− 1 in the ablated organs in a PMI of 12 hs. SeMet administration increased GPx1 concentration, especially in the liver. GPx1 concentration decreased in all the studied tissues during a PMI of 12 hours. The degradation velocity of GPx1 (VGPx1) was higher in the liver, followed by the kidneys and heart. Se degradation products were found in the range of 0.1 to 0.4 µg g− 1, higher in the liver. In kidneys, no differences in GPx1 degradation were observed in control and SeMet-administered rats. GPx1 degradation was lower in SeMet-administered rats. SeMet administration increased GPx1 concentration and decreased its degradation post mortem in the organs of rats.