The aim of the present study is to investigate oxidative stress produced by experimental hypoxia and hyperoxia in young and old pampiniform plexus rats, in order to evaluate the oxidative role of oxygen. Oxidative stress causing molecular and cellular dysfunction increases in hypertension and can therefore be considered a state of oxidative stress. This consideration makes us reflect on the responsibility of oxidative stress in the veins of the pampiniform plexus, notoriously under high hydrostatic pressure. After experimental hypoxia and hyperoxia we studied the 8-iso-PGF2alpha release (a specific index of cellular oxidative stress) in young and old left pampiniform plexus rats. The basal 8-iso-PGF2alpha release showed a statistically significant difference P=0.0067 between young and old rats PP. After hypoxia and hyperoxia, the release was higher in young rats as compared to normoxia, respectively P=0.0001 and P=0.0002. After hypoxia the release was not modified in old rats P=0.544 while after hyperoxia the release was increased in old rats as compared to control P less than 0.0001. The results show how chronic hypoxia and hyperoxia represent two important causes of oxidative stress and lipid peroxidation in pampiniform plexus rats. In young rats an increase of oxidative stress suggests that pampiniform plexus is sensitive to variations of oxygen supply. In old rats the pampiniform plexus is liable to a reduction of oxygen-sensing mechanisms and it is possible that the missing oxidative answer to the hypoxia in old rats is attributable in all likelihood to adaptation to a hypoxic condition typical of aging.
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