Cerebral plasmalogens and aldehydes in senescence-accelerated mice P8 and R1: A comparison between weaned, adult and aged mice

In contrast with senescence-accelerated mice R1, SAM P8 show abnormal aging characteristics. Changes occurring during aging could be mainly caused by free radical reactions. The brain is a plasmalogen-rich tissue. These particular phospholipids may act as endogenous antioxidants, be oxidized and release long chain aldehydes and α-hydroxyaldehydes during oxidative stress. The aim of this study was to examine by GC/MS the age- and strain-related levels of plasmalogens, aldehydes and α-hydroxyaldehydes in brain homogenates of SAM P8 and R1 at weaning, 5 months and 9 months of age in order to better understand the differences between both strains. In SAM R1, the evolution of brain plasmalogen levels corresponded to characteristics of normal aging: an increase from weaned to adult mice followed by a decrease characterizing the normal loss of myelin. By contrast to SAM R1, there was no change in the plasmalogen content in SAM P8 brain. The levels of aldehydes and α-hydroxyaldehydes were similar for both strains, they remained constant between adult and aged mice. Specific changes in the aging of SAM P8 were not explained by cerebral levels of these oxidative products. Other mechanisms related to the toxicity of aldehydes and α-hydroxyaldehydes could be considered.