It has been reported that acetyl-L-carnitine (AcCn) can reduce the degenerative processes in the central nervous system of rats, modify the fluidity of membranes and decrease the accumulation of lipofuscins in neurones. In light of these considerations we have assayed the in vitro effect of acetyl-L-carnitine on spontaneous and induced lipoperoxidation in rat skeletal muscle; in addition, the effect of AcCn on XD/XO ratio was evaluated. The presence of AcCn (10-40 mM) in incubation medium significantly reduced MDA and conjugated diene formation in rat skeletal muscle; moreover, a significant decrease in induced MDA levels was observed when microsomal preparation where incubated in the presence of 10-40 mM AcCn. Since a significant reduction of XO activity was detected in the presence of 10-80 mM AcCn, the reduced lipid peroxidation by AcCn seems to be due to an inhibition of XO activity.

The superoxide dismutase (SOD) activities in cerebral cortex of rat during aging are reported. The specific activity of cytosol SOD (Cu/Zn dismutase) decreases progressively from the 1st to the 30th month of postnatal life, whereas the specific activity of mitochondrial SOD increases with age. The alterations in the two enzymatic forms of SOD in the cerebral cortex of rat during aging may be due to separate regulation mechanisms.

Superoxide dismutase (SOD) activity and reduced glutathione (GSH) content in erythrocytes (RBC) of uremic patients on chronic dialysis were determined. Specific SOD activity and GSH content were found lower in RBC from uremic patients before hemodialysis compared to normal RBC; after hemodialysis, the specific activity of SOD and GSH content were significantly increased.

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The effect of glucose and polyamines (putrescine, spermidine and spermine) on the rate of autohemolysis in normal and thalassemic red blood cell (RBC) populations has been investigated. In addition, the specific activity of superoxide dismutase (SOD) was measured on blood samples obtained from the same patients. Our results show that glucose, and to a less extent polyamines, reduce the autohemolysis of thalassemic RBC, and that specific activity of SOD is increased in RBC from thalassemic patients compared to normal subjects.