[Role of semicarbazide-sensitive amine oxidase in disturbances of endogenic detoxication in ischemic stroke patients].

Oxidative stress is a pathogenetic factor of ischemic stroke. Enhancement in the activity of one of xenobiotic transformation enzymes and biogenic amines (serum semicarbazide-sensitive amine oxidase (SSAO)) leads to the higher production of secondary toxins stimulating oxidative stress. We studied 38 patients (mean age 69,5 +/- 7,2 years) in the early restoration period of ischemic stroke. A control group included 17 age- and sex-matched healthy people. Severity of neurological and functional deficits was assessed with the NIHSS and the Barthel index, respectively. A number of biochemical parameters: serum SSAO activity, concentration of middle-sized molecules (MSM) and malonic dialdehyde (MDA) were measured. The higher concentration of MSM (0,80 +/- 0,22 and 0,5 +/- 0,1 g/l) and MDA (4,5 +/- 1,25 and 3,66 +/- 0,15 mmol/ml), respectively, was found in patients compared to the controls (p < 0,001). The correlative increase in MSM and MDA suggest the formation of chronic oxidative stress in the 4-5 months of disease. The changes in SSAO activity in patients with ischemic stroke that differed from controls were seen in 84% of cases while the increase in SSAO activity was found in 31% of patients. The pathogenetic link between the increase in SSAO activity and severity of neurological deficit was shown. This increase might be one of the pathogenetic links in the disturbance of neuroplasticity.