FUTURE USE OF ANTIOXIDANT DEFENSE SYSTEM COMPONENTS AS MARKERS OF ORGANIC DAMAGE TO THE CENTRAL NERVOUS SYSTEM IN THE NEONATAL PERIOD IN PREMATURE NEWBORNS

Objective of the study: to assess the significance of superoxide dismutase (SOD) and glutathione as markers of severe CNS damage in premature infants. Materials and methods of research: a onestage comparative study with a control group – a part of an observational prospective longitudinal non-randomized multicenter study. The main group – 60 premature infants with gestational age (GA) less than 36 weeks inclusive (32 boys (53%) and 28 girls (47%), the control group – 25 fullterm newborns (15 boys (60%) and 10 girls (40%). In the process of dynamic observation, the main group was divided into subgroups depending on the diagnosed in the neonatal period according to instrumental methods of examination of CNS lesions. Subgroup 1 included 25 children with CNS lesions – intraventricular hemorrhages (IVH) of varying severity, periventricular leukomalacia – PVL; 14 boys (56%), 11 girls (44%). Subgroup 2 included 35 preterm infants without CNS damage – 18 boys (51%), 17 girls (49%) The indicators of oxidative stress, antioxidant capacity, blood levels of SOD and glutathione enzymes in reduced (GSH) and oxidized (GSSG) states were studied once in the early neonatal period. Results: statistically significant differences were found when comparing the control group, 1st and 2nd subgroups by body weight (BW) (K–V, p<0.0001). BW at birth in premature infants with CNS lesions was statistically significantly less than in premature infants without CNS lesions (M–U, p=0.0019). When analyzing GA, statistically significant differences were also found when comparing the three groups with each other (K–U, p<0.0001). The gestational period of premature infants with CNS lesions was statistically significantly lower than in premature infants without CNS lesions (M–U, p=0.0013). All three groups differed statistically significantly in terms of SOD (C–V, p=0.0045). Premature infants with CNS lesions in the neonatal period had a statistically significantly lower SOD value than children without CNS lesions (M–U, p=0.0021). Statistically significant differences were found when comparing the three groups in terms of GSSG content (K–V, p<0.0001). Also, in premature infants with CNS lesions, the GSSG values were statistically significantly lower than in premature infants without CNS lesions in the neonatal period (M–V, p=0.0001). The GSH level in all studied groups was statistically significantly different (C–C, p<0.0001). In premature infants with CNS lesions, the GSH level was statistically significantly lower than in infants without CNS lesions in the neonatal period (М–У, p=0.0001). When determining the TAS/TAC (antioxidant capacity), statistically significant differences were found when comparing the three groups (K–V, p=0.0002). In premature infants with CNS damage, TAS/TAC was statistically significantly lower than in the group of premature infants without CNS damage in the neonatal period (M–U, p=0.0001). In all cases of comparison of the studied parameters, the control group and premature babies without CNS damage did not differ statistically significantly. When comparing premature infants with and without damage to the CNS with GA of more than 31 weeks, it was revealed that the groups differed statistically significantly in all the studied parameters: in the group of children with CNS lesions, the studied parameters were lower (SOD, M–U, p=0.0249; GSSG, M–U, p=0.0055; GSH M–U, p=0.0055; TAS/TAC, p=0.0019). The study revealed that premature infants with CNS damage experience greater oxidative stress than infants without CNS damage in the neonatal period (Fisher's exact test, two-sided, p=0.0012, Infinity [NaN; Infinity]). Conclusions: Premature infants differ in antioxidant protection; children with lower antioxidant status are prone to the development of severe organic lesions of the central nervous system in the neonatal period. SOD and glutathione can be used in clinical practice as markers of organic lesions of the central nervous system in the neonatal period in premature infants.