Oxidative stress and antioxidative defense in fetuses and newborn children with spina bifida in cerebrospinal fluid.

BACKGROUND

Spina bifida remains the most prevalent defect of the central nervous system and second most common congenital birth anomaly. Oxidative stress is one of the key factors affecting the extent of tissue damage during fetal life. Harmful effects of Reactive Oxygen Species (ROS) are exacerbated by rapid growth and development of tissues, coupled with weak antioxidant defenses, and lead to protein, lipid and DNA damage, ultimately resulting in cell death through apoptosis or necrosis.

METHODS

A total of 62 samples of the cerebrospinal fluid from children with spina bifida were collected: 31 fetuses-prenatal repair (Group 1) and 31 newborns-postnatal repair on day 1, within the first 24 h of life (Group 2). The activity of glutathione reductase (GR), catalase (KAT), superoxide dismutase (SOD) and its mitochondrial isoenzyme (MnSOD), as well as Total Antioxidant Capacity (TAC) and Total Oxidative Status (TOC) levels, were compared.

RESULTS

Both the activity of the antioxidant enzymes (SOD, MnSOD, GR, KAT) and TAC and TOS levels were statistically significantly higher in the fetuses as compared to the newborns.

CONCLUSIONS

Significantly higher antioxidant enzyme activity and TAC and TOS levels were found in the cerebrospinal fluid samples in the prenatal as compared to the postnatal repair groups. These results suggest insufficient antioxidant protection in the postnatal repair group, which may increase the risk of oxidative damage, potentially affecting the neurological system more severely than in the fetuses. Extinguishment of the enzymatic activity of the antioxidant system during fetal life may lead to irreversible damage to the exposed structures of the central and peripheral nervous system in fetuses with spina bifida.