Neonatal brain injury as a consequence of insufficient cerebral oxygenation.

Neonatal brain hypoxic-ischemic injury represents a serious health care and socio-economical problem since it is one of the most common causes of mortality and morbidity of newborns. Neonatal hypoxic-ischemic encephalopathy is often associated with signs of perinatal asphyxia, with an incidence of about 2-4 per 1,000 live births and mortality rate up to 20%. In about one half of survivors, cerebral hypoxic-ischemic insult may result in more or less pronounced neuro-psychological sequelae of immediate or delayed nature, such as seizures, cerebral palsy or behavioural and learning disabilities, including attention-deficit hyperactivity disorder. Hypoxic-ischemic injury develops as a consequence of transient or permanent restriction of blood supply to the brain. Severity of hypoxic-ischemic encephalopathy varies depending on the intensity and duration of hypoxia-ischemia, on the type and size of the brain region affected, and on the maturity of the foetal/neonatal brain. Though a primary cause of hypoxic-ischemic injury is lack of oxygen in the neonatal brain, underlying mechanisms of subsequent events that are critical for developing hypoxic-ischemic encephalopathy are less understood. Their understanding is however necessary for elaborating effective management for newborns that underwent cerebral hypoxic-ischemic insult and thus are at risk of a negative outcome. The present paper summarizes current knowledge on cerebral hypoxic-ischemic injury of the neonate, fundamental processes involved in etiopathogenesis, with a special focus on cellular and molecular mechanisms and particular attention on certain controversial aspects of oxidative stress involvement.

Effect of venlafaxine on scavenging free radicals in vitro.

UNLABELLED: O BJECTIVE: Venlafaxine (VLF) was examined as a potential donor of H atom(s) to scavenge hydroxyl and peroxy-type radicals generated under aerobic conditions by catalytic oxidation of ascorbate with Cu²âº ions. Kinetics of the electron-donor property of VLF was investigated by standard ABTS and DPPH assays. Electron paramagnetic resonance measurements were applied to prove/disprove the VLF ability to scavenge superoxide anion radical. RESULTS: Results indicated that the drug venlafaxine was slightly capable of donating ·H, this way VLF scavenged the in situ generated hydroxyl radicals. Under the experimental conditions VLF was not able to inhibit/retard the propagation of the peroxy-type radicals. Regarding to the drug electron donating property, VLF did not show any ABTS·âº or DPPH· radical quenching property. Venlafaxine was not effective in scavenging O2·â». CONCLUSION: Results of ABTS and DPPH assay showed a negligible redox activity of venlafaxine to both DPPH· and ABTS·âº. Venlafaxine was not capable of scavenging the superoxide anion radical generated in KO2/DMSO system, which indicates that VLF is not an efficient electron/proton donor molecule.