EFFECT OF MELATONIN ON OXIDATIVE STRESS AFTER NEONATAL ANOXIA

• Grant number: 23/01234-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: July 01, 2023
• End date: June 30, 2024
• Field of knowledge: Biological Sciences - Morphology - Cytology and Cell Biology
• Principal Investigator: Silvia Honda Takada
• Grantee: Yeda Junqueira
• Host Institution: Centro de Matemática, Computação e Cognição (CMCC). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil

Abstract

Neonatal anoxia is defined as total deprivation of oxygen supply at birth and its incidence in low-birth-weight preterm infants is approximately 60%. One of the experimental models developed to study this condition is the neonatal anoxia model, global and non-invasive, which has the advantage of simulating clinical conditions of premature newborns. In this model, death was observed in the glial and neuronal populations of the hippocampus, a decrease in neurogenesis and volume in this region and changes in memory and learning in animals exposed to the insult. The hippocampus is especially vulnerable to oxygen deficit and astrocytes play an important role in protecting against oxidative stress and, in cases of injury, can express proteins at high levels, contributing to neuronal death. Among the treatment possibilities for this injury is melatonin, produced by the pineal gland and peripheral tissues, which exerts a regulatory function on circadian rhythms, as well as on the defense system, being a powerful antioxidant acting in the neutralization of reactive oxygen species and in stimulating the activity of antioxidant enzymes. Therefore, this study intends to analyze the effect of melatonin on oxidative stress after neonatal anoxia.