CHANGES OF BIOMETALS IN THE RAT FOREBRAIN IN THE EARLY PERIOD OF BLAST-INDUCED TRAUMATIC BRAIN INJURY

Abstract

Blast-induced traumatic brain injury is a complex of impairments caused by the rapid transfer of energy from the explosion to the brain. The main pathogenic factor is the blast wave, which leads to primary diffuse damage. The question of the biometals participation in the pathogenesis of secondary damage in various structures of the brain, in particular in the forebrain in the early period of mild blast-induced traumatic brain injury, is attracting considerable interest at present. The experiment carried out on 36 sexually mature male Wistar rats weighing 220-270 g in the laboratory of the Department of Pathological Anatomy, Forensic Medicine and Pathological Physiology of the Dnipro State Medical University in compliance with current legislation on ethical treatment of animals. Rats were kept in standard vivarium conditions and were randomly divided into 2 groups: experimental (subjected to anaesthesia and exposure to a baroacoustic wave of 26-36 kPa) and intact groups. On the 14th, 21st, and 28th days of the post-traumatic period, the animals were euthanized with halothane followed by removal of the brain and separation of the forebrain. Spectral research was carried out using energy-dispersive X-ray fluorescence analysis. The analysis of the results showed an intragroup increase in the level of Fe by 3% and Cu by 36% and a decrease in Zn by 36%, but all these biometals and their ratios (Cu/Fe, Cu/Zn, Zn/Fe) were more in the experimental rats. We consider that these biometals lead to oxidative stress, damage to the neurons and mitochondria membranes, development of energy deficit, excitation of neurons, disruption of axonal conduction and synaptic transmission. The obtained data can be suggested as factors of secondary damage and used as diagnostic and prognostic markers of this injury type; they can also be used as the foundation for developing pathogenetically validated neuroprotection.