The release of reactive oxygen species accompanying oxidative stress is one of the most significant damaging mechanisms during brain ischemia. Some aspects of the neuroprotective activity of the thyronamine T0AM synthetic analogue, 4-4-(2-aminoethoxy)benzylaniline (ABA), were studied and discussed in two independent experiments using a model of acute cerebral ischemia. Antioxidant effects were evaluated in adult male and female Wistar rats (Rattus norvegicus), while neurological outcomes were assessed in adult male outbred white rats. Administration of the ABA in a rat brain hemisphere ischemia model was associated with significant changes in redox markers: malondialdehyde, glutathione peroxidase and superoxide dismutase levels in the ischemic hemisphere. Also, the introduction of ABA into the model of acute cerebral ischemia contributed to a reduction in neurological deficit compared to untreated controls. It was revealed that the considered thyronamine T0AM analogue could control redox status in acute brain ischemia. Mono protonated form of ABA (ABA-H+) is considered to be the main species at pH 6.9 ÷ 7.2. Structural models of the neutral (ABA), protonated (ABA-H+) thyronamine and its solvate (DMSO…ABA-H+) were used in DFT calculations, followed by estimation of molecular and supramolecular level descriptors.
Filimonov et al. (Tue,) studied this question.