Antiapoptotic potential of spider toxins
Автор: Yurova Elena Valerevna, Beloborodov Evgeniy Alekseevich, Tazintseva Elizaveta Dmitrievna, Sugak Dmitriy Evgenevich, Rastorgueva Evgeniya Vladimirovna
Журнал: Ульяновский медико-биологический журнал @medbio-ulsu
Статья в выпуске: 2, 2021 года.
Arthropod peptide toxins rich in disulfide bonds are one of the potential sources of bioactive substances. Due to their structure, toxins have increased stability and are able to bind to ion channels, blocking them or changing the gating mechanism. Some spider toxins bind to different types of calcium channels. Calcium ions, in turn, play an important role in many cellular processes, namely, apoptosis. The aim of this paper is to investigate the effect of a number of toxins - arachnid ion-channel blockers in -on intracellular processes associated with the induction of apoptosis in mammalian cells. Materials and Methods. Toxins ω-hexatoxin-Hv1a, ω-theraphotoxin-Hhn2a were used in the study, as they are inhibitors of L- and P/Q-type calcium channels, respectively. Apoptosis was induced using the AC-1001H3 peptide. The authors used fluorescence microscopy to study the effect of toxins on the apoptosis level, oxidative stress, and mitochondrial potential in CHO-K1 cells. Results. The authors observed that incubation of cells with toxins (10 nM) and AC-1001H3 peptide led to increased ROI intracellular concentration, which should have induced apoptotic mechanisms. However, the effect was the opposite. In addition, there was an increase in the mitochondrial potential level. Despite this, the used toxins blocked apoptosis caused by AC-1001H3 and reduced the natural apoptosis level in the CHO-K1 cells. Conclusion. The study demonstrated the antiapoptotic effect of some arthropod peptide toxins. The studied toxins can be used in the treatment of pathologies associated with the activation of apoptotic mechanisms.
Apoptosis, spider toxin, peptide
Короткий адрес: https://sciup.org/14121207
IDR: 14121207 | DOI: 10.34014/2227-1848-2021-2-147-156