Efeitos da peçonha de Bothrops jararacussu em eritrócitos humanos

Abstract

Erythrocytes, which have a discoidal shape, are surrounded by a membrane consisting of a lipid bilayer formed by phospholipids – such as phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and sphingomyelin – and many proteins. Furthermore, the erythrocyte membrane is also malleable, which facilitates its movement in specific locations, such as capillaries, where blood vessels are narrowed. These distinct characteristics, together with the fact that these cells lack cytoplasmic organelles, make erythrocytes an enjoyable model for studying the effects of certain substances on the lipid bilayer. Among these substances, snake venoms are characterized by many enzymes, including phospholipase A2 (PLA2), which catalyzes the cleavage of phospholipids, particularly phosphatidylcholine (lecithin). This leads to destabilization of the erythrocyte membrane, which subsequently promotes increased osmotic fragility and, consequently, cell lysis.Therefore, this study aimed to analyze the effect of the venom of one of the most important Brazilian snakes, Bothrops jararacussu, on osmotic fragility and erythrocyte membrane structure. Tests were performed using different concentrations of NaCl and crude Bothrops jararacussu venom. Wright staining was also performed to investigate the effect of venom on erythrocyte membrane morphology. These tests demonstrated that crude Bothrops jararacussu venom alone does not increase erythrocyte osmotic fragility. However, in the presence of egg yolk, a source of exogenous glycerophospholipids, increased osmotic fragility was observed. Thus, treatment with crude venom combined with egg yolk led to a change in the standard biconcave disc shape of erythrocytes to an echinocyte shape, characterized by regularly spaced spines on their surface. This change appears to be associated with the formation of lysolecithin from the action of PLA2 on lecithin. Given these results, it can be seen that, although raw venom, when alone, is not capable of directly causing an increase in erythrocyte membrane instability, this phenomenon can appear when concentrations of glycerophospholipids are increased