Abstract

Background: It has been reported that biologically active compounds extracted from Cnidaria venom may induce damage by oxidative stress. Erythrocytes are constantly exposed to oxidative stresses, which can contribute to sulphydril (SH-) group oxidation and cell membrane deformability accompanied with activation of K-Cl co-transport and inhibition of anion transport. In this regard, Band 3 protein is responsible for mediating the electroneutral exchange of chloride (Cl<sup>-</sup>) for bicarbonate (HCO<sub>3</sub><sup>-</sup>), particularly in erythrocytes, where it is the most abundant membrane protein. The aim of this study was to elucidate the effect of crude venom extracted from Pelagia noctiluca nematocysts on Band 3 -mediated anion transport in human erythrocytes. Methods: Erythrocytes were tested for SO<sub>4</sub><sup>2-</sup> uptake, K<sup>+</sup> efflux, glutathione (GSH) levels and concentration of SH- groups. Results: The rate constant of SO<sub>4</sub><sup>2-</sup> uptake decreased progressively to 58% of control with increasing venom doses, and showed a 28% decrease after 2 mM NEM treatment. These effects can be explained by oxidative stress, which was reflected by decreased GSH levels in venom-treated erythrocytes. Hence, the decreased efficiency of anion transport may be due to changes in Band 3 structure caused by SH-group oxidation and reduced GSH concentration. In addition, an increased Cl<sup>-</sup>-dependent K<sup>+</sup> efflux was observed in venom-treated erythrocytes. Conclusion: Our results suggest that crude venom from Pelagia noctiluca alters cell membrane transport in human erythrocytes.

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