Key result
OD1 severely hampers insect para/tipE channel inactivation at ~80 nM while sparing Na(v)1.2/beta1.
Why the study?
The venom of the Iranian scorpion Odonthobuthus doriae was scarcely studied and its alpha-like toxins affecting voltage-gated Na+ channels were not characterized.
OD1 is a novel alpha-like toxin from Odonthobuthus doriae venom that selectively impairs the inactivation of insect voltage-gated sodium channels compared to mammalian isoforms.
OD1 may enable selective targeting of insect sodium channels; leaves open its development as a novel insecticide.
In this study, we isolated and pharmacologically characterized the first alpha-like toxin from the venom of the scarcely studied Iranian scorpion Odonthobuthus doriae. The toxin was termed OD1 and its primary sequence was determined: GVRDAYIADDKNCVYTCASNGYCNTECTKNGAESGYCQWIGRYGNACWCIKLPDEVPIRIPGKCR. Using the two-electrode voltage clamp technique, the pharmacological effects of OD1 were studied on three cloned voltage-gated Na+ channels expressed in Xenopus laevis oocytes (Na(v)1.2/beta1, Na(v)1.5/beta1, para/tipE). The inactivation process of the insect channel, para/tipE, was severely hampered by 200 nM of OD1 (EC50 = 80+/-14 nM) while Na(v)1.2/beta1 still was not affected at concentrations up to 5 microM. Na(v)1.5/beta1 was influenced at micromolar concentrations.
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Jalali et al. (2005) studied this question. OD1 was evaluated on Inactivation process of voltage-gated Na+ channels (EC50 = 80+/-14 nM). OD1 severely hampered the inactivation process of the insect channel para/tipE (EC50 = 80+/-14 nM), while Na(v)1.2/beta1 was unaffected up to 5 microM.
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