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Effects of the mycotoxin destruxin A on Locusta migratoria visceral muscles

Effects of the mycotoxin destruxin A on Locusta migratoria visceral muscles,10.1016/j.toxicon.2010.07.012,Toxicon,Esau Ruiz-Sanchez,Angela B. Lange,Ia

Effects of the mycotoxin destruxin A on Locusta migratoria visceral muscles  
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Destruxins, a family of cyclic peptides, are produced by various species of entomopathogenic fungi. These peptides have been shown to influence calcium-dependent processes in insect cell lines and tissues, such as skeletal muscles. To better understand the mechanism of action of these peptide toxins on insect muscular tissues, we have evaluated the effects of destruxin A on the contractions of oviducts and hindgut of Locusta migratoria. In oviducts, destruxin A increased the frequency of spontaneous contractions and induced a dose-dependent tonic contraction; the EC50 for lower lateral and upper lateral oviducts was 0.7 μM and 8.7 μM, respectively. In hindgut, destruxin A also caused an increase in the frequency of spontaneous contractions; the EC50 was 3.2 μM. The action of destruxin A was abolished in Ca2+-free saline or when the Ca2+ channel blocker CoCl2 was added to the incubation saline. Likewise, the presence of 50 μM nifedipine or 100 μM verapamil in the medium reduced the magnitude of destruxin A′s effect, particularly in hindgut. The depolarization of muscle membranes by 100 mM K+ saline prevented the action of destruxin A. Preincubation of lower lateral oviducts in the intracellular Ca2+ antagonist TMB-8 did not have any effect on destruxin A action; however, preincubation in the calmodulin inhibitor trifluoperazine greatly reduced the effect of destruxin A. Taken together, these results show that destruxin A has an excitatory effect on contractions of insect visceral muscles of L. migratoria. Destruxin A-induced contractions appear to be dependent on extracellular, but not on intracellularly-released Ca2+, which suggest that this peptide toxin might be acting on insect visceral muscle by facilitating an influx of extracellular Ca2+.
Journal: Toxicon , vol. 56, no. 6, pp. 1043-1051, 2010
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