A new muscle damaging toxin, myotoxin II, from the venom of the snake Bothrops asper (terciopelo)
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B. Lomonte and J. M. Gutiérrez. A new muscle damaging toxin, myotoxin II, from the venom of the snake Bothrops asper (terciopelo). Toxicon27, 725–733. 1989.—A new muscle damaging toxin, myotoxin II, was purified from the venom of Bothrops asper by ion-exchange chromatography on CM-Sephadex C-25. The toxin is a dimeric, basic protein with a monomer mol.wt of 13,341, according to the amino acid composition, and 16,000 on the basis of SDS-polyacrylamide gel electrophoretic mobility. It has a high number of aspartate and lysine residues, as well as of hydrophobic amino acids. Upon i.m. injection into mice, the toxin induces myonecrosis and increase in serum creatine kinase levels. In addition, myotoxin II induces edema in the mouse foot pad. Immunochemical tests, mol.wt, and amino acid composition indicate a high degree of homology between myotoxin II and a previously characterized myotoxin from this venom, myotoxin I. However, in contrast to myotoxin I, myotoxin II lacks phospholipase A2 and anticoagulant activities in vitro.
Horticultural supplements containing oxytetracycline and gentamicin, two clinically relevant biocides, are widely marketed to prevent or control infections by bacterial phytopathogens. Despite their regular consumption in the world’s less developed countries, it is unknown whether exposure of tropical farmlands to these drugs results in an enrichment of resistant bacteria, resistance genes, and/or mobile genetic elements in the soil. These concerns were investigated under field conditions by repeatedly spraying recommended amounts of a commercial product containing oxytetracycline-HCl, and gentamicin-SO4−2'>SO−24SO4−2 onto two coriander plots. Subsequent to five applications within 16 months, composite soil samples from control and treated sections were compared with respect to the abundance of resistant bacteria and the prevalence of conserved nucleotide sequences from tetracycline efflux proteins, tetracycline ribosomal protection proteins, four different families of gentamicin-modifying enzymes, and broad host range plasmids of the IncP-1 and IncQ incompatibility groups. The isolation frequency of oxytetracycline- and gentamicin-resistant bacteria and the detection rate of the aforementioned genes and elements were unrelated to application of the supplement. Despite the omnipresence of sequences from IncP-1 plasmids, conjugative plasmids conferring resistance to oxytetracycline or gentamicin were not captured in biparental matings. The widespread occurrence of resistant bacteria and resistance genes at the beginning of the trial emerges as a reasonable explanation for the lack of anticipated responses. Moreover, we assume that the biocides applied were inactivated by biotic and abiotic factors under tropical conditions.
