Therapeutic Approaches to the Treatment of Botulism

Abstract

Work during the past year has focused on three problems: i) defining the conditions that maximize the binding of toxin to nerve endings. ii) evaluating possibility that botulinum is a mitochondrial poison, and iii) studying the interaction between botulinum neurotoxin and a series of monoclonal antibodies. The work on toxin binding suggests that the approach currently used by most biochemists is flawed. Their approach maximizes binding, but this binding does not appear to involve relevant receptors. The work on mitochondrial function indicates that botulinum neurotoxin is not a mitochondrial poison. If it does affect mitochondrial function, that effect is indirect. The work on monoclonals has shown that type E botulinum neurotoxin can be substantially detoxified by antibodies directed against both the heavy and light chains. It also shows that antigenic determinants on the toxin continue to be exposed after the toxin has bound to nerve endings. Keywords: Neuromuscular blockade, Experimental therapeutics, RA 1, Pharmacological antagonists, Antidotes, Antitoxins, Binding sites.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Oct 01, 1988
Accession Number
ADA206612

Entities

People

  • Lance L. Simpson

Organizations

  • Thomas Jefferson University

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Animals
  • Antibodies
  • Biomedical Research
  • Cholinergic Nerves
  • Gel Permeation Chromatography
  • Laboratory Animals
  • Materials
  • Mitochondria
  • Molecular Weight
  • Nerves
  • Neurotoxins
  • Paralysis
  • Peripheral Nervous System
  • Phrenic Nerves
  • Poisoning
  • Technical Information Centers
  • Tissues

Fields of Study

  • Biology

Readers

  • Microbial Pathology
  • Molecular and Cellular Biochemistry
  • Systems Analysis and Design