There is a unifying view of the behaviour of gentamicin.
It has been observed that stress inhibits the activity of the antibiotic, gentamicin. This critical observation leads not only to an explanation of the initial physiological behaviour of the molecule but also helps accommodate the behaviour of several other ligands in their affinity for specific biomembranes. The fundamental mechanism involved is assumed to be chemisorption of the ligands to the negatively-charged lipids that facilitates a phase separation of the associated lipids. In a condensed, mixed-lipid situation, as exists in a living membrane, such a type of reaction may lead to membrane expansion and as a consequence to leakage and signal-induction. The present hypothesis develops such a view with the aid of few supplementing data and a considerable amount of supporting data selected from published literature. The hypothesis requires the rigor of modern-day instrumentation for testing.
D000818:Animals; D001682:Biological Availability; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005839:Gentamicins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008563:Membrane Lipids / Q000378:metabolism; D008958:Models, Molecular; D008968:Molecular Conformation; D013312:Stress, Physiological / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D005839:Gentamicins; D008563:Membrane Lipids