Nitin et al. [12] evaluated the possibility of capsaicin acting as an
inhibitor of the NorA efflux pump of S. aureus. The minimum inhibitory concentration (MIC) of ciprofloxacin was reduced 2 to 4 fold in the
presence of capsaicin. This reduction was more prominent for S. aureus
SA-1199B (NorA overproducing) as compared with S. aureus SA-1199
(wild-type) up to 25 mg/L capsaicin. Beyond that, no concentration
dependent effect was observed. S. aureus SA-K1758 (norA knockout)
showed no reduction in the MIC of ciprofloxacin. Table 2 shows in
vitro ciprofloxacin/ capsaicin combination studies. Table 3 shows postantibiotic
effect (PAE) of ciprofloxacin alone and in combination with
capsaicin against S. aureus SA-1199B after exposure of 2 h. Ciprofloxacin
at 4 mg/L, at which no mutant was selected, was defined as the mutant
prevention concentration (MPC). When tested in combination with
capsaicin at 12.5 and 25 mg/L, the MPC of ciprofloxacin was reduced
to 2 and 1 mg/L, respectively. The MPC of the combination was found
to be lower than the Cmax of the ciprofloxacin (3-4 mg/L), indicating the
clinical relevance of these combinations in restricting the selection of
resistant mutants. Ethidium bromide fluoresces only when it is bound
to nucleic acids inside cells. Only the control cells without capsaicin
extruded ethidium bromide, resulting in a significant decrease in
florescence over the assay period. In the presence of capsaicin, the loss
of florescence was significantly reduced, reflecting a strong interference
with ethidium bromide efflux by capsaicin [2]. Table 4 shows the
mutation frequency of S. aureus ATCC 29213