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Fluoroquinolones (FQs) are widely used second line anti tuberculosis drug. Extensive use of FQs has increased the incidence
of resistance in Mycobacterium tuberculosis. Apart from mutation in the drug target site i.e., gyr A and gyr B the resistance
may develop due to active efflux pump. In this study, we evaluated the role of the efflux pumps in fluoroquinolone resistance
by using efflux inhibitors carbonyl cyanide m-chlorophenyl hydrazone (CCCP) which acts by decreasing the trans-membrane
electrochemical gradient and verapamil, a calcium channel blocker in clinical isolates of M. tuberculosis. A total of 50
fluoroquinolone resistant M. tuberculosis clinical isolates were tested by Resazurin micro titer assay (REMA) to observe the
changes in minimum inhibitory concentration (MIC) in presence and absence of efflux inhibitors using standard strain H37Rv.
The MIC levels showed 2-8 fold reduction in presence of CCCP (10/50 20%) and verapamil (12/50 24%). Reduction in MIC
was observed in (15/50 30%) strains when both the inhibitors were used simultaneously. Our findings suggest that an active
efflux pump could be a major contributor in development of resistance against fluoroquinolones. Significant reduction in MIC
indicates the involvement of Major Facilitator Super Family (MFS) family and ATP Binding Cassette (ABC) transporters which
are inhibited by CCCP and verapamil respectively.