ABSTRACT:
Drug resistance is an ever-increasing problem in the chemotherapy of bacterial infectious diseases. Development and clonal spread of drug-resistant bacteria and the horizontal transfer of resistance factors among bacteria have resulted in increase of the incidence of drug-resistant infection. Antibiotic resistance in bacteria may be an inherited trait of the organism. It occurs because of natural resistance, it may be acquired by means of mutation in its own DNA or resistance-conferring DNA from another source. RecA has emerged as a potential target due to its activities allows bacteria to overcome the metabolic stress induced by a range of antibacterial agents. Thus inhibition of RecA and its activity can be developed as molecular target for suppression of resistance to antibiotic. It has a structural and functional homologue in every species. It has multiple activities, all related to DNA repair, bacterial SOS response. Mutations are prominent cause of this type of resistance. RecA is found as component and responsible for DNA repair and recombinations required for mutations. Newer drugs are screened as RecA inhibitors, e.g. Suramin. These will act as future drugs with antibiotics to reduce resistance and improve therapeutic index.