Category: catabolism
Two distinct mechanisms grouped for clinical co-deployment. (1) DNA gyrase + topoisomerase IV — quinolones bind the enzyme-DNA complex → DNA strand breakage. (2) Bacterial folate synthesis — sulfonamides mimic PABA and competitively inhibit dihydropteroate synthase (DHPS, first step); trimethoprim inhibits dihydrofolate reductase (DHFR, downstream); the sulfonamide + trimethoprim combo (TMP-SMX) is sequential blockade → synergy. Metronidazole is activated by anaerobic ferredoxin/flavodoxin reduction → DNA-damaging nitro radicals; only anaerobes + microaerophilic protozoa can activate it. Nitrofurantoin is similarly activated by bacterial nitroreductases → multi-target damage (DNA, ribosome, metabolic enzymes); urinary concentration drives UTI activity despite low plasma levels.