What is the action of isoniazid in tuberculosis treatment?

Isoniazid is primarily effective against Mycobacterium tuberculosis through its inhibition of mycolic acid synthesis. Mycolic acids are essential components of the mycobacterial cell wall and are crucial for the bacterium's structural integrity, virulence, and resistance to phagocytosis and certain antibiotics. Isoniazid is a prodrug that is activated by the enzyme KatG (catalase-peroxidase) in the bacteria, leading to the formation of reactive metabolites that inhibit the enzyme InhA, a critical enzyme involved in the fatty acid synthesis pathway responsible for mycolic acid production. By interfering with this synthesis, isoniazid compromises the bacterial cell wall, thereby contributing to the bacterium's inability to survive and replicate.

Other choices do not accurately describe the mechanism of action of isoniazid. While inhibiting peptidoglycan synthesis is a mechanism associated with other antibiotic classes, such as beta-lactams, it does not apply to isoniazid's action against tuberculosis. Similarly, the inhibition of DNA gyrase and RNA polymerase pertains to other specific antibiotic classes, like fluoroquinolones and rifamycins, respectively, and not to isoniazid. Thus