Final answer:
Isoniazid inhibits mycobacterial mycolic acid synthesis, leading to toxicities such as hepatotoxicity, neurotoxicity, and hematologic toxicity. Rifampin blocks RNA polymerase activity in bacteria, resulting in hepatotoxicity due to the induction of liver enzymes that affect the metabolism of drugs.
Step-by-step explanation:
The mechanisms of action for isoniazid and rifampin involve the inhibition of components crucial to bacterial cell survival. Isoniazid is an antimetabolite that requires activation by bacterial enzymes, transforming into active molecules that prevent the synthesis of mycolic acid, an essential component of the mycobacterial cell wall. This process is specifically toxic to mycobacteria. Major toxicities of isoniazid include hepatotoxicity (liver damage), neurotoxicity (nerve damage), and hematologic toxicity (blood disorders, such as anemia).
On the other hand, rifampin is a semisynthetic member of the rifamycin family that blocks bacterial RNA polymerase activity, which is crucial for RNA synthesis and subsequent protein production. As it impedes the initiation step of RNA transcription, rifampin exhibits antibacterial properties. Major toxicities associated with rifampin include hepatotoxicity, as it can induce liver enzymes that increase metabolism of not only rifampin itself but also other drugs, potentially leading to reduced efficacy of these drugs.