Final answer:
TPMT mutations specifically affect the metabolism and toxicity of thiopurine drugs like mercaptopurine. Other antimetabolites, such as methotrexate or gemcitabine, are affected by different enzymatic pathways. It's important to consider genetic polymorphisms in these enzymes as they can alter the drug's effectiveness and patient safety.
Step-by-step explanation:
The antimetabolites affected by TPMT (thiopurine S-methyltransferase) mutations include drugs like mercaptopurine. Mercaptopurine is a purine analog that inhibits the biosynthesis of adenine nucleotides, an essential component of DNA, and acts as an antimetabolite. The efficacy and toxicity of thiopurine drugs, including mercaptopurine, are influenced by the genetic polymorphisms in the TPMT enzyme. TPMT mutations can lead to variations in enzyme activity that affect drug metabolism, potentially causing severe toxicity in patients with reduced TPMT activity.
Other antimetabolite medications, such as methotrexate, inhibit folic acid reductase, crucial in purine synthesis, although these are not specifically affected by TPMT mutations. Moreover, the nucleotide analog gemcitabine has its efficacy complicated by degradation through cytidine deaminases, not TPMT. Nonetheless, genetic variations in metabolizing enzymes, echoing the issues with TPMT, can influence the effectiveness and toxicity profiles of various antimetabolites.