In megaloblastic anemia, which macromolecule synthesis is impaired?

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Multiple Choice

In megaloblastic anemia, which macromolecule synthesis is impaired?

Explanation:
Megaloblastic anemia results from impaired DNA synthesis in rapidly dividing cells due to folate or vitamin B12 deficiency. These vitamins are required to make deoxyribonucleotides, especially thymidine triphosphate; without them, thymidylate synthesis falters and DNA replication slows. Because DNA synthesis is hindered, erythroid precursors cannot complete division at the normal rate, so the nucleus lags behind the expanding cytoplasm. This creates large, immature cells called megaloblasts with oversized nuclei. Meanwhile, RNA synthesis and ribosome production continue, leading to a basophilic, RNA-rich cytoplasm. Lipid and protein synthesis are not the primary bottlenecks here, so the key impaired process is DNA synthesis.

Megaloblastic anemia results from impaired DNA synthesis in rapidly dividing cells due to folate or vitamin B12 deficiency. These vitamins are required to make deoxyribonucleotides, especially thymidine triphosphate; without them, thymidylate synthesis falters and DNA replication slows. Because DNA synthesis is hindered, erythroid precursors cannot complete division at the normal rate, so the nucleus lags behind the expanding cytoplasm. This creates large, immature cells called megaloblasts with oversized nuclei. Meanwhile, RNA synthesis and ribosome production continue, leading to a basophilic, RNA-rich cytoplasm. Lipid and protein synthesis are not the primary bottlenecks here, so the key impaired process is DNA synthesis.

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