Final answer:
Cisplatin acts by forming covalent bonds with DNA, leading to the formation of intrastrand crosslinks, which interfere with DNA replication and transcription in fast dividing cells.
Step-by-step explanation:
Cisplatin, a platinum-based chemotherapeutic agent, exerts its cytotoxic effects by binding to DNA and forming intrastrand crosslinks. This process involves the displacement of chloride ions on cisplatin, allowing the molecule to react with purine bases in DNA, predominantly guanine. The resulting covalent bonds between cisplatin and DNA disrupt the normal structure of the double helix, causing bends and kinks.
These structural alterations hinder the ability of DNA to undergo replication and transcription. During cell division, fast dividing cells are particularly vulnerable to the interference caused by cisplatin-induced crosslinks. As cells attempt to replicate their DNA, the presence of these covalent bonds obstructs the progression of DNA polymerase, leading to the accumulation of DNA damage. This impediment triggers cell cycle arrest and, ultimately, cell death through apoptosis.
The preference for fast dividing cells is crucial in cancer treatment, as cancer cells typically exhibit higher rates of proliferation compared to normal cells. By selectively targeting rapidly dividing cells, cisplatin aims to minimize damage to healthy, non-dividing cells in the body.
In summary, cisplatin's mechanism of action involves the formation of intrastrand crosslinks with DNA, disrupting cellular processes essential for the proliferation of fast dividing cells, which is particularly advantageous in cancer therapy.