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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates these...

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Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
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Related Experiment Videos

PCNA damage caused by antineoplastic drugs.

Soo In Bae¹, Ran Zhao, Robert M Snapka

¹Department of Radiology, Division of Radiobiology, The Ohio State University, Columbus, OH 43240, United States.

Biochemical Pharmacology

|October 1, 2008

Summary

Certain cancer drugs cause covalent crosslinking of proliferating cell nuclear antigen (PCNA) when exposed to light. This photodynamic damage to PCNA and other proteins may impair DNA repair mechanisms.

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Area of Science:

Biochemistry
Cell Biology
Photochemistry

Background:

Proliferating cell nuclear antigen (PCNA) is crucial for DNA replication and repair.
Chemotherapeutic and chemopreventive drugs are widely used in cancer treatment.
Understanding drug-induced cellular damage is essential for optimizing cancer therapy.

Purpose of the Study:

To investigate the phototoxic effects of various drugs on PCNA.
To identify the mechanism and biomarkers of drug-induced photodynamic damage.
To assess the potential impact on DNA repair pathways.

Main Methods:

Exposure of mammalian cells to fluorescent light in the presence of diverse drugs.
Analysis of protein crosslinking using biochemical assays.
Investigation of reactive oxygen species involvement and protective/enhancing agents.

Main Results:

Structurally diverse drugs induced covalent crosslinking of PCNA trimers upon light exposure.
PCNA crosslinking occurred with both nuclear and cytoplasmic drug localizations, even with brief light exposure.
Singlet oxygen likely mediates PCNA photo-crosslinking, which also affects SV40 large T antigen.

Conclusions:

Drug-induced PCNA crosslinking serves as a sensitive biomarker for photodynamic damage.
Photodynamic damage to PCNA and large T antigen may compromise DNA damage signaling and repair.
Visible light exposure should be considered for patients undergoing treatment with these antineoplastic drugs.