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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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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...
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Electron Transport Chain: Complex I and II01:46

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

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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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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

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5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

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Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
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Drugs that Destabilize Microtubules01:10

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Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
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Updated: Feb 20, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Mitochondrial Dysfunction in Chemotherapy-Induced Peripheral Neuropathy (CIPN).

Annalisa Canta1, Eleonora Pozzi2, Valentina Alda Carozzi3

  • 1Experimental Neurology Unit, Department of Surgery and Translational Medicine, University of Milan-Bicocca, Via Cadore 48, 20900 Monza (MB), Italy. annalisa.canta@unimib.it.

Toxics
|October 24, 2017
PubMed
Summary

Mitochondrial dysfunction is key in chemotherapy-induced peripheral neuropathies (CIPN). Drugs like vincristine and paclitaxel disrupt neuronal energy and calcium balance, causing nerve damage.

Keywords:
Chemotherapy compoundsmitochondriamitotoxicityneuropathic painperipheral neurotoxicity

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Mitochondrial dysfunction plays a critical role in various disorders, notably chemotherapy-induced peripheral neuropathies (CIPN).
  • Dysregulation of calcium signaling, reactive oxygen species, and apoptosis pathways are implicated in CIPN pathogenesis.
  • Chemotherapy agents can directly impact mitochondrial function in neurons.

Purpose of the Study:

  • To elucidate the specific mechanisms by which different chemotherapy drugs induce mitochondrial dysfunction in peripheral neurons.
  • To understand the impact of these dysfunctions on neuronal homeostasis and excitability.

Main Methods:

  • Review of existing literature on the molecular and cellular effects of chemotherapy agents on mitochondria.
  • Analysis of pathways affected by vincristine, paclitaxel, cisplatin, oxaliplatin, and bortezomib.
  • Examination of effects on calcium signaling, reactive oxygen species, apoptosis, mitochondrial membrane potential, and gene expression.

Main Results:

  • Vincristine disrupts calcium movement in Dorsal Root Ganglia (DRG) neurons, altering mitochondrial homeostasis.
  • Paclitaxel induces mitochondrial permeability transition pore opening, leading to energy depletion and calcium release in axons.
  • Cisplatin and oxaliplatin damage mitochondrial DNA, inhibiting replication and transcription, causing energy failure in DRG neurons.
  • Bortezomib alters mitochondrial calcium homeostasis and the respiratory chain, affecting gene expression related to mitochondrial function.

Conclusions:

  • Multiple chemotherapy agents induce peripheral neuropathy through distinct but overlapping mechanisms of mitochondrial dysfunction.
  • Targeting mitochondrial pathways may offer therapeutic strategies for preventing or treating CIPN.