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Related Experiment Video

Updated: Jul 13, 2026

Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors

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Published on: February 7, 2018

Iron signaling and oxidant damage.

Balaraman Kalyanaraman¹

¹Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226-0509, USA. balarama@mcw.edu

Cardiovascular Toxicology

|July 27, 2007

Summary

This study explores how reactive oxygen species (ROS) and nitric oxide (NO) from both inside and outside cells influence doxorubicin (DOX) toxicity.

Area of Science:

Biochemistry
Cell Biology
Pharmacology

Background:

Doxorubicin (DOX) is a widely used chemotherapy agent with significant cardiotoxicity.
Cellular signaling pathways involving reactive oxygen species (ROS) and nitric oxide (NO) are implicated in drug toxicity.
Understanding the interplay of ROS and NO is crucial for mitigating DOX-induced side effects.

Purpose of the Study:

To elucidate the interrelationship between extracellular and intracellular ROS and nitric oxide (NO) signaling.
To investigate the role of these signaling molecules in doxorubicin (DOX) toxicity.

Main Methods:

Review of existing literature on ROS, NO, and doxorubicin (DOX) mechanisms.
Analysis of cellular signaling pathways affected by these molecules.

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Main Results:

Both extracellular and intracellular ROS and NO contribute to doxorubicin (DOX) toxicity through complex signaling networks.
The balance between ROS and NO production and scavenging is critical in determining the extent of cellular damage.

Conclusions:

Targeting ROS and NO signaling pathways may offer novel strategies to reduce doxorubicin (DOX)-induced toxicity.
Further research is needed to fully delineate the precise mechanisms and therapeutic potential.