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The Impact of Doxorubicin on 4 -HNE Aggresome Processing in Cardiac Cells: Analyzing Autophagy Flux

JSHS · 2025

Varsha Manikandan, Dr. Sumitra Miriyala · Kirksville Senior High School, Kirksville, MO

Overview

Doctors use doxorubicin as a chemotherapy treatment for multiple cancer types. Doxorubicin shows strong cancer treatment results, but its side effect of heart damage remains its most significant challenge. Scientists know ROS damages cell parts when doxorubicin produces these reactive oxygen species. ROS attacks lipids, producing 4 -hydroxynonenal (4-HNE), which forms covalent bonds with proteins. When proteins undergo harmful changes, the cell works to contain these misfolded proteins in aggresome structures it tries to degrade. Cells use autophagy to break down damaged parts and keep themselves healthy. The heart cells known as cardiomyocytes need perfect autophagy to handle stress from doxorubicin treatment. This research studies the capacity of MnTnBuOE -2-PyP5+ (MnP, also known as BMX -001) to break down damaged aggresomes in H9c2 cardiomyocytes through its superoxide dismutase (SOD) mimetic action. BMX-001 acts like superoxide dismutase to help cells break down ROS-caused aggresomes and reduce their harmfu l effects. We used an in vitro model to test the doxorubicin effect in H9c2 cardiomyocytes. After 24 hours of doxorubicin exposure, cell viability was assessed using the Evans Blue exclusion method. Two concentrations of BMX -001 were tested, with 10 µM and 20 µM selected for optimal cardioprotection. The treatment's impact on intracellular superoxide levels was quantified using HPLC post -DHE treatment. This research shows BMX -001 can lower oxidative stress indicators in H9c2 cells under Doxorubicin treatmen t and demonstrates its therapeutic power in heart-related cancer treatments. BMX-001 acts as a SOD2 mimetic to protect cardiomyocytes and help patients with heart conditions caused by chemotherapy -induced oxidative stress.

Competition history

  • JSHS 2025 Category not listed

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