The Effect of Deferoxamine and Ferrostatin-1 Treatments on Total ROS in HK-2 Cells

Overview

Investigations indicate that diabetic patients with myocardial infarctions (MI) have an increased risk of acute kidney injury (AKI) post-MI. In diabetic MI, blood hemoglobin (Hb) rises, which induces the production of reactive oxygen species (ROS) that cause AKI through ferroptosis. Deferoxamine (DFO) and ferrostatin-1 (Fer-1) are treatments that reduce ROS through iron-chelation or the catalysis of radical reduction, respectively. This study investigates how ROS levels in Proximal Tubular Cells (HK-2) change with concentration adjustments of Fer-1 and DFO, as well as whether a mixture of DFO and Fer-1 at 1µM causes a synergic reduction of ROS. The results indicate that DFO, treated at 1µM, 10µM, and 100µM, had a dose-dependent reduction of ROS but did not achieve a significant reduction of ROS (p>0.05) at 1µM. Conversely, DFO 1µM significantly increased ROS in the second experiment, indicating possible prooxidant interactions of DFO at low concentrations. Fer-1, treated at 1µM, 5µM, and 10µM, indicated a dose-dependent response until 5µM. However, there was no significant reduction in ROS between 5µM and 10µM due to the unsaturation of Fer-1 past 5µM. When Fer-1 and DFO were mixed at 1µM, the ROS was not significantly different from Fer-1 1µM, so there was no synergic effect (p>0.05). Hence, future treatments of Fer-1 and DFO should be done independently, DFO should be treated at concentrations of at least 10µM, where there is a significant reductive effect, and Fer-1 should be treated up to 5µM, where there is maximal ROS reduction.

Awards (1)

• Third Award of $1,000 $1,000

Competition history

• ISEF 2021 Biomedical and Health Sciences · Entry BMED056

Resources

• ISEF abstract page ↗

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