β-Lapachone-Induced Oxidative Stress Causes PARP-Dependent NAD+-Depletion that Affects the Energy Metabolism of Cultured Primary Rat Astrocytes

Description

Johanna Elisabeth Willker and Ralf Dringen wrote a 2026 cell study of oxidative stress in astrocytes, the brain's support cells, which have strong antioxidant defenses. They exposed cultured rat astrocytes to beta-lapachone, a compound that triggers oxidative stress through an enzyme called NQO1. The team tracked key molecules for cell energy and redox balance, meaning the balance of oxidation and reduction reactions, including NAD-related compounds and ATP, the cell's main energy currency.

Exposure rapidly oxidized those molecules and drained total NAD content over time, while the cells stayed alive. Treated cells partly lost ATP and could not raise lactate production when their breathing chain was blocked. Blocking certain enzymes called PARPs lessened the NAD and ATP losses and preserved that backup energy response. After the stress ended, cells given a NAD precursor restored their levels and function.

Catalog record

Source: https://europepmc.org/article/MED/PMC13260131