The cytotoxic mechanism of malondialdehyde and protective effect of carnosine via protein cross-linking/mitochondrial dysfunction/reactive oxygen species/MAPK pathway in neurons
Laboratory studyOther animals
- Design
- Laboratory study
- What was measured
- Viability, apoptosis and necrosis, intracellular ROS, mitochondrial membrane potential, protein cross-linking and JNK and ERK activation in cultured cortical neurons exposed to malondialdehyde, with carnosine or N-acetylcysteine.
What the authors reported
Malondialdehyde reduced neuronal viability in a time- and dose-dependent way, causing apoptosis and necrosis, ROS accumulation, loss of mitochondrial membrane potential and JNK and ERK activation. Carnosine protected better than N-acetylcysteine, relieving protein cross-linking, membrane potential loss, ROS burst and kinase activation, whereas N-acetylcysteine inhibited only the kinase activation.
Limits of this study
Primary neuron culture; concentrations not stated in abstract. Abstract only.
Source
PubMed 20868662 · doi:10.1016/j.ejphar.2010.09.033
Entry checked against PubMed abstract (E-utilities) on 2026-10-19. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.