Recently, Redox Biology, a well-known magazine in the field of oxidative stress, published Succinate accumulation induces mitochondrial reactive oxygen species generation and promotes status epilepticus in the kainic acid rat model. This is the latest work by Associate Professor Sun Hongliu from School of Pharmacy.
Sun Hongliu’s research group found that kainic acid induced status epilepticus, and the levels of succinate and mitochondrial ROS in the brain of SD rats increased simultaneously; inhibited succinate dehydrogenase (SDH) or inhibited malate/aspartate shuttle (MAS) and Purine Nucleotide Cycle (PNC) can alleviate the accumulation of succinate to varying degrees, the level of mitochondrial ROS is reduced, and thereby the neuronal damage and the severity of seizures is reduced.
This study suggested that the accumulation of succinate may be an important factor in the enhancement of mitochondrial ROS and neuronal damage in status epilepticus. And the study further revealed that the accumulation of succinic acid may originate from the MAS and PNC pathways, and finally form through the reverse catalysis of SDH. Inhibiting the accumulation of succinic acid may be a potential means to reduce neuronal damage and to suppress epileptic seizures.
Redox Biology is an influential journal in the biology category, with an impact factor of 7.793 in Biology I in 2018. This paper is another high-level paper with complete intellectual property rights of the university. Associate Professor Sun Hongliu from School of Pharmacy is the sole corresponding author, graduate students Zhang Yurong and Zhang Mengdi from School of Pharmacy are the first author and co-first author, and Binzhou Medical University is the only correspondent unit.
Source of Paper
https://www.sciencedirect.com/science/article/pii/S2213231719311425DOI: 10.1016/J.redox.2019.101365
BY: Li Shucui
SOURCE: Science and Technology Department
