Dimethyl Malonate is a Succinate Dehydrogenase inhibitor.

Inhibiting Succinate Dehydrogenase by Dimethyl Malonate Alleviates Brain Damage in a Rat Model of Cardiac Arrest.Dimethyl malonateinhibited the activation of caspase-3 and enhanced the expression of HIF-1α. Moreover, Dimethyl malonate inhibited excessive hyperpolarization of MMP after CPR, and prevented the release of cytochrome C. Therefore, inhibiting SDH by Dimethyl malonate alleviated brain damage after CA, and the main mechanisms included inhibiting the excessive hyperpolarization of MMP, reducing the generation of mtROS and stabilizing the structure of HIF-1α.

Rats were subjected to a 6?min of CA, and cardiopulmonary resuscitation (CPR) was performed with administration of normal saline or dimethyl malonate (DMM, a competitive inhibitor of SDH). After the return of spontaneous circulation, neurological function of the rats was assessed by a tape removal test for 3?days. The rats were then sacrificed, and their brains were used to assess neuronal apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Hippocampal tissues were used for Western blotting analysis and biochemical detection. In addition, hippocampal mitochondria during CA and CPR were isolated. The relative mitochondrial membrane potential (MMP) and cytochrome C in the cytosol were detected.