Yibing Li

TL;DR: Cytochemical analysis revealed a severe reduction in succinate dehydrogenase and aconitase activities in the heart and, to a lesser extent, in other organs, which indicates that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.

TL;DR: It is suggested that O2−overproduced in a mitochondrial compartment, when uncoupled from antioxidant defenses, induces impairment of mitochondrial function and causes exacerbation of cerebral infarction after ischemia.

TL;DR: In situ imaging of superoxide radical distribution by hydroethidine oxidation in vulnerable neurons suggested that superoxide radicals play a role in the delayed ischemic death of hippocampal CA1 neurons, and SOD1 Tg rats are useful tools for studying the role of oxygen radicals in the pathogenesis of neuronal death after transient global cerebral ischemia.

TL;DR: It has been demonstrated that the 3-fold increase in S OD-1 transgene activity in SOD-1 Tg mice offers protection against cerebral ischemia and reperfusion in two different models of focal cerebral isChemia, as compared to nontransgenic wild-type littermates.

TL;DR: The data suggest that striatal cells die by apoptosis following administration of 3-NP, and this mechanism is similar to that of programmed death in mice treated with the mitochondrial toxin, 3-nitropropionic acid.