The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as stroke from cerebral ischemia. It was well-documented that mitochondria-dependent apoptotic pathway involves pro- and anti-apoptotic protein binding, release of cytochrome c, leading ultimately to neuronal death. On the other hand, mitochondria also play a role to counteract the detrimental effects elicited by excessive oxidative stress. Recent studies have revealed that oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves peroxisome proliferative activated receptor-γ (PPARγ) co-activator 1α (PGC1-α). PGC1-α is a master regulator of ROS scavenging enzymes including manganese superoxide dismutase 2 and the uncoupling protein 2, both are mitochondrial proteins, and may contribute to neuronal survival. PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after stroke. This review aims to summarize the current knowledge focusing on the molecular mechanisms underlying cerebral ischemia involving ROS, mitochondrial dysfunction, apoptosis, mitochondrial proteins capable of ROS scavenging, and mitochondrial biogenesis.

The interfacial charge carrier dynamics for core-shell Au-CdS nanocrystals with various shell thicknesses were investigated and presented. Due to the difference in band structures between Au and CdS, a pronounced photoinduced charge separation took place at the interface of Au and CdS, resulting in the electron-charged Au core and the hole-enriched CdS shell. The electron-charging of Au core in Au-CdS nanocrystals was revealed with the corresponding XPS analysis and photocurrent measurement. Time-resolved PL spectra were measured to quantitatively analyze the electron transfer event between CdS shell and Au core for Au-CdS nanocrystals. An increase in the electron-transfer rate constant was observed for Au-CdS nanocrystals with increasing shell thickness, probably due to the less pronounced electron-hole interaction of thicker CdS, which enabled a fuller extent of participation of photoexcited electrons in the charge separation process. On the other hand, the hole-enriched CdS shell of Au-CdS nanocrystals upon light illumination was characterized with a photocatalytic process. The photocatalytic activity of Au-CdS nanocrystals was found to increase with increasing shell thickness, attributable to the greater capability of light absorption achieved by the extensive growth of the CdS shell. The correlation of photocatalytic activity with the shell thickness of Au-CdS nanocrystals corresponded well with that of the electron-transfer rate constant. As compared to the relevant commercial products like N-doped P-25 TiO 2 and CdS powders, the as-synthesized Au-CdS nanocrystals exhibited superior photocatalytic performance under visible light illumination, demonstrating their potential as an effective visible-light-driven photocatalyst. Furthermore, the result of performance evaluation under natural sunlight shows that the present Au-CdS nanocrystals can be used as highly efficient photocatalysts which may practically harvest energy from sunlight.

Summary Purpose:  One cellular consequence of status epilepticus is apoptosis in the hippocampal CA3 subfield. We evaluated the hypothesis that the repertoire of cellular events that underlie such elicited cell death entails mitochondrial dysfunction induced by an excessive production of nitric oxide synthase II (NOS II)‐derived NO, increased superoxide anion (O2−) production, and peroxynitrite formation. Methods:  In Sprague‐Dawley rats, kainic acid was microinjected unilaterally into the hippocampal CA3 subfield to induce bilateral seizure‐like electroencephalography (EEG) activity. The effects of pretreatments with various test agents on the induced O2− production, peroxynitrite formation, mitochondrial respiratory chain enzyme activities, cytochrome c/caspase‐3 signaling, and DNA fragmentation in bilateral CA3 subfields were examined. Results:  Significantly and temporally correlated increase in O2− and peroxynitrite levels (3 to 24 h), depressed mitochondrial Complex I activity (3 h), enhanced translocation of cytochrome c to cytosol (day 1), and augmented activated caspase‐3 (day 7) and DNA fragmentation (day 7) were detected bilaterally in hippocampal CA3 subfields after the elicitation of sustained seizure. Pretreatment with microinjection into the bilateral hippocampal CA3 subfield of a water‐soluble formulation of coenzyme Q10; a selective NOS II inhibitor, S‐methylisothiourea; a superoxide dismutase mimetic, 4‐hydroxy‐2,2,6,6‐tetramethylpiperidine‐1‐oxyl; an active peroxynitrite decomposition catalyst, 5,10, 15,20‐tetrakis‐(N‐methyl‐4‐pyridyl)‐ porphyrinato iron (III); or a peroxynitrite scavenger, L‐cysteine significantly blunted these cellular events. Discussion:  Prolonged seizures prompted NO‐, O2−‐, and peroxynitrite‐dependent reduction in mitochondrial respiratory enzyme Complex I activity, leading to cytochrome c/caspase‐3‐dependent apoptotic cell death in the hippocampal CA3 subfield after induction of experimental temporal lobe status epilepticus.