Generation of hydrogen peroxide mediates hanging death-induced neuronal cell apoptosis in the dentate gyrus of the rat brain

Role of synaptic and nonsynaptic glutamate receptors in ischaemia induced neurotoxicity

“…Glutamate (Glu) released into the extracellular space stimulates nonsynaptic NR2B-containing NMDA receptors and results in excitotoxicity. Catecholamines (DA) acting extrasynaptically, nonsynaptically in the extraneuronal space due to monoaminooxydase (MAO) activity decomposed to the toxic aldehydes (Burke et al, 2004) and also produce in H2O2 (Khatun et al, 2013). Note that hydrogen peroxide is not a radical because it contains no unpaired electrons.…”

p53 activation and mitochondria-mediated pathway are involved during hanging death-induced neuronal cell apoptosis in dentate gyrus region of the rat brain

“…Although hanging is one of the most common approaches to commit suicide in human worldwide (Emet et al 2010), the underlying mechanism during HD-induced neuronal cell apoptosis remains to be elucidated. We recently reported that HD induces generation of reactive oxygen species (ROS) and neuronal cell apoptosis in the DG region of rat brain (Khatun et al 2013). Based on these studies, we proposed that the HD-induced generation of hydrogen peroxide may trigger neuronal cell apoptosis through the activation of p53 and mitochondria-mediated pathway.…”

“…Models of rats hanged by the neck with a rope have already been developed for the induction of the expression of hypoxia-inducible factor −1 (HIF-1), a marker of hypoxia (Zhang et al 2006). We have recently reported that HD induces generation of reactive oxygen species (ROS) and neuronal cell apoptosis in the dentate gyrus (DG) region of rat brain (Khatun et al 2013) but the underlying mechanism during HD-induced neuronal cell apoptosis remains to be elucidated. Hence, present study was aimed to find out whether activation of p53 and mitochondria-mediated pathway are involved during HD-induced neuronal cell apoptosis.…”

Molecular pathways of mitochondrial dysfunctions: Possible cause of cell death in anesthesia-induced developmental neurotoxicity

“…Defects in ETC occur during critical developmental stages leads to high amounts of ROS production indirectly. These results indicate that early and long duration exposure to anesthetics causes the susceptibility of developing neurons to ROS accumulation inside mitochondria, which then increase in mitochondrial membrane potential (MMP) depolarization, morphological changes and DNA damage by direct contact or through lipid peroxidation, ultimately leading to apoptosis (Zhang et al, 2010;Khatun et al, 2013), which we will discuss in the following paragraphs. Thus, preventing excessive ROS accumulation may be an essential step to protect mitochondria for safe use of GA during early stages of brain development.…”

“…However, another study found that isoflurane can increase the pro-apoptotic factor Bax levels and decrease the anti-apoptotic factor Bcl-2 levels in H4-APP cells and primary neurons from naïve mice; isoflurane can also enhance ROS accumulation, facilitate cytochrome c release from the mitochondria to the cytosol, induce caspase-9 activation and cause apoptosis (Zhang et al, 2012). In addition, another findings demonstrated that the inhalation anesthetic isoflurane can increase ROS levels, induce mPTP opening, reduce MMP and ATP levels, activate caspase-3 to induce cell apoptosis (Khatun et al, 2013;Zhang et al, 2012). Moreover, one study investigated the effect of propofol on rat embryonic neural stem cells and found that propofol inhibited stem cell growth and induced cell apoptosis in a dose-dependent manner, and propofol activated caspase-3, -8 and -9 and cytochrome c (Zou et al, 2013).…”