It is actually responsible for programmed cell death, apoptosis, necrotic cell death and harm to DNA and membrane fatty acids which suggests that lipid signalling would be altered and lipid peroxidation elevated. It would influence gene expression and proteolysis contributing to neurodegeneration [114-118]. Additionally, antioxidant enzymes (dismutase superoxide, catalase and glutathione peroxidase) show therapeutic efficacy in neurodegenerative models [120, 121]. Another vital factor is nitrosative strain. One of many modifications attributable to nitric oxide metabolism imbalance is S-nitrosylation of protein cysteine residues [122]. Overproduction of NO could compromise neural energy and lead to neurodegeneration [122]. It inhibits cellular respiration and superoxide anions will be released, interacting with NO superoxide anions created by the mitochondria producing peroxynitrite which can be a powerful oxidant causing neurotoxicity [123]. Yet another common characteristic shared by depression and inflammation is IDO (indoleamine 2,3-dioxygenase) activation, an enzyme that induces the catabolism of tryptophan into TRYCATs (tryptophan catabolites along the IDO pathway), for instance kynurenine together with the consequent improve in TRYCATs [124-126]. Some TRYCATs, including quinolinic acid and kynurenine, are particularly neurotoxic [127, 128], as quinolinic acid causes acute tumefaction and also the destruction of post-synaptic components, induces nerve cell degeneration, including hippocampal cell death and selective necrosis of granular cells, amongst others. Quinolinic acid causes a dose-dependent decrease in cholinergic circuits and may empty dopamine, choline, GABA and encephalin deposits [129-133]. The areas most impacted by the neurotoxic effects of quinolinic acid would be the striatum, the pallidal formation and the hippocampus [134]. The neurotoxic effects of quinolinic acid could possibly be because of: 1) Agonism at NMDA receptor level [135, 136] two) Pro-oxidant impact by means of the formation of ferrous quinolinate chelates inducing lipid peroxidation three) Exacerbation of the neurotoxic effects of corticosterone and IL-1 (interleukine-1) [135, 137]. According to Ma.<br />

    Humphrey Bang
    By Humphrey Bang
    Pending Moderator Review