PMC:7463108 / 6984-8029 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7463108","sourcedb":"PMC","sourceid":"7463108","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7463108","text":"Up to 90% of post-mortem tissues sampled from opiate abusers display brain edema (Buttner 2011), astrogliosis and microgliosis especially in the hippocampus (Oehmichen et al. 1996), white matter, and subcortical regions at autopsy (Tomlinson et al. 1999; Anthony et al. 2005; Buttner et al. 2006; Buttner and Weis 2006). The reactive gliosis is accompanied by increases in proinflammatory cytokines and inflammatory mediators, including TNF-α, IL-1β, and nitric oxide synthase (NOS) (Dyuizen and Lamash 2009). Opiates especially drive the enhanced activation of heme-oxygenase, NOS, and cyclic GMP-dependent-protein kinase (Liang and Clark 2004) and production of reactive nitrogen species (RNS) such as peroxynitrite (Salvemini 2009), and resultant nitrosative damage (Zou et al. 2011). Nitrosative damage is an important endpoint for opiate exposure (Pasternak et al. 1995; Liang and Clark 2004; Salvemini 2009) and key site of convergence for the oxidative stress accompanying HIV protein exposure (Hauser and Knapp 2014; McLane et al. 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