Anti-C3 polyclonal antibody [FITC]

Potentially neurotoxic systems involved in traumatic and degenerative diseases of the brain were assessed in acute psychosis. Astrocyte-derived exosomes (ADEs) and neuron-derived exosomes (NDEs) were immunoprecipitated from plasma of ten untreated first-episode psychotics (FPs) and ten matched normal controls (Cs). Neural mitochondrial electron transport and complement proteins were extracted, quantified by ELISAs and normalized with levels of CD81 exosome marker. Levels of subunits 1 and 6 of NADH-ubiquinone oxidoreductase (complex I) and subunit 10 of cytochrome b-c1 oxidase (complex III), but not of subunit 1 of cytochrome C oxidase (complex IV) or superoxide dismutase 1 (SOD1) were significantly lower in ADEs and NDEs of FPs than Cs. This dysregulated pattern of electron transport proteins is associated with increased generation of reactive oxygen species. ADE glial fibrillary acidic protein levels were significantly higher in FPs than Cs, indicating a higher percentage of inflammatory astrocytes in FPs. ADE levels of C3b opsonin were significantly higher and those of C5b-9 attack complex was marginally higher in FPs than Cs. A significantly lower ADE level of the C3 convertase inhibitor CD55 may explain the higher levels of C3 convertase-generated C3b. ADE levels of the neuroprotective protein leukemia inhibitory factor (LIF) were significantly lower in FPs than Cs, whereas levels of IL-6 were no different. Plasma neural exosome levels of electron transport and complement proteins may be useful in predicting FP and guiding therapy. SOD mimetics, C3 convertase inhibitors and LIF receptor agonists also may have therapeutic benefits in FP.

Gas-phase oxidation of PAHs can result in formation of oxygenated PAHs (OPAHs) and nitro-PAH (NPAHs) as well as a series of secondary pollutants which contribute to formation of SOA. Acenaphthene (ACE) is one of the PAHs with three rings which exists mainly as gaseous form in the atmosphere, where the oxidation is mainly initiated by reaction with OH radical. In this study, the atmospheric oxidation mechanism of ACE initiated by OH radical is investigated using high level quantum chemistry (at the ROCBS-QB3 level) and kinetic calculations, and the overall rate coefficient obtained here is in good agreement with previous experimental values. The reaction starts with OH radical additions to the C3-, C5-site and H atom abstraction from C1/C2 of ACE, and the fates of main adducts formed as ACE-n-OH (ACE3 and ACES in short) and R2 are further considered. ACE3 and ACES would react with O-2 at different sites, of which all the additions are reversible. An overall effective removal rate of similar to 9 s(-1) for ACES with O-2 are calculated here using steady state approximately, which allows their reaction with NO2 to a relative significant extent in the atmosphere. We predicted significant 4-NACE formation from ACES. Reaction of ACE3 with O-2 is fast enough of similar to 10(7) s(-1) that 9-NACE is expected to form in smaller quantities. Additionally, a number of cyclic OPAHs and multifunctional compounds are formed in the oxidation of ACE3, ACES and R2 under the high/low NOx concentration as observed in previous investigations.