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Involvement of NAD(P)H oxidase in acrolein‐induced oxidative stress (1106.14)
Author(s) -
Yousefipour Zivar,
Newaz Mohammad
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1106.14
Subject(s) - acrolein , nad(p)h oxidase , nad+ kinase , oxidative stress , chemistry , xanthine oxidase , oxidase test , toxicity , biochemistry , enzyme , organic chemistry , catalysis
Acrolein toxicity has been linked to oxidative stress & inflammation. NAD(P)H oxidase plays an important role in oxidative stress. gp91phox, an essential component of NAD(P)H oxidase, maintains the functionality of the enzyme. The precise contribution of NAD(P)H in acrolein‐induced toxicity is not fully explored. We investigated the involvement of NAD(P)H oxidase in acrolein toxicity using gp91phox knock‐out (KO) mice. Male gp91 KO mice (20‐25 g) or wild type (WT) control were treated with acrolein (0.5 μg/kg; 1 week). Animals were sacrificed and liver was used for biochemical analysis. KO mice generated low (1.43±.02 pg/μg protein) free radical as evident by 8‐Isoprostane compare to the WT mice (2.19±0.1). Acrolein increased 8‐Isoprostane in WT (P<0.05) but not in KO mice. Xanthine Oxidase (XO) activity was higher (p<0.05) in KO (0.56±0.06 μunit/μg protein). Acrolein reduced XO in KO mice while significantly increased it in WT. Cycloxygenase (COX) activity was not different between WT and KO mice although acrolein increased COX in WT. KO mice exhibited a significantly low (2.1±0.2 μmol/mg protein) total antioxidant status (TAS) compared to the WT (3.5±0.3). Acrolein reduced TAS in both WT and KO mice in an equal manner. These data suggests that NAD(P)H oxidase contributes significantly in acrolein‐induced oxidative stress. We suggests that in absence of NAD(P)H oxidase XO and COX play a definitive role in this process. We also suggest that besides generating free radical, acrolein reduces antioxidant ability thus compounding the effects of oxidative stress. Grant Funding Source : Supported by NIH‐SC3