Disease relevance of 8-Isoprostane

• 8-Isoprostane as a biomarker of oxidative stress in interstitial lung diseases [1].
• We have reported that 8-isoprostane stimulated the production of endothelin (ET)-1, a potent vasoconstrictor and critical mediator of chronic pulmonary hypertension, by infant rat pulmonary artery smooth muscle cells (PASMCs), through stimulation of the thromboxane A(2) receptor [2].
• Release of proinflammatory cytokines and 8-isoprostane from placenta, adipose tissue, and skeletal muscle from normal pregnant women and women with gestational diabetes mellitus [3].
• RESULTS: Concentrations of 8-isoprostane in the breath condensate of patients with stable cystic fibrosis were increased about threefold compared with normal subjects (42.7 (4.5) pg/ml vs 15.2 (1.7) pg/ml; p<0.005, 95% CI 14.6 to 40.9) [4].
• Treatment of DOCA-salt rats with either MnTBAP or NS-398 alleviated hypertension, normalized aortic pD2 values for norepinephrine and restored serum 8-isoprostane concentrations towards those observed in Sham group rats [5].

Psychiatry related information on 8-Isoprostane

• We measured plasma 8-isoprostane levels in 157 healthy Japanese volunteers divided into three groups (64 non-habitual drinkers, 56 moderate drinkers and 37 habitual drinkers) according to their alcohol consumption per week [6].

High impact information on 8-Isoprostane

• To confirm this, we looked for other evidence of in vivo granulocyte activation and found it in drastically elevated plasma levels of 8-isoprostane, a product of lipid peroxidation and a marker of oxidative stress [7].
• Colonic mucosae and tumors were analyzed for COX, 15-PGDH, and 8-isoprostane levels [8].
• RECENT FINDINGS: Recent studies indicate that scavenger receptor A activity can be regulated by phosphorylation, glucosidases, 8-isoprostane, high glucose and nobiletin [9].
• In the HAGE-HF group, plasma 8-isoprostane was higher (P < 0.01) and adiponectin lower (P < 0.001) than control mice, while in the LAGE-HF group, these were more modestly affected (P < 0.05) [10].
• Methylglyoxal and 3DG levels reflected dicarbonyl stress, while reduced glutathione (GSH) and urine 8-isoprostane (8-IP) measured oxidative stress [11].

Chemical compound and disease context of 8-Isoprostane

• Antioxidant status was evaluated measuring ferric reducing ability of plasma and vitamin E. There was no difference between preeclampsia and control groups regarding median plasma concentration of 8-isoprostane in umbilical vein (955 versus 780 pg/mL, p = 0.41) or in umbilical artery (233 versus 276 pg/mL, p = 0.65) [12].
• OBJECTIVE: To determine serum levels and clinical correlation of 8-isoprostane, which is produced in vivo through free radical-catalysed peroxidation of arachidonic acid and reflects oxidative stress, in patients with systemic sclerosis (SSc) [13].
• CONCLUSIONS: Our data show that cardioplegia-induced myocardial ischemia and reperfusion is associated with nitrotyrosine and 8-isoprostane formation mainly in the coronary endothelium, indicating injury mediated by both peroxynitrite and oxygen-derived free radicals [14].
• To explore the mechanisms by which this combined inhibiting effect against colon carcinogenesis comes about, we have investigated protein kinase C (PKC), tyrosine protein kinase (TPK), diacylglycerol kinase (DGK) activities and 8-isoprostane levels in colonic mucosa and tumor tissues in an azoxymethane (AOM)-induced rat colon cancer model [15].
• METHODS: We started 40mg/day valsartan treatment in 15 type 2 diabetic subjects with hypertension, and metabolic parameters, lipid peroxide, paraoxonase activity, platelet-activating factor acethylhydrolase activity, AGEs and urine 8-isoprostane were measured at baseline and after 3 and 6 months of treatment [16].

Biological context of 8-Isoprostane

• Reperfusion increased lipid peroxidation (tissue 8-isoprostane concentration) in the bowel, liver, and lung, and caused histologically apparent bowel injury; however, none of these effects was altered by TH [17].
• 8-Isoprostane concentrations were negatively correlated with forced expiratory volume in one second in patients with cystic fibrosis (r = -0.61; p<0.005) [4].
• Although the increase in 8-isoprostane levels preceded cell death, exogenously added 8-isoprostane had no cytotoxic effects [18].
• Similarly, edaravone dose-dependently inhibited H(2)O(2)-induce apoptosis of cultured endothelial cells in parallel with the inhibition of 8-isoprostane formation, 4-hydroxy-2-nonenal (4-HNE) accumulation and VCAM-1 expression [19].
• Exposure to 10% CO(2) attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling [20].

Anatomical context of 8-Isoprostane

• Induced sputum 8-isoprostane concentrations in inflammatory airway diseases [21].
• 8-Isoprostane-induced endothelin-1 production by infant rat pulmonary artery smooth muscle cells is mediated by Rho-kinase [2].
• The data presented in this study demonstrate that there is a differential release of 8-isoprostane from fetal (placenta) and maternal (adipose tissue and skeletal muscle) tissues obtained from normal pregnant women and women with GDM [3].
• Finally, newborn but not adult pulmonary arteries exposed to ONOO- showed a 10-fold increase in 8-isoprostane production, a possible mediator of ONOO- -induced contraction [22].
• These findings further support a link between oxidative stress/lipid peroxidation and inflammation in human macrophages and suggest a role for 8-isoprostane in this process [23].

Associations of 8-Isoprostane with other chemical compounds

• High-salt intake for 4 weeks markedly elevated systolic arterial pressure, urinary excretion of protein, 8-isoprostane, and H(2)O(2), and the enzyme activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase along with the elevated expression of its subunits gp91phox and p47phox at the levels of mRNA and protein [24].
• Urinary excretion of 8-isoprostane F2alpha (8-iso-PGF2alpha) was used as an index of whole-body lipid peroxidation [25].
• In conclusion, cPLA2, PGE2, and ROS formation was activated by all particle types, whereas LTB4 production and 8-isoprostane were strongly dependent on particles' oxidative potential [26].
• RESULTS: Compared with control subjects, exhaled LTE 4 ( P <.001), LTB 4 ( P <.001), and 8-isoprostane ( P <.001) levels were increased in both steroid-naive and steroid-treated atopic asthmatic children but not in atopic nonasthmatic children (LTE 4 , P=.14; LTB 4 , P=.23; and 8-isoprostane, P=.52) [27].
• RESULTS: 8-Isoprostane, nitrogen oxides, and pH were significantly higher in EBC than in BAL (3.845 vs. 0.027 ng/ml, 28.4 vs. 3.8 muM, and 7.35 vs. 6.4, respectively; p < 0.001) [28].

Gene context of 8-Isoprostane

• CONCLUSIONS: We show that 8-isoprostane increases IL-8 expression in human macrophages involving both ERK 1/2 and p38 MAPK, but not NF-kappaB signaling pathway [23].
• By contrast, breathing air through the same face mask for 1 hour had no significant effects on 8-isoprostane or IL-6 concentrations in normal subjects or those with COPD [29].
• Our data with 8-isoprostane also indicates that COX-2 plays a major role in ROS production in LPS-activated microglia [30].
• In this process, 8-isoprostane induced the activation of two major MAP-kinases; ERK 1/2 and p38 MAPK [23].
• With the exception of LPL, levels of other cytokines and 8-isoprostane were not increased in the supernatants of macrophages of FH patients [31].

Analytical, diagnostic and therapeutic context of 8-Isoprostane

• Exhaled 8-isoprostane was measured by an enzyme immunoassay [32].
• The incubation medium was collected and assayed for type II phospholipase A(2) tissue content, IL-6, IL-8, TNFalpha, and 8-isoprostane release by ELISA [33].
• 8-Isoprostane is a biomarker of oxidative stress, and its concentration is increased in the bronchoalveolar lavage fluid of patients with interstitial lung diseases [34].
• There was no correlation between 8-isoprostane and lung function tests in any group of patients [34].
• Plasma EC-SOD activity was measured using in-gel activity staining and spectrophotometric assays, EC-SOD protein level was measured using Western blotting, nitrotyrosine was measured using slot blotting, 8-isoprostane was measured with an enzyme immunoassay, and plasma copper and zinc concentrations were measured using an atomic absorption assay [35].

References