Disease relevance of Amph cpd

• Single-stranded M13mp19 plasmids were incubated with a range of concentrations of the azo initiator 2,2'-azobis(2-amidinopropane) hydrochloride, and then transfected into competent, SOS-induced Escherichia coli JM105 cells [1].
• Oxidative hemolysis and lipid/protein peroxidation of erythrocytes induced by the aqueous peroxyl radical [2,2'-Azobis(2-amidinopropane) dihydrochloride, AAPH] were suppressed by A. camphorata mycelia in a time-and concentration-dependent manner [2].
• Contact dermatitis due to 2,2'-azobis(2-amidinopropane) dihydrochloride: an outbreak in production workers [3].
• The induced hyperthyroidism caused a significant increase in the serum concentration of the lipid peroxidation end-product malondialdehyde and lowered erythrocyte resistance to oxidative stress when subjected to the free radical generator 2,2'-azobis(2-amidinopropane) hydrochloride in vitro [4].

High impact information on Amph cpd

• Exposure of liver proteins to a metal-catalyzed oxidation system (ascorbate/Fe(II)/H2O2) or a peroxyl radical generating system, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) led to increases of 2% or 30% in surface hydrophobicity, respectively [5].
• A chemical model based on the thermal decomposition of AAPH (2,2'-azobis(2-amidinopropane) dihydrochloride is used for the production of peroxyl radicals [6].
• The radical initiators, water-soluble 2,2'-azobis(2-amidinopropane) (AAPH) and lipid-soluble 2,2'-azobis(2,4-dimethylvaleronitrile (AMVN), when thermally decomposed at 37 degrees C under air, produced a constant rate of lipid peroxidation in microsomes and lag times inversely related to their concentrations [7].
• The peroxidation was initiated thermally by a water-soluble azo initiator 2,2'-azobis(2-methylpropionamidine) dihydrochloride (AAPH), and the reaction kinetics were studied by monitoring the formation of linoleic acid hydroperoxides [8].
• Rat liver mitochondria were exposed to increasing concentrations of the water-soluble radical initiator 2,2'-azobis(2-amidinopropane) dihydrochoride (ABAP), and damage was assessed by monitoring mitochondrial respiration, alpha-TH oxidation, and lipid peroxidation [9].

Chemical compound and disease context of Amph cpd

• It was determined that the oxidative hemolysis and lipid/protein peroxidation of erythrocytes induced by the aqueous peroxyl radical [2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)] were suppressed by both EtOH (50-150 microg/ml) and EA/EtOH (25-75 microg/ml) extracts of B. pilosa in concentration- and time-dependent manners [10].

Biological context of Amph cpd

• It inhibited the Cu2+-mediated oxidation of LDL (IC50: 5.3 microM) and 2,2'-azobis(2-methylpropionamidine) dihydrochloride (AAPH)-mediated oxidation of LDL (IC50: 2.8 microM) in the thiobarbituric acid-reactive substances (TBARS) assay as well as the macrophage-mediated LDL oxidation (73% inhibition at 5 microM) [11].
• Cell growth, anthocyanin content, phenylalanine ammonia-lyase (PAL) activity and furanocoumarin production were determined after treatment with H(2)O(2), 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), X-ray and yeast extract, independently [12].
• A water extract of Artemisia capillaris Thunberg (Compositae) was investigated for protective effects against oxidative stress induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) in Sprague-Dawley male rats [13].

Anatomical context of Amph cpd

• In erythrocytes that were 80% depleted of intracellular ascorbate by treatment with the nitroxide Tempol, both 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and ferricyanide oxidized alpha-tocopherol to a greater extent than in cells not depleted of ascorbate [14].
• Upon exposure to 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH), which induces lipid peroxidation in membrane, a significant decrease in both cytosolic and mitochondrial ICDH activities were observed in U937 cells [15].
• The antioxidant activities of compounds endogenous to bovine rod outer segments (ROS) were investigated by measuring the loss of polyunsaturated fatty acids (PUFA's) from membranes exposed to the water-soluble oxidant 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) [16].
• The development of embryos to blastocysts was suppressed (P < .05) when oxygen radicals were generated in culture medium by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) under both 5% and 20% O2 [17].

Associations of Amph cpd with other chemical compounds

• (E)-Retinoic acid (RA) was shown to stimulate the rate of 2,2'-azobis(2-amidinopropane) (AAPH)-initiated autoxidation of linoleic acid (18:2) in sodium dodecyl sulfate (SDS) micelles [18].
• We examined the role of in vivo and in vitro supplementation with beta-carotene on metal ion-dependent (cupric ions, Cu2+) and metal ion-independent (2,2'-azobis[2-amidinopropane]dihydrochloride, AAPH) oxidation of LDL as measured by the formation of conjugated dienes (absorbance at 234 nm) [19].
• NAC inhibited in vitro LDL oxidation induced by copper sulfate, 2,2'-azobis(2-amidinopropane) dihydrochloride, and UV light, and protected LDL against depletion of antioxidant vitamins [20].
• The antioxidant effects of L-arginine, N-alpha-acetyl-arginine and vitamin E in combination with L-arginine were measured after initiation of free radical generation with either copper or 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH) [21].
• Twelve major anthocyanins identified in bilberry extracts were studied in vitro using capillary zone electrophoresis (CZE) for their reactions towards 2,2'-azobis(2-amidinopropane) (AAPH) radicals, hydrogen peroxides (H(2)O(2)) and tert-buthylhydroperoxides (t-BuOOH) [22].

Gene context of Amph cpd

• The study of the interaction of alkylperoxyl radicals generated by the aerobic thermolysis of 2,2'-azobis(2-amidinopropane) (AAP) with yeast alcohol dehydrogenase (YADH) revealed a high reactivity of the enzyme, with an average of about 20 radicals per added YADH tetramer being needed to elicit its total inactivation [23].
• The 2,2'-azobis(2-amidinopropane) (AAPH)-induced inactivation and oxidative modification of lysozyme, as determined by the loss of tryptophan-associated fluorescence (TAF) and the increase in dinitrophenylhydrazine-reactive carbonyl groups (CO), were studied in the absence and in the presence of antioxidants [24].
• Oxidative modification of glutamine synthetase by 2,2'-azobis(2- amidinopropane) dihydrochloride [25].
• Prooxidants included ADP-chelated iron with reductants (NADPH and ascorbate), or compounds that generate peroxyl radicals (tert-butyl hydroperoxide and 2,2'-azobis(2-amidinopropane)), or free metal ions (Fe2+ and Cu2+) [26].
• The methods of ultrasound velocity and density measurements were used to study the adiabatic compressibility of bovine serum albumin (BSA) during its oxidation by the prooxidants Cu2+ and 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH) [27].

Analytical, diagnostic and therapeutic context of Amph cpd

• However, when 2,2'-azobis(2-amidinopropane) dihydrochloride (ABAP) was used to initiate oxidation, there was no difference in conjugated-diene generation between CAPD and the control [28].
• The formation of oxidized cholesterol in 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH)-mediated oxidation of rat plasma was also inhibited when the rats were given diets containing 0.5% ECG or EGCG [29].

References