sodium-hypochlorite and 1-1-diphenyl-2-picrylhydrazyl

A xanthouronic acid sodium salt called xanthouronan was produced from xanthan by regioselective oxidation with NaOCl/NaBr using 2,2,6,6-tetramethylpiperidine-1-oxy radical (TEMPO) as catalyst. The efficiency of the one pot TEMPO-mediated oxidation was confirmed by HPAEC-PAD, (13)C NMR, and FT-IR. The oxidation degree was close to 98% and the mass yield of this new polyglucuronic acid was higher than 90% (w/w). The macromolecular characterization of xanthouronan using SEC-MALLS showed a molecular size reduced by a third due to the oxidation treatment and the degree of polymerization (DP) of the xanthouronan form was about 665. The evaluation of the enzymatic degradation of this C-6 carboxylated xanthan by various polysaccharide hydrolases and one polysaccharide lyase showed its high resistant to biodegradation. The antioxidant activity of xanthouronan was also tested by using the 2,2'-diphenyl-1-picrylhydrazyle (DPPH) and hydroxyl radical procedures. At 1 g/L, xanthouronan presented 75% of the ascorbic acid antioxidant activity.

Topics: Antioxidants; Biphenyl Compounds; Bromides; Catalysis; Cyclic N-Oxides; Oxidation-Reduction; Picrates; Polysaccharides; Polysaccharides, Bacterial; Sodium Compounds; Sodium Hydroxide; Sodium Hypochlorite; Uronic Acids

TEMPO (2,2,6,6-tetramethylpiperidine-1-oxyl radical)-mediated 6-carboxy β-chitin derivatives (T-chitin) with different carboxylate content were successfully synthesized by controlling the addition level of NaClO as the primary oxidant. The structural and biochemical properties of the derivatives were investigated. The carboxylate contents of the derivatives calculated by electrical conductivity titration were 1.33, 1.68, 1.80, and 2.08 mmol/g, respectively. The yield of T-chitin with carboxylate content of 2.08 mmol/g reached 74.55%. T-chitin exhibited stronger bile acid binding capacities than that of β-chitin. The scavenging ability of T-chitin against hydroxyl radicals improved with increasing concentration, and EC(50) values were below 1.2 mg/mL. All T-chitin exhibited a strong ferrous ion chelating effect. At 8 mg/mL, the chelating effects of T-chitin with carboxylate content of 0.81 mmol/g reached 80.15%. These results showed that T-chitin had good bile acid binding capacity and antioxidant activities and it may be a potential antioxidant in vitro.

Topics: Animal Shells; Animals; Bile Acids and Salts; Biphenyl Compounds; Bromides; Carboxylic Acids; Chitin; Cyclic N-Oxides; Decapodiformes; Free Radical Scavengers; Hydroxyl Radical; Iron Chelating Agents; Oxidation-Reduction; Picrates; Sodium Compounds; Sodium Hypochlorite

The effect of various concentrations of essential alpha-amino acids on the luminol-sodium hypochlorite chemiluminescence (CL) has been studied. It was found that all tested compounds have an inhibiting effect. Amino acids with phenolic groups present higher inhibition than basic, acidic or neutral amino acids. The calculated antioxidant activities by the CL method are compared with those of the N,N-diphenyl-picryl hydrazyl (DPPH) method.

Topics: Amino Acids; Amino Acids, Acidic; Amino Acids, Basic; Amino Acids, Neutral; Antioxidants; Biphenyl Compounds; Indicators and Reagents; Luminescent Measurements; Luminol; Oxidation-Reduction; Phenols; Picrates; Sodium Hypochlorite; Structure-Activity Relationship

The effect of beta-blockers (alprenolol, oxprenolol, atenolol, acebutolol) and the non-steroidal anti-inflammatory drug, diclofenac, on modification of low-density lipoproteins (LDL) by sodium hypochlorite (NaOCl) was investigated in vitro. Beta-blockers and diclofenac inhibit the formation of thiobarbituric acid reactive substances in LDL modified by NaOCl. Beta-blockers, but not diclofenac, inhibit the hypochlorite-induced aggregation of LDL which was determined by photon correlation spectroscopy. The intracellular accumulation of cholesterol esters in J774 macrophages is inhibited by addition of beta-blockers, but not diclofenac, to LDL prior to the addition of NaOCl. The modification inhibiting effect of beta-blockers is inversely correlated to the binding capabilities of these substances to LDL which were assessed by laser electrophoresis. Inhibition of LDL modification in vivo by beta-blockers may reduce the risk of atherosclerosis and, therefore, compensate for the cholesterol-raising effect of these drugs in human plasma.

Topics: Acebutolol; Adrenergic beta-Antagonists; Alprenolol; Anti-Inflammatory Agents, Non-Steroidal; Arteriosclerosis; Atenolol; Bepridil; Biphenyl Compounds; Chemical Phenomena; Chemistry; Cholesterol Esters; Diclofenac; Free Radicals; Humans; Lipoproteins, LDL; Macrophages; Molecular Structure; Oxprenolol; Particle Size; Picrates; Sodium Hypochlorite; Spectrum Analysis; Thiobarbituric Acid Reactive Substances