scholarly journals Involvement of the superoxide anion in sulphoxidation (Short Communication)

1974 ◽  
Vol 137 (1) ◽  
pp. 119-121 ◽  
Author(s):  
K. Prema ◽  
K. P. Gopinathan

Sulphoxidation of compounds capable of undergoing biological sulphoxidation has been demonstrated in a model system (NADH–phenazine methosulphate–O2), known to generate superoxide anions (O2-). Addition of superoxide dismutase to this system results in complete inhibition, suggesting the involvement of O2- in sulphoxidation.

2016 ◽  
Vol 12 (1) ◽  
pp. 274-282
Author(s):  
Tsutomu Ishihara ◽  
Misaki Shibui ◽  
Takaya Hoshi ◽  
Tohru Mizushima

Superoxide dismutase covalently bound to four lecithin molecules (PC-SOD) on plasma membrane has been found to have beneficial therapeutic effects.


2017 ◽  
Vol 19 (34) ◽  
pp. 23176-23186 ◽  
Author(s):  
Mauritz Johan Ryding ◽  
Israel Fernández ◽  
Einar Uggerud

Reactions between water clusters containing the superoxide anion, O2˙−(H2O)n (n = 0–4), and formic acid, HCO2H, were studied experimentally in vacuo and modelled using quantum chemical methods.


1994 ◽  
Vol 80 (3) ◽  
pp. 476-483 ◽  
Author(s):  
Yasukazu Kajita ◽  
Yoshio Suzuki ◽  
Hirofumi Oyama ◽  
Toshihiko Tanazawa ◽  
Masakazu Takayasu ◽  
...  

✓ To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 µmol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.


1980 ◽  
Vol 43 (1) ◽  
pp. 19-20 ◽  
Author(s):  
MALGORZATA KORYCKA-DAHL ◽  
THOMAS RICHARDSON

Photogenerated superoxide anion might be involved in the oxidative deterioration of foods. For this reason, purines, pyrimidines and related compounds were illuminated with fluorescent light in the presence of riboflavin to examine their capacity to photogenerate superoxide anion (measured from suppression of its reduction of nitro blue tetrazolium by superoxide dismutase). Superoxide anion was photogenerated in the presence of guanine, xanthine, 6-thioguanine, thymine, uracil, 6-methyl uracil, orotic acid and 5- as well as 6-amino uracil but not in the presence of 24 other related compounds examined. Replacing the oxygen at the 6-position of guanine with sulfur or attachment of an amino group to the 5- or 6-carbon of uracil greatly increased superoxide anion generation as compared to guanine and uracil, respectively. The attachment of a carboxyl group at the 6-position of uracil augmented superoxide anion photogeneration to a much smaller extent and thymine and 6-methyl uracil did not yield any more superoxide anion than did uracil. In general, only those compounds which had an oxo group at the 6-position of purines or the 4-position of pyrimidines, and either an oxo or an amino group in the 2-position of either ring served as substrates for photogeneration of superoxide anion. Additionally, presence of purines and pyrimidines in an enol and/or amino form and an unsubstituted imidazole ring for purines were required for photogeneration of superoxide anion.


Blood ◽  
1994 ◽  
Vol 83 (12) ◽  
pp. 3705-3716 ◽  
Author(s):  
T Arnould ◽  
C Michiels ◽  
J Remacle

Abstract Several pieces of evidence are reported for the accumulation of activated neutrophils in ischemic and reperfused tissues leading to the transformation of the ischemic tissue into an inflammatory territory and to an enhancement of tissue damages during reoxygenation. However, the molecular mechanisms responsible for these observations and the precise role played by endothelial cells in this process are still poorly understood. In this study, an in vitro model that mimics this situation was used to investigate the effects of hypoxia-incubated human umbilical vein endothelial cells (HUVEC) on polymorphonuclear leukocyte (PMN) functions. A strong PMN activation characterized by an increase in intracellular calcium concentration as well as by superoxide anion release and leukotriene B4 production was observed when these cells were coincubated with hypoxic HUVEC. On the other hand, conditioned medium from hypoxia-incubated HUVEC failed to activate PMN, as determined by the lack of PMN calcium concentration increase, the failure of superoxide anion production enhancement, as well as the absence of effects on the integrin CD18, CD11a, and CD11b expression. These results indicate that the presence of hypoxia- incubated HUVEC is necessary to obtain an activation of the PMN, probably via the adherence process. Once activated by coincubation with hypoxic HUVEC, PMN became cytotoxic, as evidenced by 51Cr released from prelabeled HUVEC. This cytotoxic effect of activated PMN for hypoxic endothelial cells could be prevented by a combination of superoxide dismutase and catalase (94% inhibition), whereas superoxide dismutase alone was inefficient. Antiprotease (alpha 2-macroglobulin) and a specific elastase inhibitor (MAAPV-CMK) were also inefficient. These results correlate very well with the fact that no increase in elastase release could be observed in supernatants from PMN coincubated with hypoxic HUVEC. Furthermore, when adherence process was blocked by oleic acid or by anti-ICAM-1 monoclonal antibodies, protection was, respectively, 90% and 72%. We thus evidenced that free radicals but not elastase released from activated PMN coincubated with hypoxic HUVEC are involved in HUVEC injury. We conclude from these results that PMN activation is initiated by PMN adherence to hypoxic HUVEC. These observations indicate that hypoxic HUVEC may be partly responsible for neutrophil activation observed in ischemic tissues, which is part of the amplification process of tissue damage.


1999 ◽  
Vol 277 (6) ◽  
pp. L1089-L1095
Author(s):  
Tetsuya Koyama ◽  
Masahiro Oike ◽  
Sohtaro Komiyama ◽  
Yushi Ito

We examined the effects of superoxide anion ([Formula: see text]) on the intracellular Ca2+ concentration in cultured human nasal epithelial cells. The cells were exposed to[Formula: see text] by pretreatment with xanthine (X) and xanthine oxidase (XO); control cells were treated with X alone. When Ca2+-containing Krebs solution was reperfused in the thapsigargin-treated, store-depleted cells, reapplication-induced intracellular Ca2+ concentration elevation was significantly smaller in X/XO-treated cells than in the control cells, suggesting that [Formula: see text] impairs Ca2+ release-activated Ca2+ entry (CRAC). Bath application of ATP induced a steep Ca2+ transient in both control and X/XO-treated cells. However, the concentration-response curve of the ATP-induced Ca2+ transient was shifted to a higher concentration in X/XO-treated cells. The impairments of CRAC and ATP-induced Ca2+ transient induced by X/XO were reversed by superoxide dismutase. Furthermore, all these X/XO-induced effects were also observed in cells pretreated with pyrogallol, also an [Formula: see text] donor. These results indicate that [Formula: see text] impairs at least two mechanisms involved in Ca2+ mobilization in human nasal epithelial cells, i.e., CRAC and ATP-induced Ca2+ release.


2004 ◽  
Vol 286 (5) ◽  
pp. C1152-C1158 ◽  
Author(s):  
A. McArdle ◽  
J. van der Meulen ◽  
G. L. Close ◽  
D. Pattwell ◽  
H. Van Remmen ◽  
...  

Contractions of skeletal muscles produce increases in concentrations of superoxide anions and activity of hydroxyl radicals in the extracellular space. The sources of these reactive oxygen species are not clear. We tested the hypothesis that, after a demanding isometric contraction protocol, the major source of superoxide and hydroxyl radical activity in the extracellular space of muscles is mitochondrial generation of superoxide anions and that, with a reduction in MnSOD activity, concentration of superoxide anions in the extracellular space is unchanged but concentration of hydroxyl radicals is decreased. For gastrocnemius muscles from adult (6–8 mo old) wild-type ( Sod2+/+) mice and knockout mice heterozygous for the MnSOD gene ( Sod2+/-), concentrations of superoxide anions and hydroxyl radical activity were measured in the extracellular space by microdialysis. A 15-min protocol of 180 isometric contractions induced a rapid, equivalent increase in reduction of cytochrome c as an index of superoxide anion concentrations in the extracellular space of Sod2+/+ and Sod2+/- mice, whereas hydroxyl radical activity measured by formation of 2,3-dihydroxybenzoate from salicylate increased only in the extracellular space of muscles of Sod2+/+ mice. The lack of a difference in increase in superoxide anion concentration in the extracellular space of Sod2+/+ and Sod2+/- mice after the contraction protocol supported the hypothesis that superoxide anions were not directly derived from mitochondria. In contrast, the data obtained suggest that the increase in hydroxyl radical concentration in the extracellular space of muscles from wild-type mice after the contraction protocol most likely results from degradation of hydrogen peroxide generated by MnSOD activity.


The Analyst ◽  
2018 ◽  
Vol 143 (5) ◽  
pp. 1242-1249 ◽  
Author(s):  
Ji Yang ◽  
Xianglong Liu ◽  
Honglei Wang ◽  
Haoqi Tan ◽  
Xiaoxu Xie ◽  
...  

A new turn-on near-infrared fluorescence probe (BDP) based on dibenzo[a,c]phenazine for superoxide anion detection with AIE properties and a large Stokes shift was developed.


Marine Drugs ◽  
2019 ◽  
Vol 17 (1) ◽  
pp. 23 ◽  
Author(s):  
Xiu-Rong Yang ◽  
Lun Zhang ◽  
Dong-Ge Ding ◽  
Chang-Feng Chi ◽  
Bin Wang ◽  
...  

In this report, protein of hairtail (Trichiurus japonicas) muscle was separately hydrolyzed using five kinds of proteases (alcalase, trypsin, neutrase, pepsin, and papain), and the papain- and alcalase-hydrolysates showed higher 2,2-diphenyl-1-picrylhydrazyl radicals (DPPH•) and hydroxyl radical (HO•) scavenging activity than other three protease hydrolysates. Therefore, the protein hydrolysate of hairtail muscle (HTP) was prepared using binary-enzymes hydrolysis process (papain + alcalase). Subsequently, eight antioxidant peptides were purified from HTP using membrane ultrafiltration and chromatography technology, and their amino acid sequences were identified as Gln-Asn-Asp-Glu-Arg (TJP1), Lys-Ser (TJP2), Lys-Ala (TJP3), Ala-Lys-Gly (TJP4), Thr-Lys-Ala (TJP5), Val-Lys (TJP6), Met-Lys (TJP7), and Ile-Tyr-Gly (TJP8) with molecular weights of 660.3, 233.0, 217.1, 274.1, 318.0, 245.1, 277.0, and 351.0 Da, respectively. TJP3, TJP4, and TJP8 exhibited strong scavenging activities on DPPH• (EC50 0.902, 0.626, and 0.663 mg/mL, respectively), HO• (EC50 1.740, 2.378, and 2.498 mg/mL, respectively), superoxide anion radical (EC50 2.082, 2.538, and 1.355 mg/mL, respectively), and 2,2′-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) radical (EC50 1.652, 0.831, and 0.586 mg/mL, respectively). Moreover, TJP3, TJP4, and TJP8 showed higher reducing power and inhibiting ability on lipid peroxidation in a linoleic acid model system. These results suggested that eight isolated peptides (TJP1 to TJP8), especially TJP3, TJP4, and TJP8 might serve as potential antioxidants applied in the pharmaceutical and health food industries.


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