Oxidative burst inhibition

Au(CN)2] inhibits the oxidative burst of polymorphonuclear leukocytes and the proliferation of lymphocytes in vitro (both types of cells actively participate in the development and maintenance of inflammatory processes of rheumatoid disease) [71]. It is also far more toxic than gold(I) thiolates to bacteria, plants and animals. 

In the production of formic acid, a slimy of calcium formate in 50% aqueous formic acid containing urea is acidified with strong nitric acid to convert the calcium salt to free acid, and interaction of formic acid (reducant) with nitric acid (oxidant) is inhibited by the urea. When only 10% of the required amount of urea had been added (unwittingly, because of a blocked hopper), addition of the nitric acid caused a thermal runaway (redox) reaction to occur which burst the (vented) vessel. A small-scale repeat indicated that a pressure of 150-200 bar may have been attained. A mathematical model was developed which closely matched experimental data. 

That the oxidative burst is directly involved in the chemical defense of these algae is clear. This reaction can be inhibited by diphenyleneiodonium, a suicide inhibitor of NADPH-oxidase which suppresses both the production of reactive oxygen species and the natural resistance to epiphytic bacteria. In addition a role in the defense against endophytes was indicated, since pre-treatment with oligomeric guluronates resulted in decreased infection of L. digitata with the pathogen Laminariocolax tomentosoides [141]. 

A common metabolite found in the urine and plasma of patients treated with gold drugs is [Au(CN)2], an ion which readily enters cells and can inhibit the oxidative burst of white blood cells. It may therefore be an active metabolite of gold drugs. It also exhibits anticancer and anti-HIV activity. The high Au contents of red blood cells of smokers receiving gold therapy has been attributed to the inhalation of HCN in smoke (420). 

Broussochalcone A (32) Antioxidant activity (inhibition of lipid peroxidation) Inhibition of cyclooxygenase Inhibition of nitric oxide production Inhibition of respiratory burst in neutrophils Platelet aggregation inhibitory activity1 [42] [431 [42] [44] [431... 

Human neutrophils Inhibition of oxidative burst Bouma et al. 1997 Gessi et al. 2002... 

In conclusion as for the role of A3 receptors in the inhibition of TNF-a production in macrophages discrepant results have been obtained and not only due to the different species considered. For example some studies attributed reduction of TNF-a to A3 receptors either in human and mouse species (Sajjadi et al. 1996 McWhinney et al. 1996), whilst other found this effect to be mediated essentially by A2A and in minor part by A2B without the involvement of the A3 receptors again in both human and mouse species (Zhang et al. 2005 Kreckler et al. 2006). Therefore it is difficult in this case to verify the relevance of the A3 receptor-induced cellular response when other adenosine subtypes like A2A and A2B are also activated. As for the effects exerted by the A3 subtype in human monocytes and macrophages it is possible to find support for an anti-inflammatory role for this receptor as attested by reduction of tissue factor, oxidative burst and perhaps TNF-a release. Also the recent discovery of an increase in MMP9 supports a role for A3 agonists in the therapy of myocardial infarction (Velot et al. 2008) (Fig. 12.4). 

Pilette C, Ouadrhiri Y, Van Snick J, Renauld JC, et al. 2002. Interleukin-9 inhibits oxidative burst in LPS-stimulated human blood monocytes through TGF-(i. J Immunol. 168 4103—4 111. 

It appears probable that this sensitivity to oxidation is both part of the homeostatic control mechanism for HLE and a possible basis for some disease processes. At physiological concentrations, the ti/2jnact increases from 0.64 ms for apPI to 1.3 s for ai-PI,x, and the latter compound is ineffective in vivo as an inhibitor of HLE [45]. It is now believed that the oxidative burst of an activated neutrophil deactivates any a,-PI in close proximity by conversion to ai-PIo, thus allowing elastase to remain active. Since the effective range of oxidative radicals is very limited, ai-PI outside the immediate vicinity of the neutrophil retains its activity and inhibits systemic HLE. 

Narayanan PK, Carter WO, Ganey PE, et al. 1998. Impairment of human neutrophil oxidative burst by polychlorinated biphenyls inhibition of superoxide dismutase activity. J Leukoc Biol 63(2) 216-224. 

NONCOMPETITIVE INHIBITION OF LANTHANIDE-INDUCED OXIDATIVE BURST BY ZINC IN TOBACCO BY-2 CELLS ... 

Noncompetitive Inhibition of Lanthanide-Induced Oxidative Burst... 

The major difference between the secreted and membrane-bound acid phosphatase is that the latter is approximately 40-fold more resistant to the inhibitory effects of sodium tartrate. Furthermore, non-specific antibodies to the extracellular enzyme do not cross-react with membrane-bound enzyme. The secreted enzyme also does not appear to inhibit neutrophil oxidative burst, unlike its membranous counterpart. The biological role of the secreted enzyme is unknown, but may be involved in modification of host activities. 

In sub-acute toxicity study of over 90 days, picroliv was found to be safe in rats and monkeys [6, 15-18]. Of the minor components, apocynin has been shown to inhibit neurophil oxidative burst in addition to being a powerful anti-inflammatory agent, and the curcubitacins to be highly cytotoxic. 

PAF-induced oxidative burst in human PMNL. In guinea pigs, yangambin inhibited PAF-induced thrombocytopenia but did not affect leukocytopenia. 

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