Anti-oxidant effects of gold compounds

Yoshioka, Akira; Imamura, Sadao; Niwa, Yukie

doi:10.1111/j.1365-2133.1987.tb05789.x

Cited by 52 publications

(9 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two ROS other than 02-, i.e. hydrogen peroxide (H202) (8)(9)(10)(11) and hydroxyl radical (OH.) (10-14), are considered to be important in causing injury of host tissues as major toxic candidates because of their potent oxidative activity.…”

mentioning

confidence: 99%

Inhibitory effect of local anaesthetics on reactive oxygen species production by human neutrophils

Mikawa

Akamatsu

Nishina

et al. 1997

Acta Anaesthesiol Scand

Self Cite

View full text Add to dashboard Cite

In conclusion, in the present in vitro system, only concentrations of lidocaine and mepivacaine 100-fold higher than clinically feasible ones reduced ROS production by human neutrophils. However, the local anaesthetics at clinically relevant blood concentrations had no suppressive effect. Further studies using in vivo systems are required to elucidate the inhibitory effects of local anaesthetics on ROS generation in clinical settings.

show abstract

mentioning

confidence: 99%

Inhibitory effect of local anaesthetics on reactive oxygen species production by human neutrophils

Mikawa

Akamatsu

Nishina

et al. 1997

Acta Anaesthesiol Scand

Self Cite

View full text Add to dashboard Cite

show abstract

“…This was confirmed in several papers [200,201] with immune complexes and frustrated phagocytosis, and the effect was irreversible by washing. A number of other laboratories have reported similar findings, occasionally also finding the same effect with antimalarials [202,203]. Auranofin was also shown to quench singlet oxygen in a organic solvent system and was proposed as a protector of lipid peroxidation [204].…”

Section: Effects Of Anti-rheumatics Drugs On Oxygen Radical Productiomentioning

confidence: 49%

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

Cuzzocrea

2006

CPD

View full text Add to dashboard Cite

A vast amount of circumstantial evidence implicates oxygen-derived free radicals, especially reactive oxygen species and nitric oxide as mediators of inflammation and/or tissue destruction in inflammatory and arthritic disorders. The aim of the current article is to overview the recent developments in this field, as it relates to the roles of nitric oxide (NO) and reactive oxygen species in the pathogenesis of this condition. The first part of the review focuses on the biochemical impact of NO and reactive oxygen species. The second part of the review deals with the novel findings related to the recently identified regulatory roles of the inducible isoform of nitric oxide synthase (iNOS) in the expression of pro-inflammatory mediators in inflammation. Reactive oxygen species can initiate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3phosphate dehydrogenase, inhibition of membrane sodium/potassium ATP-ase activity, inactivation of membrane sodium channels, and other oxidative modifications of proteins. All these toxicities are likely to play a role in the pathophysiology of inflammation. Reactive oxygen species are all potential reactants capable of initiating DNA single strand breakage, with subsequent activation of the nuclear enzyme poly (ADP ribose) synthetase (PARS), leading to eventual severe energy depletion of the cells, and necrotic-type cell death. Recently it has been demonstrated that iNOS inhibitor prevents the activation of poly (ADP ribose) synthetase, and prevents the organ injury associated with inflammation. Although the severity and duration of inflammation may dictate the timing and extent of NOS expression, it is now evident that the up-regulation of NOS can take place during sustained inflammation. Thus, induced nitric oxide, in addition to being a "final common mediator" of inflammation, is essential for the up-regulation of the inflammatory response. Furthermore, a picture of a pathway is evolving that contributes to tissue damage both directly via the formation of reactive oxygen species, with them associated toxicities, and indirectly through the amplification of the inflammatory response.

show abstract

“…To address this need histopathologieal studies of spleen, bone marrow, thymus, and small intestine were conducted in parallel with immunological studies of animals exposed to LD50/0 irradiation (8. The observed decrease in skin Cu2Zn2SOD following a single ultraviolet irradiation was also reduced by pretreatment with liposomes containing Cu2Zn2SOD [62]. Increased ultraviolet radiation-induced keratinocyte proliferation was also found to be associated with a decrease in total SOD activity which was due mainly to a decrease in Cu2Zn2SOD [63].…”

Section: Chemical Consequences Of Ionizing Radiationmentioning

confidence: 66%

Essential Metalloelement Chelates Facilitate Repair of RadiationInjury

et al. 2001

View full text Add to dashboard Cite

Treatment with essential metalloelement (Cu, Fe, Mn, and Zn) chelates or combinations of them before and/or after radiation injury is a useful approach to overcoming radiation injury. No other agents are known to increase survival when they are used to treat after irradiation, in a radiorecovery treatment paradigm. These chelates may be useful in facilitating de novo syntheses of essential metalloelement-dependent enzymes required to repair radiation injury. Reports of radioprotection, which involves treatment before irradiation, with calcium-.channel blockers, acyl Melatonin homologs, and substituted anilines, which may serve as chelating agents after biochemical modification in vivo, as well as Curcumin, which is a chelating agent, have been included in this review. These inclusions are intended to suggest additional approaches to combination treatments that may be useful in facilitating radiation recovery. These approaches to radioprotection and radiorecovery offer promise in facilitating recovery from radiation-induced injury experienced by patients undergoing radiotherapy for neoplastic disease and by individuals who experience environmental, occupational, or accidental exposure to ultraviolet, x-ray, or ,-ray radiation. Since there are no existing treatments of radiation-injury intended to facilitate tissue repair, studies of essential metalloelement chelates and combinations of them, as well as combinations of them with existing organic radioprotectants, seem worthwhile.

show abstract

Anti-oxidant effects of gold compounds

Cited by 52 publications

References 24 publications

Inhibitory effect of local anaesthetics on reactive oxygen species production by human neutrophils

Inhibitory effect of local anaesthetics on reactive oxygen species production by human neutrophils

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

Essential Metalloelement Chelates Facilitate Repair of RadiationInjury

Contact Info

Product

Resources

About