Differential role of hydrogen peroxide and organic hydroperoxides in augmenting ferric nitrilotriacetate (Fe-NTA)-mediated DNA damage: Implications for carcinogenesis

Iqbal, Mohammad; Sharma, Som D.; Mizote, Akiko; Fujisawa, Masayoshi; Okada, Shigeru

doi:10.1002/tcm.10045

Cited by 9 publications

(4 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Much of the cytotoxicity of H 2 O 2 is the result of oxidative DNA damage induced by hydroxyl radicals generated through Fenton chemistry 27,28 . Hydroxyl radicals can trigger direct strand breakage through the oxidation of the ribose moieties of the DNA backbone 27,29,30 . In addition, the nucleobases can be oxidized, with guanine being one of the major targets of oxidation 31 .…”

Section: Relevant Chemistry Of Hydrogen Peroxide and Reactive Oxygen mentioning

confidence: 99%

Live and let die: Hydrogen peroxide production by the commensal flora and its role in maintaining a symbiotic microbiome

Redanz

Xing

Giacaman

et al. 2018

Molecular Oral Microbiology

View full text Add to dashboard Cite

The majority of commensal oral streptococci are able to generate hydrogen peroxide (H O ) during aerobic growth, which can diffuse through the cell membrane and inhibit competing species in close proximity. Competing H O production is mainly dependent upon the pyruvate oxidase SpxB, and to a lesser extent the lactate oxidase LctO, both of which are important for energy generation in aerobic environments. Several studies point to a broad impact of H O production in the oral environment, including a potential role in biofilm homeostasis, signaling, and interspecies interactions. Here, we summarize the current research regarding oral streptococcal H O generation, resistance mechanisms, and the ecological impact of H O production. We also discuss the potential therapeutic utility of H O for the prevention/treatment of dysbiotic diseases as well as its potential role as a biomarker of oral health.

show abstract

Section: Relevant Chemistry Of Hydrogen Peroxide and Reactive Oxygen mentioning

confidence: 99%

Live and let die: Hydrogen peroxide production by the commensal flora and its role in maintaining a symbiotic microbiome

Redanz

Xing

Giacaman

et al. 2018

Molecular Oral Microbiology

View full text Add to dashboard Cite

show abstract

“…Ferric nitrilotriacetate (Fe III -NTA) is a wellknown renal carcinogen, and Fe III -NTA-injected animals have been used as a model of free-radical carcinogenesis (Iqbal et al 2003;Mizote et al 2002). Free radical injuries by repeated injections of Fe III -NTA were clearly demonstrated, and resulted in renal carcinoma (Okada 1996(Okada , 2003.…”

Section: Introductionmentioning

confidence: 99%

Oxidative renal tubular injuries induced by aminocarboxylate-type iron (III) coordination compounds as candidate renal carcinogens

et al. 2006

Self Cite

View full text Add to dashboard Cite

Oxidative renal tubular injuries and carcinogenesis induced by Fe(III)-nitrilotriacetate (NTA) and Fe(III)-ethylenediamine-N,N'-diacetate (EDDA) have been reported in rodent kidneys, but the identity of iron coordination structure essential for renal carcinogenesis, remains to be clarified. We compared renal tubular injuries caused by various low molecular weight aminocarboxylate type chelators with injuries due to NTA and EDDA. We found that Fe(III)-iminodiacetate (IDA), a novel iron-chelator, induced acute tubular injuries and lipid peroxidation to the same extent. We also prepared Fe(III)-IDA solutions at different pHs, and studied resultant oxidative injuries and physicochemical properties. The use of Fe(III)-IDA at pH 5.2, 6.2, and 7.2 resulted in renal tubular necrosis and apoptotic cell death, but neither tubular necrosis nor apoptosis was observed at pH 8.2. Spectrophotometric data suggested that Fe(III)-IDA had the same dimer structure from pH 6.2 to 7.2 as Fe(III)-NTA; but at a higher pH, iron polymerized and formed clusters. Fe(III)-IDA was crystallized, and this was confirmed by X-ray analysis and magnetic susceptibility measurements. These data indicated that Fe(III)-IDA possessed a linear mu-oxo bridged dinuclear iron (III) around neutral pH.

show abstract

“…As predicted, the tumorpromoting organic peroxides (33,39), benzoylperoxide and dicumyl peroxide, inhibited GJIC and activated extracellular kinase (ERK)-MAPK, and the nonpromoting peroxide (33,39), t-butylperoxide, had no effect on these two endpoints (102), yet t-butylperoxide caused considerably more oxidative DNA damage than BzOOH (45). Resveratrol, an antioxidant found in the products of grapes, such as red wine, and peanuts, prevented the inhibition of GJIC by dicumyl peroxide, which closed gap junction channel through a phosphatidylcholine-specific phospholipase C (PC-PLC) but not benzoylperoxide, which closed channels in a PC-PLC-independent way (102).…”

Section: Signaling Pathway-specificity Of Antioxidants: Implications mentioning

confidence: 67%

Oxidative-Dependent Integration of Signal Transduction with Intercellular Gap Junctional Communication in the Control of Gene Expression

Upham

Trosko

2009

Antioxidants & Redox Signaling

View full text Add to dashboard Cite

Research on oxidative stress focused primarily on determining how reactive oxygen species (ROS) damage cells by indiscriminate reactions with their macromolecular machinery, particularly lipids, proteins, and DNA. However, many chronic diseases are not always a consequence of tissue necrosis, DNA, or protein damage, but rather to altered gene expression. Gene expression is highly regulated by the coordination of cell signaling systems that maintain tissue homeostasis. Therefore, much research has shifted to the understanding of how ROS reversibly control gene expression through cell signaling mechanisms. However, most research has focused on redox regulation of signal transduction within a cell, but we introduce a more comprehensive-systems biology approach to understanding oxidative signaling that includes gap junctional intercellular communication, which plays a role in coordinating gene expression between cells of a tissue needed to maintain tissue homeostasis. We propose a hypothesis that gap junctions are critical in modulating the levels of second messengers, such as low molecular weight reactive oxygen, needed in the transduction of an external signal to the nucleus in the expression of genes. Thus, any comprehensive-systems biology approach to understanding oxidative signaling must also include gap junctions, in which aberrant gap junctions have been clearly implicated in many human diseases. Antioxid. Redox Signal. 11, 297-307. 297Oxidative Damage vs. Oxidative Signaling O XIDATIVE STRESS HAS LONG BEEN AFFILIATED with acute and chronic human diseases, and was believed to be primarily a consequence of indiscriminate, cumulative damage to proteins, lipids, and DNA from the vigorous production of reactive oxygen species (ROS) that overwhelm the cell's antioxidant defense system. However, pathological causes of many chronic diseases, particularly cancer, have also been linked with noncytotoxic nongenotoxic events, and the role of ROS and antioxidants in human diseases must also address epigenetic events (10,15,29,76,99).Oxygen was first implicated in cancer as far back as the 1920s by Otto Warburg (111). Initially his theory of altered oxidative metabolism fell mostly on deaf ears. However, recently there has been a renewed interest in how cancer cells shift their energy production from oxidative phosphorylation to anaerobic glycolysis, the "Warburg Effect," that is now considered a fundamental property of cancer cells and not just a consequence of malignant cell transformation (3,54,116). In contrast to this role of low oxygen tensions in cancer, the discovery of superoxide dismutase in 1968 by McCord and Fridovich (70) led to an explosion of research on the role of reactive oxygen, a product of high oxygen tensions, in the pathologies of biological organisms, and has been specifically connected with not only cancer but also many other human diseases (1, 41). For many years, research in oxidative stress at high oxygen tensions focused primarily on determining the mechanisms by which ROS damage cel...

show abstract

Differential role of hydrogen peroxide and organic hydroperoxides in augmenting ferric nitrilotriacetate (Fe-NTA)-mediated DNA damage: Implications for carcinogenesis

Cited by 9 publications

References 34 publications

Live and let die: Hydrogen peroxide production by the commensal flora and its role in maintaining a symbiotic microbiome

Live and let die: Hydrogen peroxide production by the commensal flora and its role in maintaining a symbiotic microbiome

Oxidative renal tubular injuries induced by aminocarboxylate-type iron (III) coordination compounds as candidate renal carcinogens

Oxidative-Dependent Integration of Signal Transduction with Intercellular Gap Junctional Communication in the Control of Gene Expression

Contact Info

Product

Resources

About