Endogenous generation of reactive oxidants and electrophiles and their reactions with DNA and protein

Marnett, Lawrence J.; Riggins, James N.; West, James D.

doi:10.1172/jci18022

Cited by 172 publications

(142 citation statements)

References 132 publications

(60 reference statements)

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“…The sequential reduction of molecular oxygen can generate a group of ROS such as superoxide anion ( • O 2 -), hydrogen peroxide (H 2 O 2 ) and hydroxyl radical (•OH). The •OH radical was an extremely strong and highly diffusible oxidant with redox potential of 2.8 V, which can mediate DNA damage by adding to double bonds of DNA bases or abstracting hydrogen atoms from sugar moiety (Marnett et al 2003).…”

Section: Effects Of Scavengers In the Damage Of Pbr322dnamentioning

confidence: 99%

Oxidative damage to DNA by 1,10-phenanthroline/l-threonine copper (II) complexes with chlorogenic acid

Wang

Zhang

et al. 2009

Biometals

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The oxidative DNA damage by copper (II) complexes in the presence of chlorogenic acid was explored using agarose gel electrophoresis. The extent of pBR322 DNA damage was enhanced significantly with increasing concentration of [Cu-phen-Thr] complex and incubation time. A fluorescence quenching activity of calf thymus DNA-EB was observed more remarkably with chlorogenic acid than without chlorogenic acid. The fluorescence measurements suggested that [Cu-phen-Thr] complex not only can bind to DNA by intercalation but also can damage the double strand DNA in the presence of chlorogenic acid. Further, 8-hydroxy-2'-deoxyguanosine, a biomarker of DNA oxidative damage was determined by electrochemical method. The control experiments revealed that the structure of copper (II) complexes affected capability of complex to DNA damage. The planar structure copper (II) complex showed high efficiency to DNA damage. The chlorogenic acid as biological reductant could improve copper (II) complex to DNA damage. A mechanism on [Cu-phen-Thr] complex to DNA damage in the presence of chlorogenic acid was proposed.

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Section: Effects Of Scavengers In the Damage Of Pbr322dnamentioning

confidence: 99%

Oxidative damage to DNA by 1,10-phenanthroline/l-threonine copper (II) complexes with chlorogenic acid

Wang

Zhang

et al. 2009

Biometals

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“…Because of the now appreciated association between chronic infl ammation, ROS and preneoplastic genomic instability, it is tempting to speculate that ROS might be a trigger for MIN and CIN. ROS are produced constantly by normal metabolic processes, acute and chronic infl ammation, and exposure to exogenous toxins and radiation [102]. ROS include hydrogen peroxide (H2O2), superoxide (O2 -), and hydroxyl ( .…”

Section: Genomic Instability and Oxidative Dna Damagementioning

confidence: 99%

“…OH) radicals. These short-lived but highly reactive agents can mediate the oxidation of proteins, lipids and DNA, particularly in association with certain metal ions such as Fe ++ [102]. The consequences of DNA damage include the chemical modifi cation of bases with resultant mispairing [103].…”

Section: Genomic Instability and Oxidative Dna Damagementioning

confidence: 99%

“…Because of the potentially deleterious consequences of maintaining an oxidative environment, a number of defenses have evolved to inactive ROS. These include superoxide dismutase, which converts superoxide to H2O2; catalase and glutatione peroxidase, which convert H2O2 to water; and peroxiredoxins, which utilize thioredoxin as an electron donor and also scavenge peroxide [102]. Non-enzymatic ROS scavengers include ascorbate (vitamin C), tocopherols (vitamin E and its derivatives), glutathione, selenium and carotenoids.…”

Section: Genomic Instability and Oxidative Dna Damagementioning

confidence: 99%

“…Non-enzymatic ROS scavengers include ascorbate (vitamin C), tocopherols (vitamin E and its derivatives), glutathione, selenium and carotenoids. The number and functional redundancy of these molecules underscores the importance of ROS inactivation and the need to regulate tightly the cellular re-dox state [102,104].…”

Section: Genomic Instability and Oxidative Dna Damagementioning

confidence: 99%

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Functional and physical communication between oncoproteins and tumor suppressors

Prochownik

2005

Cell. Mol. Life Sci.

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The discovery of oncogenes (c-onc's) and tumor suppressors (TS's) has led to the concept that cancer arises from defects in each of these classes of genes or their products. More recently, it has been appreciated that c-onc and TS proteins often affect one another's functions. Within this context, I review the two classical TS's, p53 and the retinoblastoma protein, and the consequences of their inactivation. The various forms of genomic instability (GI) that underly the high mutation rates of transformed cells are then discussed. Particular emphasis is placed upon the concept that GI is not only an integral part of the transformed state but is a prerequisite. Increased oxidative DNA damage, and/or an inabiliy to repair it, can lead to GI. The review then discusses recent observations showing that loss of the TS protein peroxiredoxin 1 (prdx 1) and increased expression of the c-onc protein c-Myc, each leads to increased oxidative DNA damage. The critical nature of the c-onc-TS interaction is underscored by that occurring between prdx1 and c-Myc, with the former protein regulating the production of DNA-damaging reactive oxygen species by the latter. The intimate association between these proteins and others serves as a paradigm for the exquisite balancing act that c-onc's and TS's must maintain in order to properly control normal DNA replication and cellular proliferation while simultaneously minimizing the acquisition of potentially neoplastic mutations.

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Antioxidants in patients receiving total parenteral nutrition after gastrointestinal cancer surgery

Szpetnar

Matras

Kiełczykowska

et al. 2011

Cell Biochemistry & Function

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Total parenteral nutrition (TPN) is essential for patients with postoperative impairing gastrointestinal function who are unable to receive and absorb oral/enteral feeding for at least 7 days. Oxidative stress plays a major role in the ethiopathogenesis of cancers. In this study, total antioxidant status (TAS), glutathione peroxidase (GPx), superoxide dismutase, malondialdehyde and ascorbic acid were studied in patients operated because of small intestine, colorectal or pancreatic cancer and subsequently receiving TPN in comparison with patients receiving standard nutrition after the operation. TAS level and GPx activity were decreased in patients with small intestine cancer but did not differ in patients with colorectal and pancreatic cancer before and after surgery. In all patient groups receiving TPN, superoxide dismutase activity after the surgery was kept at the same level as before. On the fifth day after the surgery, malondialdehyde concentration in each group was restored to the value observed before surgery. On the fifth day of TPN treatment, ascorbic acid concentration was increased in every group of patients. TPN applied during the postoperative period alleviates oxidative stress resulting from surgery. In the case of small intestine cancer, the addition of vitamins and antioxidants to the nutrition mixture seems to result in depletion of antioxidant enzymes' activities.

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Endogenous generation of reactive oxidants and electrophiles and their reactions with DNA and protein

Cited by 172 publications

References 132 publications

Oxidative damage to DNA by 1,10-phenanthroline/l-threonine copper (II) complexes with chlorogenic acid

Oxidative damage to DNA by 1,10-phenanthroline/l-threonine copper (II) complexes with chlorogenic acid

Functional and physical communication between oncoproteins and tumor suppressors

Antioxidants in patients receiving total parenteral nutrition after gastrointestinal cancer surgery

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