Redox redux: The control of oxidative stress responses

Demple, Bruce; Amábile-Cuevas, Carlos F.

doi:10.1016/0092-8674(91)90355-3

Cited by 239 publications

(120 citation statements)

References 17 publications

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“…They control the gene expression of antioxidant enzymes responsible for the removal of H202 and 02, respectively (128). (ii) Antioxidant enzyme regulation in eukaryotic cells is poorly understood, however, AP-1 and NF-KB are two transcription factors that play an iml~ortant role and that are regulated by the redox state of the cell (129). (iii) NF-KB is activated by a variety of pro-oxidants, including ROS (130).…”

Section: Summary Of Findingsmentioning

confidence: 99%

Exercise and oxidative stress: Sources of free radicals and their impact on antioxidant systems

Leichtweis

1997

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Strenuous exercise is characterized by increased oxygen consumption and the disturbance between intracellular pro-oxidant and antioxidant homeostasis. At lease three biochemical pathways (i.e., mitochondrial electron transport chain, xanthine oxidase, and polymorphoneutrophil) have been identified as potential sources of intracellular free radical generation during exercise. These deleterious reactive oxygen species pose a serious threat to the cellular antioxidant defense system, such as diminished reserves of antioxidant vitamins and glutathione. However, enzymatic and non-enzymatic antioxidants have demonstrated great versitility and adaptability in response to acute and chronic exercise. The delicate balance between pro-oxidants and antioxidants suggests that supplementation with antioxidants may be desirable for physically active individuals under certain physiological conditions by providing a larger protective margin.

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Section: Summary Of Findingsmentioning

confidence: 99%

Exercise and oxidative stress: Sources of free radicals and their impact on antioxidant systems

Leichtweis

1997

AGE

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“…The genetic response to oxidative stress has been studied intensively in bacteria [reviewed in Refs. [14][15][16]. In Escherichia coli.…”

Section: The Oxidant Stress Responsementioning

confidence: 99%

Redox signalling by transcription factors NF-κB and AP-1 in lymphocytes

Schulze‐Osthoff

Łos

Baeuerle

1995

Biochemical Pharmacology

253

146

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“…For example, reactive oxygen species generated during aerobic metabolism damage DNA bases and sugar residues. Specific oxygen radical detoxification and DNA repair mechanisms prevent or remove this damage (13,14). The increase in the rate of spontaneous mutagenesis in bacteria and yeast mutants that are specifically deficient in the repair of aberrantly methylated DNA bases indicates that methylation of DNA also occurs endogenously (16,34,52,53).…”

mentioning

confidence: 99%

Generation of an endogenous DNA-methylating agent by nitrosation in Escherichia coli

Taverna¹,

Sedgwick²

1996

J Bacteriol

143

113

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Escherichia coli ada ogt mutants, which are totally deficient in O 6 -methylguanine-DNA methyltransferases, have an increased spontaneous mutation rate. This phenotype is particularly evident in starving cells and suggests the generation of an endogenous DNA alkylating agent under this growth condition. We have found that in wild-type cells, the level of the inducible Ada protein is 20-fold higher in stationary-phase and starving cells than in rapidly growing cells, thus enhancing the defense of these cells against DNA damage. The increased level of Ada in stationary cells is dependent on RpoS, a stationary-phase-specific sigma subunit of RNA polymerase. We have also identified a potential source of the mutagenic agent. Nitrosation of amides and related compounds can generate directly acting methylating agents and can be catalyzed by bacterial enzymes. E. coli moa mutants, which are defective in the synthesis of a molybdopterin cofactor required by several reductases, are deficient in nitrosation activity. It is reported here that a moa mutant shows reduced generation of a mutagenic methylating agent from methylamine (or methylurea) and nitrite added to agar plates. Moreover, a moa mutation eliminates much of the spontaneous mutagenesis in ada ogt mutants. These observations indicate that the major endogenous mutagen is not S-adenosylmethionine but arises by bacterially catalyzed nitrosation.Only a few types of cancer have been attributed to environmental agents. Other carcinogens of primary concern may be transient but highly reactive metabolites that arise during normal metabolism (24, 36). Indeed, several metabolites of amino acids, sugars, oxygen, and lipids are known to be mutagenic. It is, therefore, important to identify metabolites that damage DNA in vivo and result in spontaneous mutagenesis in the absence of adequate DNA repair. For example, reactive oxygen species generated during aerobic metabolism damage DNA bases and sugar residues. Specific oxygen radical detoxification and DNA repair mechanisms prevent or remove this damage (13,14). The increase in the rate of spontaneous mutagenesis in bacteria and yeast mutants that are specifically deficient in the repair of aberrantly methylated DNA bases indicates that methylation of DNA also occurs endogenously (16,34,52,53). Rodent cells may be similarly affected (2).The major mutagenic adduct induced in DNA by methylating agents is O 6 -methylguanine (O 6 -meG). This modified base mispairs with thymine during DNA replication, resulting in GC-to-AT transition mutations. In wild-type cells, O 6 -meG is repaired by ubiquitous O 6 -meG-DNA methyltransferases that directly transfer the methyl group from the modified base to one of their own cysteine residues. As a result of this process, the methyltransferases are inactivated (25). Escherichia coli has two O 6 -meG-DNA methyltransferases, a constitutive Ogt protein and an inducible Ada protein. Each exponentially growing cell contains only two to four molecules of Ada protein and 10-fold more Ogt protein (32,3...

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Redox redux: The control of oxidative stress responses

Cited by 239 publications

References 17 publications

Exercise and oxidative stress: Sources of free radicals and their impact on antioxidant systems

Exercise and oxidative stress: Sources of free radicals and their impact on antioxidant systems

Redox signalling by transcription factors NF-κB and AP-1 in lymphocytes

Generation of an endogenous DNA-methylating agent by nitrosation in Escherichia coli

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