Role of sulfiredoxin as a regulator of peroxiredoxin function and regulation of its expression

Jeong, Woojin; Bae, Soo Han; Toledano, Michel B.; Rhee, Sue Goo

doi:10.1016/j.freeradbiomed.2012.05.020

Cited by 116 publications

(96 citation statements)

References 115 publications

(172 reference statements)

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“…NRF2 also promotes the expression of glutathione peroxidase, glutathione reductase, and thioredoxin reductase ( Fig. 1; Hayes and McMahon 2009;Abbas et al 2011;Jeong et al 2012;Hawkes et al 2014;Lu and Holmgren 2014), as well as proteins such as ferritin, which blocks the formation of free radicals, and NADPH:quinone oxidoreductase 1, which inhibits the Figure 1. Endogenous antioxidant mechanisms.…”

Section: Antioxidant Mechanisms For Ros Defensementioning

confidence: 99%

Cancer, Oxidative Stress, and Metastasis

Gill

Piskounova

Morrison

2016

Cold Spring Harb Symp Quant Biol

231

164

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Reactive oxygen species (ROS) are highly reactive molecules that arise from a number of cellular sources, including oxidative metabolism in mitochondria. At low levels they can be advantageous to cells, activating signaling pathways that promote proliferation or survival. At higher levels, ROS can damage or kill cells by oxidizing proteins, lipids, and nucleic acids. It was hypothesized that antioxidants might benefit high-risk patients by reducing the rate of ROS-induced mutations and delaying cancer initiation. However, dietary supplementation with antioxidants has generally proven ineffective or detrimental in clinical trials. High ROS levels limit cancer cell survival during certain windows of cancer initiation and progression. During these periods, dietary supplementation with antioxidants may promote cancer cell survival and cancer progression. This raises the possibility that rather than treating cancer patients with antioxidants, they should be treated with pro-oxidants that exacerbate oxidative stress or block metabolic adaptations that confer oxidative stress resistance.

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Section: Antioxidant Mechanisms For Ros Defensementioning

confidence: 99%

Cancer, Oxidative Stress, and Metastasis

Gill

Piskounova

Morrison

2016

Cold Spring Harb Symp Quant Biol

231

164

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“…With age, the cellular milieu becomes more pro-oxidizing, and the thiol/disulfide ratio declines. Both the degree and level of protein thiol oxidation are enhanced, resulting in a slower reversion of the post-translational modifications, dictated by either the need to replace modified protein through turnover, or, as in the case of sulfinic acid reduction, reliance on the kinetically slower reactions of the sulfiredoxin (Srx) enzymes (39,92). As members of the enzymatic resolution machinery (TrxR, peroxiredoxin [Prx], Trx, and Grx) are themselves redox-sensitive, the thiol/disulfide switching mechanisms would be further compromised, and it is imagined that in older animals, this would result in the loss of efficiency in the maintenance of redox homeostasis.…”

Section: The Redox Stress Hypothesis Of Agingmentioning

confidence: 99%

“…Reaction kinetics of thiol reduction will vary as a function of the degree of oxidation of both the target protein thiols as well as the Trxs/Grxs/Srxs that reduce the oxidized thiols belonging to the target proteins. Thus, the reduction of Prx S-S or Prx SOH by Trx or GSH + GST is considerably faster than the reduction of Prx SO 2 H by Srx (39,92,94). The heights of the curved arrows represent the relative rate of resolution of these post-translational modifications as a function of the increasing pro-oxidizing state that accompanies age.…”

Section: Fig 2 Schematic Changes In the Resolution Of Redox Switchementioning

confidence: 99%

Involvement of Redox State in the Aging ofDrosophila melanogaster

Orr

Radyuk

Sohal

2013

Antioxidants & Redox Signaling

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Significance: The main objective of this review was to provide an exposition of investigations, conducted in Drosophila melanogaster, on the role of reactive oxygen species and redox state in the aging process. While early transgenic studies did not clearly support the validity of the oxidative stress hypothesis of aging, predicated on the accumulation of structural damage, they spawned a broader search for redox-related effects that might impact the aging process. Recent Advances: Initial evidence implicating the thiol redox state as a possible causative factor in aging has been obtained in Drosophila. Overexpression of genes, such as GCL, G6PD, Prx2, and Prx5, which are involved in the maintenance of thiol redox homeostasis, has strong positive effects on longevity. Further, the depletion of peroxiredoxin activity in the mitochondria through the double knockdown of Prx5 and Prx3 not only results in a redox crisis but also elicits a rapid aging phenotype. Critical Issues: Herein, we summarize the present status of knowledge about the main components of the machinery controlling thiol redox homeostasis and describe how age-related redox fluctuations might impact aging more acutely through disruption of the redox-sensitive signaling mechanisms rather than via the simple accumulation of structural damage. Future Directions: Based on these initial insights into the plausible impact of redox fluctuations on redox signaling, future studies should focus on the pathways that have been explicitly implicated in aging, such as insulin signaling, TOR, and JNK/FOXO, with particular attention to elements that are redox sensitive. Antioxid. Redox Signal. 19, 788-803. Historical BackgroundLinkage between energy utilization and life span S tudies in the fruit fly, Drosophila melanogaster, have historically made important contributions toward the development of basic concepts in many areas of biology, including the aging process, especially in defining the role of oxygen metabolism in the determination of life span. In 1917, Loeb and Northrop showed that the life span of D. melanogaster is inversely associated with the ambient temperature (61), which, in turn, was later demonstrated to be linked to the rate of oxygen consumption within the physiological range, whose upper limit for long-term survival and optimal fecundity is *27°C (67). A major advance in the field of aging that can be largely credited to the Drosophila model was Pearl's (77) interpretation of the effects of temperature on longevity, namely, shorter life spans at elevated temperatures are ascribable to a relatively higher physical activity or the rate of living (ROL). As originally proposed, the length of life of an individual organism is governed by two distinct factors: (i) a genetically determined metabolic potential, that is, the total amount of energy consumed during life, which varies in different genotypes, and (ii) the rate at which this metabolic potential is expended by the individual or the rate of its metabolism. It is a widely recognized phe...

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“…Hyperoxidation increases the affinity constant of the decamer and may also enhance the ability of Prxs to act as chaperones (12). It is readily observed in cells treated with H 2 O 2 and can be induced by stresses such as high ethanol exposure (13). The physiological relevance of hyperoxidation can also be inferred from findings of sulfiredoxin acting synergistically with Prxs in protecting cells from oxidative stress (14).…”

mentioning

confidence: 99%

Hyperoxidation of Peroxiredoxins 2 and 3

Peskin

Dickerhof

Poynton

et al. 2013

Journal of Biological Chemistry

152

109

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Background: H 2 O 2 oxidizes peroxiredoxins (Prxs) to sulfenic acid intermediates which form disulfides or become hyperoxidized. Results: Rate constants for hyperoxidation and disulfide formation were obtained for Prx2 and Prx3. Conclusions: Prx2 is more susceptible than Prx3 to hyperoxidation due to slower disulfide formation. Significance: H 2 O 2 reacts with Prx sulfenic acid faster than with most reduced thiols.

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Role of sulfiredoxin as a regulator of peroxiredoxin function and regulation of its expression

Cited by 116 publications

References 115 publications

Cancer, Oxidative Stress, and Metastasis

Cancer, Oxidative Stress, and Metastasis

Involvement of Redox State in the Aging ofDrosophila melanogaster

Hyperoxidation of Peroxiredoxins 2 and 3

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