Thiol–Disulfide Balance: From the Concept of Oxidative Stress to that of Redox Regulation

Ghezzi, Pietro; Bonetto, Valentina; Fratelli, Maddalena

doi:10.1089/ars.2005.7.964

Cited by 226 publications

(158 citation statements)

References 81 publications

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“…A vast majority of these studies showed thiol/disulphide balance shifted toward disulphide formation under oxidative stress. 22 These results support that thiol/disulphide homeostasis shifts in favor of increased oxidative stress in inflammatory and/or oxidative diseases. In recent years, there have been some reports that support the idea that depression is an inflammatory disorder and the underlying neurobiological mechanism is associated with oxidative stress.…”

Section: Anadolu Psikiyatri Derg 2018; 19(2):135-142supporting

confidence: 60%

Dynamic thiol/disulphide homeostasis as a novel oxidative stress marker in women with major depressive disorder

Baykan¹,

Durmaz²,

Baykan³

et al. 2018

Anadolu Psikiyatri Derg

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Section: Anadolu Psikiyatri Derg 2018; 19(2):135-142supporting

confidence: 60%

Dynamic thiol/disulphide homeostasis as a novel oxidative stress marker in women with major depressive disorder

Baykan¹,

Durmaz²,

Baykan³

et al. 2018

Anadolu Psikiyatri Derg

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“…In senescing rose petals, decline of GSH leads to shift the cellular redox toward more oxidized state . GSH can directly react with ROS and act as a substrate for enzymes scavenge ROS (Ghezzi et al, 2005;Szalai et al, 2009). In the enzymatic scavenging of ROS, glutathione reductase (GR) reduces oxidized glutathione (GSSG) to reduced GSH by use of NAD(P)H (Rogers, 2012).…”

Section: Introductionmentioning

confidence: 99%

Chitooligosaccharide Prolongs Vase Life of Cut Roses by Decreasing Reactive Oxygen Species

Jing

HuanQing²

2015

HST

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Chitooligosaccharide (COS), as antioxidant, extensively applied to food and juice preservation. In the present study, influences of COS on vase life and ornamental value of cut roses were investigated. Results showed that vase life of cut roses treated by COS was longer 6.4 days than one of control and ornamental character of cut roses was improved effectively by COS. The increase of vase life and ornamental value were chiefly governed by that COS improved water absorption capacity of cut roses. Besides that, COS decreased the contents of superoxide anion and hydrogen peroxide and lowered the levels of malondialdehyde in turn during the senescence process of cut roses. That was because that COS not only enhanced activities of antioxidant enzymes glutathione reductase, but also improved reduced glutathione contents in petals of cut rose. Therefore, COS could be used in commercial preservatives to improve the longevity of cut roses.

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“…To function properly, cells need to maintain an adequate redox balance (7). Recent work indicates a role for reduced cell surface thiols (ϪSH) as targets of redox regulation in the immune system (8).…”

mentioning

confidence: 99%

T cell surface redox levels determine T cell reactivity and arthritis susceptibility

Gelderman

Hultqvist

Holmberg

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

215

199

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Rats and mice with a lower capacity to produce reactive oxygen species (ROS) because of allelic polymorphisms in the Ncf1 gene (which encodes neutrophil cytosolic factor 1) are more susceptible to develop severe arthritis. These data suggest that ROS are involved in regulating the immune response. We now show that the lower capacity to produce ROS is associated with an increased number of reduced thiol groups (؊SH) on T cell membrane surfaces. Artificially increasing the number of reduced thiols on T cells from animals with arthritis-protective Ncf1 alleles by glutathione treatment lowered the threshold for T cell reactivity and enhanced proliferative responses in vitro and in vivo. Importantly, T cells from immunized congenic rats with an E3-derived Ncf1 allele (DA.Ncf1 E3 rats) that cannot transfer arthritis to rats with an arthritis-associated Dark Agouti (DA)-derived mutated Ncf1 allele (DA.Ncf1 DA rats) became arthritogenic after increasing cell surface thiol levels. This finding was confirmed by the reverse experiment, in which oxidized T cells from DA.Ncf1 DA rats induced less severe arthritis compared with controls. Therefore, we conclude that ROS production as controlled by Ncf1 is important in regulating surface redox levels of T cells and thereby suppresses autoreactivity and arthritis development.Ncf1 ͉ reactive oxidative species ͉ p47 phox ͉ NADPH ͉ glutathione R eactive oxygen species (ROS) are generally thought to be harmful and to play a disease-enhancing role in autoimmune diseases such as arthritis (1, 2). However, we have found that a decreased capacity to produce ROS because of polymorphisms in Ncf1 increases susceptibility for autoimmunity and arthritis (3, 4). Ncf1 encodes neutrophil cytosolic factor 1 (Ncf1, also known as p47phox), the activating protein in the NADPH oxidase complex that produces ROS upon activation. In the rat, a SNP in the Ncf1 gene was identified by positional cloning to be one of the strongest genes in regulating both oxidative burst and arthritis (3). In the mouse, a spontaneous mutation was identified that affects splicing and results in expression of truncated, less functional Ncf1 protein (5), which also resulted in increased arthritis and autoimmunity (4). Hence, it was clear that the Ncf1 gene that controls oxidative burst also controlled the autoimmune response and severity of arthritis in both rats and mice.It has been shown that arthritis as induced by immunization with pristane in rats and collagen in mice expressing polymorphic Ncf1 is T cell dependent. In the rat model, only T cells from DA.Ncf1 DA rats [Dark Agouti (DA) rats with the mutated Ncf1 DA allele from the DA rat] can transfer disease to naïve DA.Ncf1 DA recipients, whereas T cells from the congenic DA.Ncf1 E3 rats (DA rats with the WT Ncf1 E3 allele from the E3 rat) cannot (3, 6). In the mouse model, a mutation in Ncf1 results in an increased delayed-type hypersensitivity response and serum levels of anti-collagen type II (CII) IgG antibodies (4), indicating enhanced activation of autoreactive T ...

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Thiol–Disulfide Balance: From the Concept of Oxidative Stress to that of Redox Regulation

Cited by 226 publications

References 81 publications

Dynamic thiol/disulphide homeostasis as a novel oxidative stress marker in women with major depressive disorder

Dynamic thiol/disulphide homeostasis as a novel oxidative stress marker in women with major depressive disorder

Chitooligosaccharide Prolongs Vase Life of Cut Roses by Decreasing Reactive Oxygen Species

T cell surface redox levels determine T cell reactivity and arthritis susceptibility

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