Glutathione Peroxidase-1 Protects from CD95-induced Apoptosis

Gouazé, Valérie; Andrieu‐Abadie, Nathalie; Cuvillier, Olivier; Malagarie‐Cazenave, Sophie; Frisach, Marie-Françoise; Mirault, Marc-Édouard; Levade, Thierry

doi:10.1074/jbc.m203067200

Cited by 79 publications

(49 citation statements)

References 57 publications

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“…Our findings are consistent with the known inhibitory effect of antioxidant selenoproteins on apoptosis (Fu et al, 2001;Gouaze et al, 2002). Previous studies reported elevated expression of detoxification and repair enzymes in Se-deficient mouse livers (Reiter and Wendel, 1984;Carlson et al, 2004), as well as in cells treated with high levels of Se (El-Bayoumy and Sinha, 2004;Zhao et al, 2004).…”

Section: Discussionsupporting

confidence: 81%

Selenoprotein deficiency and high levels of selenium compounds can effectively inhibit hepatocarcinogenesis in transgenic mice

et al. 2005

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The micronutrient element selenium (Se) has been shown to be effective in reducing the incidence of cancer in animal models and human clinical trials. Selenoproteins and low molecular weight Se compounds were implicated in the chemopreventive effect, but specific mechanisms are not clear. We examined the role of Se and selenoproteins in liver tumor formation in TGFa/c-Myc transgenic mice, which are characterized by disrupted redox homeostasis and develop liver cancer by 6 months of age. In these mice, both Se deficiency and high levels of Se compounds suppressed hepatocarcinogenesis. In addition, both treatments induced expression of detoxification genes, increased apoptosis and inhibited cell proliferation. Within low-to-optimal levels of dietary Se, tumor formation correlated with expression of most selenoproteins. These data suggest that changes in selenoprotein expression may either suppress or promote tumorigenesis depending on cell type and genotype. Since dietary Se may have opposing effects on cancer, it is important to identify the subjects who will benefit from Se supplementation as well as those who will not.

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Section: Discussionsupporting

confidence: 81%

Selenoprotein deficiency and high levels of selenium compounds can effectively inhibit hepatocarcinogenesis in transgenic mice

et al. 2005

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“…This is surprising, as the efficacy of pharmacological antioxidants such as GSH, NAC, deferoxamine (283,420,425), and antioxidant enzymes such as catalase or GPx (149,283) in preventing apoptosis have been shown by several groups. Other studies, however, were unable to demonstrate any role of antioxidants in preventing apoptosis (15,66,122).…”

Section: A Extrinsic Pathways Of Cell Death and Regulation By Rosmentioning

confidence: 98%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,484

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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“…It was reported that a caspase-1 inhibitor, Ac-YVAD-cmk, blocked a later burst of ROS during GSH depletion when added early in the death program (37); thus caspase-1 may also play a role in the later phase of ROS generation, and protection from apoptosis by Bcl-X L may be related to its ability to serve as "anti-oxidant" in this system (38). Consequently, the decline of the expression of Bcl-X L might also contribute to the delayed increase of ROS.…”

Section: Discussionmentioning

confidence: 99%

Dracorhodin Perchlorate Induces Apoptosis via Activation of Caspases and Generation of Reactive Oxygen Species

Xia

Wang

et al. 2004

J Pharmacol Sci

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Abstract. Dracorhodin perchlorate inhibited proliferation of several tumor cell lines. The drug induced oligonucleosomal fragmentation of DNA in HeLa cells and increased caspase-3, -8, -9 activities followed by the degradation of caspase-3 substrates, inhibitor of caspase-dependent DNase, and poly-(ADP-ribose) polymerase. It also increased caspase-1 activity and a caspase-1 inhibitor, Ac-YVAD-cmk, and a caspase-10 inhibitor z-AEVD-fmk, also reduced dracorhodinperchlorate-induced HeLa cell death. Dracorhodin perchlorate decreased the expression of anti-apoptotic mitochondrial protein, Bcl-X L , but not Bcl-2; and it increased the expression of pro-apoptotic protein, Bax. Dracorhodin perchlorate induced a sustained generation of reactive oxygen species (ROS) in HeLa cells; caspase-1 inhibitor, Ac-YVAD-cmk, and caspase-3 inhibitor, z-DEVD-fmk, attenuated the generation of ROS. Taken together, our results indicate that dracorhodin perchlorate alters the intracellular redox status, changed the balance of Bcl-X L and Bax protein expression, and induces apoptosis through caspase pathways in HeLa cells.

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Glutathione Peroxidase-1 Protects from CD95-induced Apoptosis

Cited by 79 publications

References 57 publications

Selenoprotein deficiency and high levels of selenium compounds can effectively inhibit hepatocarcinogenesis in transgenic mice

Selenoprotein deficiency and high levels of selenium compounds can effectively inhibit hepatocarcinogenesis in transgenic mice

Reactive Oxygen Species in Inflammation and Tissue Injury

Dracorhodin Perchlorate Induces Apoptosis via Activation of Caspases and Generation of Reactive Oxygen Species

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