Antioxidants and AP-1 Activation: A Brief Overview

Arco, Pablo Gómez del; Martı́nez-Martı́nez, Sara; Calvo, Vı́ctor; Armesilla, Ángel Luis; Redondo, Juan Miguel

doi:10.1016/s0171-2985(97)80047-2

Cited by 46 publications

(19 citation statements)

References 18 publications

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“…These MAPKs are components of the signal transduction cascades that regulate the AP-1 family members at the transcriptional and posttranscriptional levels (20,26). Although we observed a clear induction of the human collagenase AP-1-dependent reporter construct and the mRNA levels of c-fos, both the AP-1 DNA-binding activity and the c-jun mRNA levels were only weakly induced in response to VEGF.…”

Section: Figmentioning

confidence: 54%

Vascular Endothelial Growth Factor Activates Nuclear Factor of Activated T Cells in Human Endothelial Cells: a Role for Tissue Factor Gene Expression

Armesilla

Lorenzo

Arco

et al. 1999

Molecular and Cellular Biology

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182

165

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Section: Figmentioning

confidence: 54%

Vascular Endothelial Growth Factor Activates Nuclear Factor of Activated T Cells in Human Endothelial Cells: a Role for Tissue Factor Gene Expression

Armesilla

Lorenzo

Arco

et al. 1999

Molecular and Cellular Biology

Self Cite

182

165

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“…Indeed, KG-1a cells exposed to HQ did not show any change in CD34 expression (data not shown), loss of which occurs concomitant with differentiation (65). The high background of NQO1 induced in our experimental systems may have resulted from transcriptional activation via the antioxidant response element͞TPA (12-O-tetradecanoylphorbol-13-acetate) response element by components of serum and͞or stressors to which cells may have been exposed during isolation procedures (66,67). For example, the DNA binding activities of Fos and Jun family members are regulated by oxidative changes (68,69) and transcription of c-fos is activated when cells are exposed to serum via a serum response element in its promoter (70).…”

Section: Discussionmentioning

confidence: 80%

A potential mechanism underlying the increased susceptibility of individuals with a polymorphism in NAD(P)H:quinone oxidoreductase 1 (NQO1) to benzene toxicity

Moran

Siegel²,

Ross³

1999

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

139

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A BSTR ACT NAD(P)H:quinone oxidoreductase 1 (NQO1) is a two-electron reductase that detoxifies quinones derived from the oxidation of phenolic metabolites of benzene. A polymorphism in NQO1, a C609T substitution, has been identified, and individuals homozygous for this change (T͞T) have no detectable NQO1. Exposed workers with a T͞T genotype have an increased risk of benzene hematotoxicity. This finding suggests NQO1 is protective against benzene toxicity, which is difficult to reconcile with the lack of detectable NQO1 in human bone marrow. The human promyeloblastic cell line, KG-1a, was used to investigate the ability of the benzene metabolite hydroquinone (HQ) to induce NQO1. A concentration-dependent induction of NQO1 protein and activity was observed in KG-1a cells cultured with HQ. Multiple detoxification systems, including NQO1 and glutathione protect against benzene metabolite-induced toxicity. Indeed, exposure to a noncytotoxic concentration of HQ induced both NQO1 and soluble thiols and protected against HQ-induced apoptosis. NQO1 protein and activity increased in wild-type human bone marrow cells (C͞C) exposed to HQ, whereas no NQO1 was induced by HQ in bone marrow cells with the T͞T genotype. Intermediate induction of NQO1 by HQ was observed in heterozygous bone marrow cells (C͞T). NQO1 also was induced by HQ in wild-type (C͞C) human bone marrow CD34 ؉ progenitor cells. Our data suggest that failure to induce functional NQO1 may contribute to the increased risk of benzene poisoning in individuals homozygous for the NQO1 C609T substitution (T͞T).

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“…In fungi, the Ap-1-like protein possesses N-and C-terminal cysteine rich domains that might act as a sensortarget of ROS such as H2O2 (Sies, 2014). Interestingly, activation of Ap-1 occurs either in anti-or pro-oxidative conditions via the signalization of different phospho-relay HogA/SakA cascades (Gomez del Arco et al, 1997). As a matter of fact, while an over-expression of ap-1 was observed upon piperine addition, the response regulator sskA (involved in the HogA/SakA pathway) was also positively modulated.…”

Section: Piperine Inhibits Afb1 Production and Modulates Bzip Transcrmentioning

confidence: 99%

Piperine inhibits aflatoxin B1 production in Aspergillus flavus by modulating fungal oxidative stress response

Caceres

Khoury

Bailly

et al. 2017

Fungal Genetics and Biology

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Aspergillus flavus, a soil-borne pathogen, represents a danger for humans and animals since it produces the carcinogenic mycotoxin Aflatoxin B1 (AFB1). Approaches aiming the reduction of this fungal contaminant mainly involve chemicals that may also be toxic. Therefore, identification and characterization of natural antiaflatoxigenic products represents a sustainable alternative strategy. Piperine, a major component of black and long peppers, has been previously demonstrated as an AFB1-inhibitor; nevertheless its mechanism of action was yet to be elucidated. The aim of the present study was to evaluate piperine's molecular mechanism of action in A. flavus with a special focus on oxidative stress response. For that, the entire AFB1 gene cluster as well as a targeted gene-network coding for fungal stress response factors and cellular receptors were analyzed. In addition to this, fungal enzymatic activities were also characterized. We demonstrated that piperine inhibits aflatoxin production and fungal growth in a dose-dependent manner. Analysis of the gene cluster demonstrated that almost all genes participating in aflatoxin's biosynthetic pathway were down regulated. Exposure to piperine also resulted in decreased transcript levels of the global regulator veA together with an over-expression of genes coding for several basic leucine zipper (bZIP) transcription factors such as atfA, atfB and ap-1 and genes belonging to superoxide dismutase and catalase's families.Furthermore, this gene response was accompanied by a significant enhancement of Version postprintComment citer ce document :

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Antioxidants and AP-1 Activation: A Brief Overview

Cited by 46 publications

References 18 publications

Vascular Endothelial Growth Factor Activates Nuclear Factor of Activated T Cells in Human Endothelial Cells: a Role for Tissue Factor Gene Expression

Vascular Endothelial Growth Factor Activates Nuclear Factor of Activated T Cells in Human Endothelial Cells: a Role for Tissue Factor Gene Expression

A potential mechanism underlying the increased susceptibility of individuals with a polymorphism in NAD(P)H:quinone oxidoreductase 1 (NQO1) to benzene toxicity

Piperine inhibits aflatoxin B1 production in Aspergillus flavus by modulating fungal oxidative stress response

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