Nuclear Factor Kb: An Oxidative Stress-Responsive Transcription Factor of Eukaryotic Cells (A Review)

Schreck, Ralf; Albermann, Kaj; Baeuerle, Patrick A.

doi:10.3109/10715769209079515

Cited by 1,351 publications

(741 citation statements)

References 51 publications

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“…It is likely that this induction of antioxidant enzymes represents a stress response to the hypoxia since Das et al have shown that Mn SOD and catalase are two of a number of stress-related genes up-regulated in cardiac biopsy tissue following repeated ischaemia [38]. Whether the anti-apoptotic effect of hypoxia relates to the induction of other stress-related proteins or changes in poly-ADP-ribose transferase activity and hence ATP levels [39,40], lipid oxidation [41], regulation of NF~B activation [42], or some alternative mechanism, requires further investigation.…”

Section: Resultsmentioning

confidence: 99%

Hypoxia prolongs neutrophil survival in vitro

et al. 1995

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~,bstract Neutrophil apoptosis represents a major mechanism ~nvolved in the resolution of inflammation. Since hypoxia induces apoptosis in several cell lines and is of particular relevance in many disease states, we studied the effect of oxygen concentration on neutrophil survival in vitro. Hypoxia caused a dramatic decrease in neutrophil apoptosis (% apoptosis 20 h: 78.7 + 2.2% in 21% 0 2, 61.4 _+ 6.5% in 2.5% 02, 23.1 + 3.2% in 0% 02, = 5). This was additive to the effect of GM-CSF (50 Ulml), not associated with induction of bcl-2 expression, and was not mimicked by methionine (5 raM), superoxide dismutase (200 pg/ml) or Trolox (10 mM) but was mimicked by catalase (250/zg/ml).Hence, hypoxia has a bcl-2-independent effect on neutrophil apoptosis that may adversely affect the clearance of these cells from an inflammatory focus.

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Section: Resultsmentioning

confidence: 99%

Hypoxia prolongs neutrophil survival in vitro

et al. 1995

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“…CHOP-regulated genes relevant for apoptosis regulation have not yet been identi®ed but may include pro-apoptotic molecules such as the Bcl-2 family member Bax, a known trigger of cytochrome c release on mitochondria (RosseÂ et al, 1998). On the other hand, it is known that activation of the transcription factor NF-kB via the EOR involves reactive oxygen species (ROS) which are produced from the oxidizing environment of the ER lumen and the action of cytochrome p450 on the ER membrane (Pahl and Baeuerle, 1997;Schreck et al, 1992). ROS can mount an oxidative stress that damages membranes, including those of mitochondria (Kowaltowski and Vercesi, 1999).…”

Section: Discussionmentioning

confidence: 99%

Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2

et al. 2000

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Apoptosis involves mitochondrial steps such as the release of the apoptogenic factor cytochrome c which are e ectively blocked by Bcl-2. Although Bcl-2 may have a direct action on the mitochondrial membrane, it also resides and functions on the endoplasmic reticulum (ER), and there is increasing evidence for a role of the ER in apoptosis regulation as well. Here we uncover a hitherto unrecognized, apoptotic crosstalk between the ER and mitochondria that is controlled by Bcl-2. After triggering massive ER dilation due to an inhibition of secretion, the drug brefeldin A (BFA) induces the release of cytochrome c from mitochondria in a caspase-8-and Bid-independent manner. This is followed by caspase-3 activation and DNA/nuclear fragmentation. Surprisingly, cytochrome c release by BFA is not only blocked by wild-type Bcl-2 but also by a Bcl-2 variant that is exclusively targeted to the ER (Bcl-2/cb5). Similar ®ndings were obtained with tunicamycin, an agent interfering with N-linked glycosylations in the secretory system. Thus, apoptotic agents perturbing ER functions induce a novel crosstalk between the ER and mitochondria that can be interrupted by ER-based Bcl-2.

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“…PCBs also can produce oxidative DMA damage, in the form of 8-hydroxydeoxyguanosine (Oakley et al 1996). We have observed that PCBs can activate NF-κB, which may be activated by oxidative stress (Li and Karin 1999;Schreck et al 1992;vandenBerg et al 2001). We examined two PCBs: 3,3′ 4,4′-tetrachlorobiphenyl (PCB-77), an Ah receptor agonist; and 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB-153), a CAR activator.…”

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress in the promoting activities of PCBs

Glauert

Tharappel

et al. 2008

Environmental Toxicology and Pharmacology

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PCBs are organic pollutants that persist and bioaccumulate in the environment. These chemicals induce and promote liver tumors in rodents. Previous studies have shown that they increase oxidative stress in the liver, including lipid peroxidation, oxidative DNA damage, and NF-κB activation. The objective of these studies was to determine if the promoting activities of PCBs could be inhibited by dietary antioxidants (vitamin E, selenium, or phytochemicals) or by knocking out the p50 subunit of NF-κB. In the antioxidant studies, female rats were first injected with DEN (150 mg/kg) and then administered 4 biweekly i.p. injections (300 μmol/kg/injection) of PCB-77, PCB-153, or vehicle; the number and volume of placental glutathione S-transferase (PGST)-positive foci were then quantified. Vitamin E did not influence the promoting activities of PCBs. Increasing dietary selenium above the recommended intake increased the number of foci induced but decreased their volume. Most of the phytochemicals examined (N-acetyl cysteine, β-carotene, resveratrol, EGCG) had no significant effect on the promoting activity of PCB-77. Ellagic acid increased and lycopene decreased the number of foci; ellagic acid, CoQ 10 , and curcumin decreased the volume of foci. In the NF-κB knockout study, male mice were first injected with DEN (90 mg/kg); controls not receiving DEN were also studied. Both p50 −/− and wild-type mice were then injected biweekly 20 times with PCB-153 (300 (μmol/kg). In DEN-treated and DEN + PCB-treated mice, the incidence of tumors was lower in the p50 −/− mice than in wild-type mice. In mice receiving PCB-153, the tumor incidence and tumor volume were higher. The volume of tumors that were positive for glutamine synthetase was increased in mice administered PCB-153. This study shows that the promotion of hepatocarcinogenesis by PCBs is largely unaffected by dietary antioxidants but is diminished when NF-κB activation is impaired by the absence of the p50 subunit.

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Nuclear Factor Kb: An Oxidative Stress-Responsive Transcription Factor of Eukaryotic Cells (A Review)

Cited by 1,351 publications

References 51 publications

Hypoxia prolongs neutrophil survival in vitro

Hypoxia prolongs neutrophil survival in vitro

Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2

Role of oxidative stress in the promoting activities of PCBs

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