Stimulation of reactive oxygen, but not reactive nitrogen species, in vascular endothelial cells exposed to low levels of arsenite

Barchowsky, Aaron; Klei, Linda R.; Dudek, Edward J.; Swartz, Harold M.; James, Philip E.

doi:10.1016/s0891-5849(99)00186-0

Cited by 240 publications

(140 citation statements)

References 18 publications

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“…3). Blockade of NAD(P)H oxidase by apocynin [14] or of xanthine oxidoreductase by oxypurinol [15] during the glucose normalisation period interrupted the induction of several high glucose stress markers, but not all (Fig. 3), while overexpression of the mitochondrial respiratory chain uncoupling protein UCP2 [17] during the normalisation period reduced the induction of all the stress proteins (Fig.…”

Section: Resultsmentioning

confidence: 95%

“…Effects of ROS inhibition on the 'memory' phenomenon in HUVECs In the last week of normal glucose in HUVECs, glucose was given with or without agents capable of inhibiting ROS production as follows: 62.5 μmol/l α-lipoic acid (ALA), an antioxidant working also at the mitochondria level [13]; 10 μmol/l apocynin [14]; 10 μmol/l oxypurinol [15]; 1 μmol/l PJ34 [16]; and 25 to 100 plaque-forming units per cell of an uncoupling protein 2 (UCP2) overexpressing adenovirus, used to specifically inhibit mitochondrial ROS production [17]. Inhibitors were replaced every other day and 24 h before the end of the experiment.…”

Section: Methodsmentioning

confidence: 99%

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Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling

et al. 2007

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Aims/hypothesis A long-term 'memory' of hyperglycaemic stress, even when glycaemia is normalised, has been previously reported in endothelial cells. In this report we sought to duplicate and extend this finding. Materials and methods HUVECs and ARPE-19 retinal cells were incubated in 5 or in 30 mmol/l glucose for 3 weeks or subjected to 1 week of normal glucose after being exposed for 2 weeks to continuous high glucose. HUVECs were also treated in this last condition with several antioxidants. Similarly, four groups of rats were studied for 3 weeks: (1) normal rats; (2) diabetic rats not treated with insulin; (3) diabetic rats treated with insulin during the last week; and (4) diabetic rats treated with insulin plus α-lipoic acid in the last week. Results In human endothelial cells and ARPE-19 retinal cells in culture, as well as in the retina of diabetic rats, levels of the following markers of high glucose stress remained induced for 1 week after levels of glucose had normalised: protein kinase C-β, NAD(P)H oxidase subunit p47phox, BCL-2-associated X protein, 3-nitrotyrosine, fibronectin, poly(ADPribose) Blockade of reactive species using different approaches, i.e. the mitochondrial antioxidant α-lipoic acid, overexpression of uncoupling protein 2, oxypurinol, apocynin and the poly(ADP-ribose) polymerase inhibitor PJ34, interrupted the induction both of high glucose stress markers and of the fluorescent reactive oxygen species (ROS) probe CM-H 2 DCFDA in human endothelial cells. Similar results were obtained in the retina of diabetic rats with α-lipoic acid added to the last week of normalised glucose. Conclusions/interpretation These results provide proofof-principle of a ROS-mediated cellular persistence of vascular stress after glucose normalisation.

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Section: Resultsmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling

et al. 2007

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“…Barchowsky et al (1996Barchowsky et al ( ,1999 reported that arsenic-induced oxidant stress, H 2 O 2 , and superoxide are the predominant reactive species in endothelia cells and may be the mediators for the activation of the NF-κB pathway. We showed that arsenic induced activation of NF-κB in different cell culture models.…”

Section: Blocking Nf-κb Activation Inhibits Arsenic-induced Apoptosismentioning

confidence: 99%

The molecular mechanisms of arsenic-induced cell transformation and apoptosis.

Dong

2002

Environ Health Perspect

106

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“…Exogenously added catalase was also shown to significantly inhibit intracellular H 2 O 2 formation in cells induced by H 2 O 2 14,15) , and abolish H 2 O 2 -generated DNA strand breaks 16) . Arsenic was shown to increase both extracellular and intracellular levels of H 2 O 2 and superoxide (O 2 -) [17][18][19] . DMSO has been reported to be one of the strongest scavengers for ·OH-induced DNA strand breaks 16,20) .…”

Section: 14)mentioning

confidence: 99%

Arsenic induces DNA damage via reactive oxygen species in human cells

Morimoto

Takeshita

et al. 2001

Environ Health Prev Med

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To elucidate arsenic-induced oxidative DNA damage, the genotoxicity of arsenic in human cells was comparatively studied with single cell gel electrophoresis (SCGE) assay in combination with the observation of the protective effects of dimethyl sulfoxide (DMSO) and catalase. Arsenic, at the concentration of 2.4 mM by coincubation for 24 hours, significantly induced DNA damage in HL60, a human promyelocytic leukemia cell line. In contrast, significant DNA damage was found in human mononucleocytes at the concentration of 4.8 mM or above. The cells were incubated separately with DMSO (12 mM/l), a well-known hydroxyl radical (OH ----) scavenger, and catalase (1,300 U/ml), a hydrogen peroxide (H 2 O 2 ) scavenger, for 6 hours and then further coincubated with various concentrations of arsenic for 24 hours at 37°°°°C and 5% CO 2 . The findings showed that both DMSO and catalase significantly reduced the arsenic-induced tail moment, a parameter of total damaged DNA, in HL60 and mononucleocytes. Hence our findings indicate that arsenic, with micromolar concentrations, induces typical and various extents of DNA damage in human cells via reactive oxygen species in a dose-dependent manner.

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Stimulation of reactive oxygen, but not reactive nitrogen species, in vascular endothelial cells exposed to low levels of arsenite

Cited by 240 publications

References 18 publications

Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling

Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling

The molecular mechanisms of arsenic-induced cell transformation and apoptosis.

Arsenic induces DNA damage via reactive oxygen species in human cells

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