scholarly journals Acute apoptosis by cisplatin requires induction of reactive oxygen species but is not associated with damage to nuclear DNA

2006 ◽  
Vol 120 (1) ◽  
pp. 175-180 ◽  
Author(s):  
Maria Berndtsson ◽  
Maria Hägg ◽  
Theocharis Panaretakis ◽  
Aleksandra Mandic Havelka ◽  
Maria C. Shoshan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nuclear Dna ◽  
Reactive Oxygen ◽  
Oxygen Species

Activation of NF-κB induced by H2O2 and TNF-α and its effects on ICAM-1 expression in endothelial cells

2000 ◽  
Vol 279 (2) ◽  
pp. L302-L311 ◽  
Author(s):  
Andrea L. True ◽  
Arshad Rahman ◽  
Asrar B. Malik
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Nuclear Dna ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Intercellular Adhesion Molecule ◽  
Oxygen Species ◽  
Tnf Α

Reactive oxygen species have been proposed to signal the activation of the transcription factor nuclear factor (NF)-κB in response to tumor necrosis factor (TNF)-α challenge. In the present study, we investigated the effects of H2O2 and TNF-α in mediating activation of NF-κB and transcription of the intercellular adhesion molecule (ICAM)-1 gene. Northern blot analysis showed that TNF-α exposure of human dermal microvascular endothelial cells (HMEC-1) induced marked increases in ICAM-1 mRNA and cell surface protein expression. In contrast, H2O2 added at subcytolytic concentrations failed to activate ICAM-1 expression. Challenge with H2O2 also failed to induce NF-κB-driven reporter gene expression in the transduced HMEC-1 cells, whereas TNF-α increased the NF-κB-driven gene expression ∼10-fold. Gel supershift assay revealed the presence of p65 (Rel A), p50, and c-Rel in both H2O2- and TNF-α-induced NF-κB complexes bound to the ICAM-1 promoter, with the binding of the p65 subunit being the most prominent. In vivo phosphorylation studies, however, showed that TNF-α exposure induced marked phosphorylation of NF-κB p65 in HMEC-1 cells, whereas H2O2 had no effect. These results suggest that reactive oxygen species generation in endothelial cells mediates the binding of NF-κB to nuclear DNA, whereas TNF-α generates additional signals that induce phosphorylation of the bound NF-κB p65 and confer transcriptional competency to NF-κB.

scholarly journals Cytotoxic Effect of Curcumin on Malaria Parasite Plasmodium falciparum: Inhibition of Histone Acetylation and Generation of Reactive Oxygen Species

2006 ◽  
Vol 51 (2) ◽  
pp. 488-494 ◽  
Author(s):  
Long Cui ◽  
Jun Miao ◽  
Liwang Cui
Keyword(s):  
Reactive Oxygen Species ◽  
Plasmodium Falciparum ◽  
Cytotoxic Effect ◽  
Nuclear Dna ◽  
Reactive Oxygen ◽  
Multidrug Resistant ◽  
Oxygen Species ◽  
Mammalian Cell Lines ◽  
Parasite Plasmodium Falciparum

ABSTRACT The emergence of multidrug-resistant parasites is a major concern for malaria control, and development of novel drugs is a high priority. Curcumin, a natural polyphenolic compound, possesses diverse pharmacological properties. Among its antiprotozoan activities, curcumin was potent against both chloroquine-sensitive and -resistant Plasmodium falciparum strains. Consistent with findings in mammalian cell lines, curcumin's prooxidant activity promoted the production in P. falciparum of reactive oxygen species (ROS), whose cytotoxic effect could be antagonized by coincubation with antioxidants and ROS scavengers. Curcumin treatment also resulted in damage of both mitochondrial and nuclear DNA, probably due to the elevation of intracellular ROS. Furthermore, we have demonstrated that curcumin inhibited the histone acetyltransferase (HAT) activity of the recombinant P. falciparum general control nonderepressed 5 (PfGCN5) in vitro and reduced nuclear HAT activity of the parasite in culture. Curcumin-induced hypoacetylation of histone H3 at K9 and K14, but not H4 at K5, K8, K12, and K16, suggested that curcumin caused specific inhibition of the PfGCN5 HAT. Taken together, these results indicated that at least the generation of ROS and down-regulation of PfGCN5 HAT activity accounted for curcumin's cytotoxicity for malaria parasites.

scholarly journals Mitochondrial reactive oxygen species are scavenged by Cockayne syndrome B protein in human fibroblasts without nuclear DNA damage

2014 ◽  
Vol 111 (37) ◽  
pp. 13487-13492 ◽  
Author(s):  
James E. Cleaver ◽  
Angela M. Brennan-Minnella ◽  
Raymond A. Swanson ◽  
Ka-wing Fong ◽  
Junjie Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Nuclear Dna ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Cockayne Syndrome ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Fas ligand expression in rat kupffer cells in response to lipopolysaccharide is mediated by reactive oxygen species

2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ligand Expression
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