Polyamine stimulation perturbs intracellular Ca2+ homeostasis and decreases viability of breast cancer BT474 cells

2020 ◽  
Vol 75 (3-4) ◽  
pp. 65-73
Author(s):  
Louis W.C. Chow ◽  
Kar-Lok Wong ◽  
Lian-Ru Shiao ◽  
King-Chuen Wu ◽  
Yuk-Man Leung
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Er Stress ◽  
Cyclopiazonic Acid ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Cytotoxic Effects ◽  
Store Depletion ◽  
Species Formation ◽  
Cancer Cell Survival

AbstractIntracellular polyamines such as spermine and spermidine are essential to cell growth in normal and especially in cancer cells. However, whether extracellular polyamines affect cancer cell survival is unknown. We therefore examined the actions of extracellular polyamines on breast cancer BT474 cells. Our data showed that spermine, spermidine, and putrescine decreased cell viability by apoptosis. These polyamines also elicited Ca2+ signals, but the latter were unlikely triggered via Ca2+-sensing receptor (CaSR) as BT474 cells have been demonstrated previously to lack CaSR expression. Spermine-elicited Ca2+ response composed of both Ca2+ release and Ca2+ influx. Spermine caused a complete discharge of the cyclopiazonic acid (CPA)-sensitive Ca2+ pool and, expectedly, endoplasmic reticulum (ER) stress. The Ca2+ influx pore opened by spermine was Mn2+-impermeable, distinct from the CPA-triggered store-operated Ca2+ channel, which was Mn2+-permeable. Spermine cytotoxic effects were not due to oxidative stress, as spermine did not trigger reactive oxygen species formation. Our results therefore suggest that spermine acted on a putative polyamine receptor in BT474 cells, causing cytotoxicity by Ca2+ overload, Ca2+ store depletion, and ER stress.

scholarly journals Type I toxin-dependent generation of superoxide affects the persister life cycle of Escherichia coli

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Daniel Edelmann ◽  
Bork A. Berghoff
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Life Cycle ◽  
Type I ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation ◽  
Genes Encoding ◽  
Oxidative Challenge ◽  
Detailed Work

Abstract Induction of growth stasis by bacterial toxins from chromosomal toxin-antitoxin systems is suspected to favor formation of multidrug-tolerant cells, named persisters. Recurrent infections are often attributed to resuscitation and regrowth of persisters upon termination of antibiotic therapy. Several lines of evidence point to oxidative stress as a crucial factor during the persister life cycle. Here, we demonstrate that the membrane-depolarizing type I toxins TisB, DinQ, and HokB have the potential to provoke reactive oxygen species formation in Escherichia coli. More detailed work with TisB revealed that mainly superoxide is formed, leading to activation of the SoxRS regulon. Deletion of the genes encoding the cytoplasmic superoxide dismutases SodA and SodB caused both a decline in TisB-dependent persisters and a delay in persister recovery upon termination of antibiotic treatment. We hypothesize that expression of depolarizing toxins during the persister formation process inflicts an oxidative challenge. The ability to counteract oxidative stress might determine whether cells will survive and how much time they need to recover from dormancy.

scholarly journals Kallistatin attenuates endothelial apoptosis through inhibition of oxidative stress and activation of Akt-eNOS signaling

2010 ◽  
Vol 299 (5) ◽  
pp. H1419-H1427 ◽  
Author(s):  
Bo Shen ◽  
Lin Gao ◽  
Yi-Te Hsu ◽  
Grant Bledsoe ◽  
Makato Hagiwara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Oxygen Species ◽  
Phosphatidylinositol 3 Kinase ◽  
Reactive Oxygen Species Formation ◽  
Endothelial Apoptosis ◽  
Species Formation ◽  
Tnf Α

Kallistatin is a regulator of vascular homeostasis capable of controlling a wide spectrum of biological actions in the cardiovascular and renal systems. We previously reported that kallistatin inhibited intracellular reactive oxygen species formation in cultured cardiac and renal cells. The present study was aimed to investigate the role and mechanisms of kallistatin in protection against oxidative stress-induced vascular injury and endothelial cell apoptosis. We found that kallistatin gene delivery significantly attenuated aortic superoxide formation and glomerular capillary loss in hypertensive DOCA-salt rats. In cultured endothelial cells, kallistatin suppressed TNF-α-induced cellular apoptosis, and the effect was blocked by the pharmacological inhibition of phosphatidylinositol 3-kinase and nitric oxide synthase (NOS) and by the knockdown of endothelial NOS (eNOS) expression. The transduction of endothelial cells with adenovirus expressing dominant-negative Akt abolished the protective effect of kallistatin on endothelial apoptosis and caspase activity. In addition, kallistatin inhibited TNF-α-induced reactive oxygen species formation and NADPH oxidase activity, and these effects were attenuated by phosphatidylinositol 3-kinase and NOS inhibition. Kallistatin also prevented the induction of Bim protein and mRNA expression by oxidative stress. Moreover, the downregulation of forkhead box O 1 (FOXO1) and Bim expression suppressed TNF-α-mediated endothelial cell death. Furthermore, the antiapoptotic actions of kallistatin were accompanied by Akt-mediated FOXO1 and eNOS phosphorylation, as well as increased NOS activity. These findings indicate a novel role of kallistatin in the protection against vascular injury and oxidative stress-induced endothelial apoptosis via the activation of Akt-dependent eNOS signaling.

scholarly journals Increased Reactive Oxygen Species Formation and Oxidative Stress in Rheumatoid Arthritis

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0152925 ◽  
Author(s):  
Somaiya Mateen ◽  
Shagufta Moin ◽  
Abdul Qayyum Khan ◽  
Atif Zafar ◽  
Naureen Fatima
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation ◽  
And Oxidative Stress

Increased Demethylmenaquinone‐Dependent Reactive Oxygen Species Formation by Β-Lactams in Enterococcus Faecalis

2018 ◽  
Author(s):  
Loïc Léger ◽  
Aurélie Budin-Verneuil ◽  
Margherita Cacaci ◽  
Abdellah Benachour ◽  
Axel Hartke ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Enterococcus Faecalis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

Carcinogenic metal induced sites of reactive oxygen species formation in hepatocytes

2003 ◽  
Vol 17 (5-6) ◽  
pp. 803-810 ◽  
Author(s):  
Jalal Pourahmad ◽  
Peter J O‘Brien ◽  
Farzaneh Jokar ◽  
Bahram Daraei
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

scholarly journals Roles of Superoxide dismutase(SOD) , Malondialdehyde (MDA), 8-iso-prostaglandinF2α ( 8-iso-PGF2α)as oxidative stress in development and progression of Brest cancer in Iraqi females patients

2020 ◽  
Vol 25 (1) ◽  
pp. 1-4
Author(s):  
Ferdous Abbas Jabir ◽  
Ahmed Sabah Shaker
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Patients ◽  
Antioxidant Defenses ◽  
Blood Levels ◽  
P Value ◽  
Oxygen Species ◽  
Breast Cancer Patients ◽  
Markers Of Oxidative Stress ◽  
The Mean

               Oxidative stress occurs as a result of disturbance in the balance between the production of reactive oxygen species (free radicals) and antioxidant defenses. Markers of oxidative stress were measured the markers of oxidative stress in breast cancer patients after diagnosis of breast cancer and compared these plasma blood levels controls This study was conducted to three markers of oxidative stress ;these are (SOD) enzyme ,malondialdehyde (MDA)and8-iso-prostaglandinF2α plasma of patients with breast cancer and compare with controls .In this study ;  the mean MDA (ng/ml) levels for the breast cancer patients and the controls were55.91±3.31 and40.61±3.76  respectively, while the SOD (pg/ml) levels were1530.37±80.4 and1851.4 9±93.65  respectively and the 8-iso-PGF2α (ng/ml ) levels were 40.16±3.31 and 30.16±2.34  difference of the mean were statistically significant (p value <0.05).                                                                                                                       

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