Water-Soluble Dinitrosyl Iron Complex (DNIC): a Nitric Oxide Vehicle Triggering Cancer Cell Death via Apoptosis

2016 ◽  
Vol 55 (18) ◽  
pp. 9383-9392 ◽  
Author(s):  
Shou-Cheng Wu ◽  
Chung-Yen Lu ◽  
Yi-Lin Chen ◽  
Feng-Chun Lo ◽  
Ting-Yin Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Cancer Cell ◽  
Iron Complex ◽  
Water Soluble ◽  
Dinitrosyl Iron Complex ◽  
Cancer Cell Death ◽  
Dinitrosyl Iron

scholarly journals Statin-Induced Breast Cancer Cell Death: Role of Inducible Nitric Oxide and Arginase-Dependent Pathways

2007 ◽  
Vol 67 (15) ◽  
pp. 7386-7394 ◽  
Author(s):  
Srigiridhar Kotamraju ◽  
Carol L. Willams ◽  
Balaraman Kalyanaraman
Keyword(s):  
Breast Cancer ◽  
Nitric Oxide ◽  
Cell Death ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Death ◽  
Inducible Nitric Oxide

scholarly journals GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

2021 ◽  
Vol 22 (2) ◽  
pp. 622
Author(s):  
Mikhail G. Akimov ◽  
Alina M. Gamisonia ◽  
Polina V. Dudina ◽  
Natalia M. Gretskaya ◽  
Anastasia A. Gaydaryova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Nitric Oxide Synthase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Receptor Activation ◽  
Gene Expression Measurement ◽  
Fatty Acid Amides ◽  
Cancer Cell Death ◽  
Oxide Synthase

GPR55 is a GPCR of the non-CB1/CB2 cannabinoid receptor family, which is activated by lysophosphatidylinositol (LPI) and stimulates the proliferation of cancer cells. Anandamide, a bioactive lipid endocannabinoid, acts as a biased agonist of GPR55 and induces cancer cell death, but is unstable and psychoactive. We hypothesized that other endocannabinoids and structurally similar compounds, which are more hydrolytically stable, could also induce cancer cell death via GPR55 activation. We chemically synthesized and tested a set of fatty acid amides and esters for cell death induction via GPR55 activation. The most active compounds appeared to be N-acyl dopamines, especially N-docosahexaenoyl dopamine (DHA-DA). Using a panel of cancer cell lines and a set of receptor and intracellular signal transduction machinery inhibitors together with cell viability, Ca2+, NO, ROS (reactive oxygen species) and gene expression measurement, we showed for the first time that for these compounds, the mechanism of cell death induction differed from that published for anandamide and included neuronal nitric oxide synthase (nNOS) overstimulation with concomitant oxidative stress induction. The combination of DHA-DA with LPI, which normally stimulates cancer proliferation and is increased in cancer setting, had an increased cytotoxicity for the cancer cells indicating a therapeutic potential.

scholarly journals Endogenous Conjugation of Biomimetic Dinitrosyl Iron Complex with Protein Vehicles for Oral Delivery of Nitric Oxide to Brain and Activation of Hippocampal Neurogenesis

JACS Au ◽  
2021 ◽  
Author(s):  
Cheng-Ru Wu ◽  
Yi-Da Huang ◽  
Yong-Huei Hong ◽  
Ya-Hsin Liu ◽  
Manmath Narwane ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oral Delivery ◽  
Iron Complex ◽  
Hippocampal Neurogenesis ◽  
Dinitrosyl Iron Complex ◽  
Dinitrosyl Iron

scholarly journals Water-soluble SCR7 Can Abrogate DNA End Joining and Induce Cancer Cell Death

2020 ◽  
pp. 1-7
Author(s):  
Sathees C. Raghavan ◽  
Ujjayinee Ray ◽  
Anjana Elizabeth Jose ◽  
Rohini Suresh ◽  
Uthara Kaloor ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Water Soluble ◽  
Nonhomologous End Joining ◽  
Dependent Manner ◽  
End Joining ◽  
Cancer Cell Death ◽  
Subtle Effect ◽  
Ligase Iv ◽  
Dose Dependent

Small molecule inhibitors targeting DNA repair pathways in cancer cells is a novel and promising approach in cancer therapy, which can improve current therapeutic regimen. Although various attempts have been made for designing inhibitors against DNA damage response and repair proteins, reports on Nonhomologous End Joining (NHEJ) inhibitors are limited. Of the several chemical moieties identified, SCR7 and its oxidized form are novel and potent DNA Ligase IV inhibitors involved in the abrogation of DNA end joining thereby leading to cell death. In the present study, we have synthesized sodium salt of SCR7 to generate a water-soluble version of the molecule, referred to as water-soluble SCR7 (WS-SCR7). WS-SCR7 inhibits NHEJ in Ligase IV dependent manner, with a subtle effect on Ligase III at higher concentration. No effect on Ligase I mediated joining was observed. WS-SCR7 shows cytotoxicity in cancer cell lines, leading to induction of apoptosis in a dose-dependent manner.

Effects of the donor of nitric oxide, dinitrosyl iron complex with glutathione, on blood circulation in healthy animals

BIOPHYSICS ◽  
2008 ◽  
Vol 53 (5) ◽  
pp. 442-447
Author(s):  
M. I. Remizova ◽  
N. I. Kochetygov ◽  
K. A. Gerbut ◽  
A. F. Vanin
Keyword(s):  
Nitric Oxide ◽  
Blood Circulation ◽  
Iron Complex ◽  
Dinitrosyl Iron Complex ◽  
Dinitrosyl Iron

A water-soluble analog of triptolide induces ovarian cancer cell death in vitro and in vivo

2013 ◽  
Vol 130 (1) ◽  
pp. e130
Author(s):  
C. Rivard Hunt ◽  
M. Geller ◽  
C. Evans ◽  
R. Vogel ◽  
S. Ramakrishnan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Water Soluble ◽  
Cancer Cell Death

Abstract 3334: GSTP1-activated nitric oxide-releasing/PARP inhibitor hybrid prodrugs induce cancer cell death through ROS/RNS, DNA damage, ER stress, and apoptosis.

2013 ◽  
Author(s):  
Anna E. Maciag ◽  
Joseph E. Saavedra ◽  
Ryan J. Holland ◽  
Youseung Kim ◽  
Vandana Kumari ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Cell Death ◽  
Er Stress ◽  
Cancer Cell ◽  
Parp Inhibitor ◽  
Cancer Cell Death ◽  
Nitric Oxide Releasing

Selective Delivery of Nitric Oxide to a Cellular Target: A Pseudosubstrate-Coupled Dinitrosyl–Iron Complex Inhibits the Enteroviral Protease 2A

Nitric Oxide ◽  
2002 ◽  
Vol 6 (3) ◽  
pp. 305-312 ◽  
Author(s):  
Cornel Badorff ◽  
Birgit Fichtlscherer ◽  
Alexander Muelsch ◽  
Andreas M. Zeiher ◽  
Stefanie Dimmeler
Keyword(s):  
Nitric Oxide ◽  
Iron Complex ◽  
Dinitrosyl Iron Complex ◽  
Cellular Target ◽  
Dinitrosyl Iron ◽  
Selective Delivery ◽  
Protease 2A
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