Anticancer organorhodium and -iridium complexes with low toxicity in vivo but high potency in vitro: DNA damage, reactive oxygen species formation, and haemolytic activity

2019 ◽  
Vol 55 (80) ◽  
pp. 12016-12019 ◽  
Author(s):  
Shahida Parveen ◽  
Muhammad Hanif ◽  
Euphemia Leung ◽  
Kelvin K. H. Tong ◽  
Annie Yang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Haemolytic Activity ◽  
Iridium Complexes ◽  
Oxygen Species ◽  
High Potency ◽  
Reactive Oxygen Species Formation ◽  
Species Formation ◽  
Low Toxicity

Dinuclear RhIII(Cp*) and IrIII(Cp*) complexes demonstrated potent in vitro anticancer activity while exhibiting low toxicity in haemolysis studies and in vivo zebrafish models.

scholarly journals Cytotoxic and Antitumor Activity of Sulforaphane: The Role of Reactive Oxygen Species

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Piero Sestili ◽  
Carmela Fimognari
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Cancer Therapies ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

According to recent estimates, cancer continues to remain the second leading cause of death and is becoming the leading one in old age. Failure and high systemic toxicity of conventional cancer therapies have accelerated the identification and development of innovative preventive as well as therapeutic strategies to contrast cancer-associated morbidity and mortality. In recent years, increasing body ofin vitroandin vivostudies has underscored the cancer preventive and therapeutic efficacy of the isothiocyanate sulforaphane. In this review article, we highlight that sulforaphane cytotoxicity derives from complex, concurring, and multiple mechanisms, among which the generation of reactive oxygen species has been identified as playing a central role in promoting apoptosis and autophagy of target cells. We also discuss the site and the mechanism of reactive oxygen species’ formation by sulforaphane, the toxicological relevance of sulforaphane-formed reactive oxygen species, and the death pathways triggered by sulforaphane-derived reactive oxygen species.

Hyperglycaemia modifies energy metabolism and reactive oxygen species formation in endothelial cells in vitro

2014 ◽  
Vol 542 ◽  
pp. 7-13 ◽  
Author(s):  
Dorota Dymkowska ◽  
Beata Drabarek ◽  
Paulina Podszywałow-Bartnicka ◽  
Joanna Szczepanowska ◽  
Krzysztof Zabłocki
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Energy Metabolism ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

scholarly journals Sirtuin 3 Alleviates Diabetic Cardiomyopathy by Regulating TIGAR and Cardiomyocyte Metabolism

2021 ◽  
Author(s):  
Lanfang Li ◽  
Heng Zeng ◽  
Xiaochen He ◽  
Jian‐Xiong Chen
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Cardiac Fibrosis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sirtuin 3 ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

Background Impairment of glycolytic metabolism is suggested to contribute to diabetic cardiomyopathy. In this study, we explored the roles of SIRT3 (Sirtuin 3) on cardiomyocyte glucose metabolism and cardiac function. Methods and Results Exposure of H9c2 cardiomyocyte cell lines to high glucose (HG) (30 mmol/L) resulted in a gradual decrease in SIRT3 and 6‐phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase isoform 3 (PFKFB3) expression together with increases in p53 acetylation and TP53‐induced glycolysis and apoptosis regulator (TIGAR) expression. Glycolysis was significantly reduced in the cardiomyocyte exposed to HG. Transfection with adenovirus‐SIRT3 significantly increased PFKFB3 expression and reduced HG‐induced p53 acetylation and TIGAR expression. Overexpression of SIRT3 rescued impaired glycolysis and attenuated HG–induced reactive oxygen species formation and apoptosis. Knockdown of TIGAR in cardiomyocytes by using siRNA significantly increased PFKFB3 expression and glycolysis under hyperglycemic conditions. This was accompanied by a significant suppression of HG–induced reactive oxygen species formation and apoptosis. In vivo, overexpression of SIRT3 by an intravenous jugular vein injection of adenovirus‐SIRT3 resulted in a significant reduction of p53 acetylation and TIGAR expression together with upregulation of PFKFB3 expression in the heart of diabetic db/db mice at day 14. Overexpression of SIRT3 further reduced reactive oxygen species formation and blunted microvascular rarefaction in the diabetic db/db mouse hearts. Overexpression of SIRT3 significantly blunted cardiac fibrosis and hypertrophy and improved cardiac function at day 14. Conclusions Our study demonstrated that SIRT3 attenuated diabetic cardiomyopathy via regulating p53 acetylation and TIGAR expression. Therefore, SIRT3 may be a novel target for abnormal energy metabolism in diabetes mellitus.

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