Juglone, from Juglans mandshruica Maxim, inhibits growth and induces apoptosis in human leukemia cell HL-60 through a reactive oxygen species-dependent mechanism

2012 ◽  
Vol 50 (3-4) ◽  
pp. 590-596 ◽  
Author(s):  
Hua Li Xu ◽  
Xiao Feng Yu ◽  
Shao Chun Qu ◽  
Xiang Ru Qu ◽  
Yan Fang Jiang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Leukemia Cell ◽  
Reactive Oxygen ◽  
Human Leukemia ◽  
Oxygen Species ◽  
Human Leukemia Cell ◽  
Dependent Mechanism

scholarly journals Synergistic Apoptosis-Inducing Antileukemic Effects of Arsenic Trioxide andMucuna macrocarpaStem Extract in Human Leukemic Cells via a Reactive Oxygen Species-Dependent Mechanism

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Kuan-Hung Lu ◽  
Hui-Ju Lee ◽  
Min-Li Huang ◽  
Shang-Chih Lai ◽  
Yu-Ling Ho ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arsenic Trioxide ◽  
Reactive Oxygen ◽  
Butylated Hydroxytoluene ◽  
Leukemic Cells ◽  
Human Leukemia ◽  
Oxygen Species ◽  
Folk Remedy ◽  
Human Leukemic Cells ◽  
Dependent Mechanism

The objective of this study was to examine the potential of enhancing the antileukemic activity of arsenic trioxide (ATO) by combining it with a folk remedy, crude methanolic extract ofMucuna macrocarpa(CMEMM). Human leukemia cells HL-60, Jurkat, and Molt-3 were treated with various doses of ATO, CMEMM, and combinations thereof for 24 and 48 h. Results indicated that the combination of 2.5 μM ATO and 50 μg/mL CMEMM synergistically inhibited cell proliferation in HL-60 and Jurkat cell lines. Apoptosis triggered by ATO/CMEMM treatment was confirmed by accumulation of cells in the sub-G1phase in cell cycle analyses, characteristic apoptotic nuclear fragmentation, and increased percentage of annexin V-positive apoptotic cells. Such combination treatments also led to elevation of reactive oxygen species (ROS). The antioxidantsN-acetyl cysteine (NAC), butylated hydroxytoluene, andα-tocopherol prevented cells from ATO/CMEMM-induced apoptosis. The ATO/CMEMM-induced activation of caspase-3 and caspase-9 can be blocked by NAC. In summary, these results suggest that ATO/CMEMM combination treatment exerts synergistic apoptosis-inducing effects in human leukemic cells through a ROS-dependent mechanism and may provide a promising antileukemic approach in the future.

scholarly journals Dihydroceramide accumulation and reactive oxygen species are distinct and nonessential events in 4-HPR-mediated leukemia cell death

2012 ◽  
Vol 90 (2) ◽  
pp. 209-223 ◽  
Author(s):  
Aintzane Apraiz ◽  
Jolanta Idkowiak-Baldys ◽  
Naiara Nieto-Rementería ◽  
María Dolores Boyano ◽  
Yusuf A Hannun ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Vitamin E ◽  
Leukemia Cell ◽  
Reactive Oxygen ◽  
Jurkat Cells ◽  
Human Leukemia ◽  
Ros Production ◽  
Oxygen Species ◽  
Independent Events

4-(Hydroxyphenyl)retinamide (4-HPR) is a synthetic retinoid with a strong apoptotic effect towards different cancer cell lines in vitro, and it is currently tested in clinical trials. Increases of reactive oxygen species (ROS) and modulation of endogenous sphingolipid levels are well-described events observed upon 4-HPR treatment, but there is still a lack of understanding of their relationship and their contribution to cell death. LC–MS analysis of sphingolipids revealed that in human leukemia CCRF-CEM and Jurkat cells, 4-HPR induced dihydroceramide but not ceramide accumulation even at sublethal concentrations. Myriocin prevented the 4-HPR-induced dihydroceramide accumulation, but it did not prevent the loss of viability and increase of intracellular ROS production. On the other hand, ascorbic acid, Trolox, and vitamin E reversed 4-HPR effects on cell death but not dihydroceramide accumulation. NDGA, described as a lipoxygenase inhibitor, exerted a significantly higher antioxidant activity than vitamin E and abrogated 4-HPR-mediated ROS. It did not however rescue cellular viability. Taken together, this study demonstrates that early changes observed upon 4-HPR treatment, i.e., sphingolipid modulation and ROS production, are mechanistically independent events. Furthermore, the results indicate that 4-HPR-driven cell death may occur even in the absence of dihydroceramide or ROS accumulation. These observations should be taken into account for an improved design of drug combinations.

scholarly journals JP-8 Induces Immune Suppression via a Reactive Oxygen Species NF-κβ–Dependent Mechanism

2008 ◽  
Vol 108 (1) ◽  
pp. 100-109 ◽  
Author(s):  
Gerardo Ramos ◽  
Alberto Y. Limon-Flores ◽  
Stephen E. Ullrich
Keyword(s):  
Reactive Oxygen Species ◽  
Immune Suppression ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dependent Mechanism

scholarly journals Manganese-Oxidizing Antarctic Bacteria (Mn-Oxb) Release Reactive Oxygen Species (ROS) as Secondary Mn(II) Oxidation Mechanisms to Avoid Toxicity

Biology ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1004
Author(s):  
Ignacio Jofré ◽  
Francisco Matus ◽  
Daniela Mendoza ◽  
Francisco Nájera ◽  
Carolina Merino
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Soil Formation ◽  
Ros Production ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Cell Protection ◽  
Temperature Dependent ◽  
Antarctic Soils ◽  
Dependent Mechanism

Manganese (Mn) oxidation is performed through oxidative Mn-oxidizing bacteria (MnOxb) as the main bio-weathering mechanism for Mn(III/IV) deposits during soil formation. However, with an increase in temperature, the respiration rate also increases, producing Reactive Oxygen Species (ROS) as by-products, which are harmful to microbial cells. We hypothesize that bacterial ROS oxidize Mn(II) to Mn(III/IV) as a secondary non-enzymatic temperature-dependent mechanism for cell protection. Fourteen MnOxb were isolated from Antarctic soils under the global warming effect, and peroxidase (PO) activity, ROS, and Mn(III/IV) production were evaluated for 120 h of incubation at 4 °C, 15 °C, and 30 °C. ROS contributions to Mn oxidation were evaluated in Arthrobacter oxydans under antioxidant (Trolox) and ROS-stimulated (menadione) conditions. The Mn(III/IV) concentration increased with temperature and positively correlated with ROS production. ROS scavenging with Trolox depleted the Mn oxidation, and ROS-stimulant increased the Mn precipitation in A. oxydans. Increasing the Mn(II) concentration caused a reduction in the membrane potential and bacterial viability, which resulted in Mn precipitation on the bacteria surface. In conclusion, bacterial ROS production serves as a complementary non-enzymatic temperature-dependent mechanism for Mn(II) oxidation as a response in warming environments.

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