The origin of reactive oxygen species in mouse embryos cultured in vitro

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 551-560 ◽  
Author(s):  
M.M. Nasr-Esfahani ◽  
M.H. Johnson

The increase in production of reactive oxygen species such as H2O2 at the G2/M phase of the second cell cycle may be related to the in vitro block to development of mouse 2-cell embryos. The occurrence of the H2O2 rise is independent of the activation of the embryonic genome and of passage through the S, G2 and M phases of the first cell cycle and G1 and M phases of the second cell cycle, but does require the activation of the unfertilized oocyte. The H2O2 is produced via dismutation of superoxide by the enzyme superoxide dismutase. Production of superoxide via mitochondrial, NADPH-oxidase and xanthine/xanthine oxidase systems has been investigated. The evidence suggests that superoxide, and thereby H2O2, is produced by the xanthine/xanthine oxidase system, but an involvement of the other superoxide generating systems has not been excluded. The relation between H2O2 and development in vitro is discussed.

1996 ◽  
Vol 24 (4) ◽  
pp. 345-351 ◽  
Author(s):  
H Akamatsu ◽  
Y Niwa ◽  
H Sasaki ◽  
Y Matoba ◽  
Y Asada ◽  
...  

The effects of ofloxacin, ciprofloxacin and balofloxacin on the reactive oxygen species (ROS) levels generated by human neutrophils was examined in vitro; ROS generated in a cell-free, xanthine–xanthine oxidase system was also assessed. The species investigated were superoxide radical anion (O2−), hydrogen peroxide (H2O2) and hydroxyl radical (OH·). Both ofloxacin and ciprofloxacin markedly decreased the levels of O2−, H2O2 and OH· generated by human neutrophils. On the other hand, these drugs did not affect any of the ROS examined in the xanthine-xanthine oxidase system. Balofloxacin showed no significant effect on ROS generated by either system. The present study indicates that ofloxacin and ciprofloxacin may exert an anti-inflammatory action by reducing the potent ROS species excessively generated by neutrophils at the sites of inflammation.


2007 ◽  
Vol 568 (1-3) ◽  
pp. 31-44 ◽  
Author(s):  
Jieliang Li ◽  
Hon-Yeung Cheung ◽  
Zhiqiang Zhang ◽  
Gallant K.L. Chan ◽  
Wang-Fun Fong

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Ke He ◽  
Lu Wu ◽  
Qianshan Ding ◽  
Farhan Haider ◽  
Honggang Yu ◽  
...  

At present, apatinib is considered a new generation agent for the treatment of patients with gastric cancer. However, the effects of apatinib on pancreatic cancer have not been clarified. This study investigated the impact of apatinib on the biological function of pancreatic cancer cells and the potential mechanism involved in this process. Using the Cell Counting Kit-8 method, we confirmed that apatinib treatment inhibited cell proliferation in vitro. Moreover, the migration rate of pancreatic cells was inhibited. The effects of apatinib on apoptosis and cell cycle distribution of pancreatic carcinoma cells were detected by flow cytometry. The number of apoptotic cells was significantly increased, and the cell cycle was altered. Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro. Apatinib significantly inhibited the biological function of pancreatic cancer cells. It promoted apoptosis, downregulated the expression of HIF-1α, and increased the levels of reactive oxygen species.


1996 ◽  
Vol 24 (1) ◽  
pp. 27-32 ◽  
Author(s):  
H Akamatsu ◽  
S Nishijima ◽  
M Akamatsu ◽  
I Kurokawa ◽  
H Sasaki ◽  
...  

The effect of roxithromycin (ROM), a new oral semisynthetic macrolide, on the generation of reactive oxygen species (ROS), using human neutrophils and a cell-free, xanthine-xanthine oxidase system was examined. The species investigated were the superoxide radical anion (O2−), hydrogen peroxide (H2O2), and the hydroxyl radical (OH·). ROM effectively inhibited the generation of O2−, H2O2 and OH· by human neutrophils. On the other hand, the drug did not markedly affect the ROS levels generated in the xanthine-xanthine oxidase system. The present study indicates that ROM may exert an anti-inflammatory action by inhibiting neutrophil oxygen radical generation at the sites of inflammation.


1998 ◽  
Vol 84 (3) ◽  
pp. 948-953 ◽  
Author(s):  
John M. Lawler ◽  
Z. Hu ◽  
W. S. Barnes

Reactive oxygen species (ROS) are postulated to alter low-frequency contractility of the unfatigued and fatigued diaphragm. It has been proposed that ROS affect contractility through changes in membrane excitability and excitation-contraction coupling. If this hypothesis is true, then ROS should alter depolarization-dependent K+contractures. Xanthine oxidase (0.01 U/ml) + hypoxanthine (1 mM) were used as a source of superoxide anion eliciting oxidative stress on diaphragm fiber bundles in vitro. Diaphragm fiber bundles from 4-mo-old Fischer 344 rats were extracted and immediately placed in Krebs solution bubbled with 95% O2-5% CO2. After 10 min of equilibration, a K+ contracture (Pre; 135 mM KCl) was induced. Fiber bundles were assigned to the following treatment groups: normal Krebs-Ringer (KR; Con) and the xanthine oxidase system (XO) in KR solution. After 15 min of treatment exposure, a second (Post) K+contracture was elicited. Mean time-to-peak tension for contractures was significantly decreased in Post vs. Pre (16.0 ± 0.7 vs. 19.8 ± 1.0 s) with XO; no change was noted with Con. Furthermore, peak contracture tension was significantly higher (31.5%) in the XO group Post compared with Pre; again, no significant change was found with KR. The relaxation phase was also altered with XO but not with KR. Additional experiments were conducted with application of 1 mM hypoxanthine, with results similar to the Con group. We conclude that the application of ROS altered the dynamics of K+ contractures in the rat diaphragm, indicating changes in voltage-dependent excitation-contraction coupling.


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