scholarly journals Comparative analysis of thymic subpopulations during different modes of atrophy identifies the reactive oxygen species scavenger,N‐acetyl cysteine, to increase the survival of thymocytes during infection‐induced and lipopolysaccharide‐induced thymic atrophy

Immunology ◽  
2019 ◽  
Vol 157 (1) ◽  
pp. 21-36 ◽  
Author(s):  
Shamik Majumdar ◽  
Vasista Adiga ◽  
Abinaya Raghavan ◽  
Supriya Rajendra Rananaware ◽  
Dipankar Nandi
Temperature ◽  
2014 ◽  
Vol 1 (3) ◽  
pp. 227-241 ◽  
Author(s):  
Manuel Sanchez-Alavez ◽  
Nikki Bortell ◽  
Andrea Galmozzi ◽  
Bruno Conti ◽  
Maria Cecilia G. Marcondes

2020 ◽  
Vol 332 ◽  
pp. 118-129
Author(s):  
Kush N. Shah ◽  
Parth N. Shah ◽  
Andrew R. Mullen ◽  
Qingquan Chen ◽  
Marie R. Southerland ◽  
...  

1992 ◽  
Vol 72 (4) ◽  
pp. 1549-1556 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms

The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been shown to constrict both bronchial and coronary vascular smooth muscle through the action of cyclooxygenase or lipoxygenase products. We observed that intravenous FMLP increased pulmonary vascular resistance (PVR) in isolated buffer-perfused rabbit lungs. FMLP increased the PVR (primarily in the middle segment of the pulmonary vascular bed) at concentrations greater than or equal to 10(-7) M. Maximum vasoconstriction occurred at 5 min and then slowly declined to a level that remained above baseline at 30 min. Tachyphylaxis was observed in response to FMLP. When polymorphonuclear leukocytes (PMNs) were added to the perfusate, FMLP caused a greater increase in PVR. PMN depletion with dimethylmyleran significantly reduced the PVR response to FMLP. Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate and ibuprofen, and the leukotriene synthesis blocker MK 886 had no effect on the FMLP-induced vasoconstriction. However, the reactive oxygen species scavenger catalase significantly reduced the vasoconstriction. These results suggest that FMLP induces vasoconstriction that is dependent on PMNs and mediated by reactive oxygen species with no involvement of cyclooxygenase or lipoxygenase products.


Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 257
Author(s):  
Qiang Li ◽  
Hélène San Clemente ◽  
Yongrui He ◽  
Yongyao Fu ◽  
Christophe Dunand

Eucalyptus is a worldwide hard-wood species which increasingly focused on. To adapt to various biotic and abiotic stresses, Eucalyptus have evolved complex mechanisms, increasing the cellular concentration of reactive oxygen species (ROS) by numerous ROS controlling enzymes. To better analyse the ROS gene network and discuss the differences between four Eucalyptus species, ROS gene network including 11 proteins families (1CysPrx, 2CysPrx, APx, APx-R, CIII Prx, Diox, GPx, Kat, PrxII, PrxQ and Rboh) were annotated and compared in an expert and exhaustive manner from the genomic data available from E. camaldulensis, E. globulus, E. grandis, and E. gunnii. In addition, a specific sequencing strategy was performed in order to determine if the missed sequences in at least one organism are the results of gain/loss events or only sequencing gaps. We observed that the automatic annotation applied to multigenic families is the source of miss-annotation. Base on the family size, the 11 families can be categorized into duplicated gene families (CIII Prx, Kat, 1CysPrx, and GPx), which contain a lot of gene duplication events and non-duplicated families (APx, APx-R, Rboh, DiOx, 2CysPrx, PrxII, and PrxQ). The gene family sizes are much larger in Eucalyptus than most of other angiosperms due to recent gene duplications, which could give higher adaptability to environmental changes and stresses. The cross-species comparative analysis shows gene gain and loss events during the evolutionary process. The 11 families possess different expression patterns, while in the Eucalyptus genus, the ROS families present similar expression patterns. Overall, the comparative analysis might be a good criterion to evaluate the adaptation of different species with different characters, but only if data mining is as exhaustive as possible. It is also a good indicator to explore the evolutionary process.


Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1895-1903 ◽  
Author(s):  
Michael V. Cohen ◽  
Xi-Ming Yang ◽  
James M. Downey

Background— It is unclear how reperfusion of infarcting hearts with alternating cycles of coronary reperfusion/occlusion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) formation is crucial. Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation. Methods and Results— After 30-minute regional ischemia in isolated rabbit hearts, reperfusion with buffer (pH 7.4) caused 34.4±2.2% of the risk zone to infarct, whereas 2 minutes of postconditioning (6 cycles of 10-second reperfusion/10-second occlusion) at reperfusion resulted in 10.7±2.9% infarction. One minute (3 cycles) of postconditioning was not protective. Hypercapnic buffer (pH 6.9) for the first 2 minutes of reperfusion in lieu of postconditioning caused equivalent cardioprotection (15.0±2.6% infarction), whereas 1 minute of acidosis did not protect. Delaying postconditioning (6 cycles) or 2 minutes of acidosis for 1 minute aborted protection. Reperfusion with buffer (pH 7.7) blocked postconditioning protection, but addition of the MPTP closer cyclosporin A restored protection. Reactive oxygen species scavenger N-2-mercaptopropionyl glycine, protein kinase C antagonist chelerythrine, and mitochondrial K ATP channel closer 5-hydroxydecanoate each blocked protection from 2 minutes of acidosis as they did for postconditioning. Conclusion— Thus, postconditioning prevents MPTP formation by maintaining acidosis during the first minutes of reperfusion as reoxygenated myocardium produces reactive oxygen species that activate protective signaling to inhibit MPTP formation after pH normalization.


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