Direct Visualization of Enzymatic Cleavage and Oxidative Damage by Hydroxyl Radicals of Single-Stranded DNA with a Cationic Polythiophene Derivative

2006 ◽  
Vol 128 (46) ◽  
pp. 14972-14976 ◽  
Author(s):  
Yanli Tang ◽  
Fude Feng ◽  
Fang He ◽  
Shu Wang ◽  
Yuliang Li ◽  
...  
2003 ◽  
Vol 69 (11) ◽  
pp. 6500-6506 ◽  
Author(s):  
Paula A. Belinky ◽  
Nufar Flikshtein ◽  
Sergey Lechenko ◽  
Shimon Gepstein ◽  
Carlos G. Dosoretz

ABSTRACT We studied oxidative stress in lignin peroxidase (LIP)-producing cultures (cultures flushed with pure O2) of Phanerochaete chrysosporium by comparing levels of reactive oxygen species (ROS), cumulative oxidative damage, and antioxidant enzymes with those found in non-LIP-producing cultures (cultures grown with free exchange of atmospheric air [control cultures]). A significant increase in the intracellular peroxide concentration and the degree of oxidative damage to macromolecules, e.g., DNA, lipids, and proteins, was observed when the fungus was exposed to pure O2 gas. The specific activities of manganese superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase and the consumption of glutathione were all higher in cultures exposed to pure O2 (oxygenated cultures) than in cultures grown with atmospheric air. Significantly higher gene expression of the LIP-H2 isozyme occurred in the oxygenated cultures. A hydroxyl radical scavenger, dimethyl sulfoxide (50 mM), added to the culture every 12 h, completely abolished LIP expression at the mRNA and protein levels. This effect was confirmed by in situ generation of hydroxyl radicals via the Fenton reaction, which significantly enhanced LIP expression. The level of intracellular cyclic AMP (cAMP) was correlated with the starvation conditions regardless of the oxygenation regimen applied, and similar cAMP levels were obtained at high O2 concentrations and in cultures grown with atmospheric air. These results suggest that even though cAMP is a prerequisite for LIP expression, high levels of ROS, preferentially hydroxyl radicals, are required to trigger LIP synthesis. Thus, the induction of LIP expression by O2 is at least partially mediated by the intracellular ROS.


2003 ◽  
Vol 11 (17) ◽  
pp. 3747-3751 ◽  
Author(s):  
Akimitsu Okamoto ◽  
Kazuhito Tanabe ◽  
Isao Saito

2010 ◽  
Vol 48 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Giuliano Bellapadrona ◽  
Matteo Ardini ◽  
Pierpaolo Ceci ◽  
Simonetta Stefanini ◽  
Emilia Chiancone

2015 ◽  
Vol 51 (15) ◽  
pp. 3266-3269 ◽  
Author(s):  
Soumya V. Nair ◽  
Małgorzata A. Witek ◽  
Joshua M. Jackson ◽  
Maria A. M. Lindell ◽  
Sally A. Hunsucker ◽  
...  

We report rapid enzymatic release of affinity-selected cells with 90% efficiency and cells viability of 85%.


2010 ◽  
Vol 25 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Agnieszka Zielinska ◽  
Owain T. Davies ◽  
Rosalind A. Meldrum ◽  
Nikolas J. Hodges

2009 ◽  
Vol 32 (9) ◽  
pp. 592-599 ◽  
Author(s):  
Madanahally D. Kiran ◽  
Naomi Balaban

Staphylococci are common pathogens of implant-related infections. RIP is a heptapeptide (YSPWTNF-NH2) that was shown to be very effective in preventing and treating antibiotic-resistant staphylococcal infections, in healing polymicrobial wounds, and in enhancing the effect of commonly used antibiotics. How the peptide negatively affects the survival of the bacteria in the host is not yet known. In staphylococci, RIP was shown to suppress toxin production by inhibiting the expression of agr and production of RNAIII. RIP was also shown to suppress the phosphorylation of TRAP (target of RNAIII-activating peptide), whose function was not clear. Here we show that mutant S. aureus TRAP- cells were more sensitive to oxidative stress and had higher rates of spontaneous and adaptive (agr) mutations. Furthermore, recombinant TRAP protected DNA from oxidative damage caused by hydroxyl radicals. Put together, these results suggest that TRAP is involved in DNA protection from stress. RIP may thus suppress pathogenesis through multiple independent molecular mechanisms involving both suppression of virulence and suppression of stress response.


1993 ◽  
Vol 69 (3) ◽  
pp. 789-800 ◽  
Author(s):  
Ron Kohen ◽  
Vered Shadmi ◽  
Angel Kakunda ◽  
Abraham Rubinstein

The role of the soluble non-starch polysaccharide pectin in the prevention of oxidative damage induced by peroxy, superoxide and hydroxyl radicals to the rat jejunal mucosa was studied. The oxidative stress was introduced to the rat jejunal mucosa by means of a closed-loop perfusion system and was characterized biochemically by monitoring the enterocyte activity of the enzyme lactate dehydrogenase (EC1·1·1·27) and the K+level. Aqueous solutions of pectin were perfused into the rat jejunum before the oxidative stress inducers. The possible protection effect was evaluated by comparing the mucosal integrity (as measured by biochemical variables) to the values obtained after perfusion with the oxidative stress inducers only. We found that: (a) mucosal damage was detected following the perfusion of peroxy and hydroxyl radicals in the rat jejunum, but not following perfusion of the superoxide radical; (b)a significant reduction in the mucosal damage was noted when pectin was perfused before the perfusion with the peroxy radical induction; (c)full protection against the mucosal damage induced by hydroxyl radicals was achieved when pectin was perfused before the damage induction.


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