Does hydrogen peroxide exist “free” in biological systems?

Schubert, Jack; Wilmer, J.W.G.M.

doi:10.1016/0891-5849(91)90135-p

Cited by 83 publications

(39 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mucus also is known to have antioxidant capabilities (44). The sugar moieties in mucus may act similarly to mannitol and glucose in scavenging hydroxyl radical and H202 (45,46). Mucus glycoproteins react with H202; in the process both H202 and glycoproteins are degraded (44,47,48 (52), increased nonspecific airway reactivity, increased specific airway resistance, increased respiratory frequency on exercise, and an involuntary reduction of maximal inspiratory capacity (53).…”

Section: Nonenzymatic Antioxidant Defensesmentioning

confidence: 99%

Interactions of oxygen radicals with airway epithelium.

Wright

Cohn

et al. 1994

Environ Health Perspect

View full text Add to dashboard Cite

Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable regarding potential for oxidative damage due to their potential for exposure to both endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms) oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain vitamins and low molecular weight compounds such as thiols. The enzymes superoxide dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection. Other materials associated with airway epithelium such as mucus, epithelial lining fluid, and even the basement membrane/extracellular matrix may have protective actions as well. When the normal balance between oxidants and antioxidants is upset, oxidant stress ensues and subsequent epithelial cell alterations or damage may be a critical component in the pathogenesis of several respiratory diseases. Oxidant stress may profoundly alter lung physiology including pulmonary function (e.g., forced expiratory volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and airway reactivity. ROS may induce airway inflammation; the inflammatory process may serve as an additional source of ROS in airways and provoke the pathophysiologic responses described. On a more fundamental level, cellular mechanisms in the pathogenesis of ROS may involve activation of intracellular signaling enzymes including phospholipases and protein kinases stimulating the release of inflammatory lipids and cytokines. Respiratory epithelium may be intimately involved in defense against, and pathophysiologic changes invoked by, ROS. -Environ Health Perspect 1 02(Suppl 1 0): 85-90 (1994)

show abstract

Section: Nonenzymatic Antioxidant Defensesmentioning

confidence: 99%

Interactions of oxygen radicals with airway epithelium.

Wright

Cohn

et al. 1994

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…In consideration of the widespread damage to cytoplasmic RNA in neurodegenerative diseases, RNA species are likely attacked by •OH, which is formed from the reaction of highly diffusible H 2 O 2 [90] with redox-active metals through the Fenton reaction [53]. In the AD brain, disrupted mitochondria likely play a central role in producing abundant ROS as well as supplying redox-active iron into the cytosol [8,[91][92][93].…”

Section: Sources Of Reactive Oxygen Species (Ros) Responsible For Celmentioning

confidence: 99%

Oxidative RNA Damage and Neurodegeneration

Nunomura¹,

Moreira

Takeda³

et al. 2007

CMC

View full text Add to dashboard Cite

show abstract

“…5 These free radicals may damage several molecules including DNA. Different modified DNA bases have been identified by treating mammalian cells with HP, 6 and it has been proven that the biological effect of HP is mediated by hydrogen bonded HP adducts, 7 which could be due to the enhanced HP stability by adduct formation. In addition, neutral HP adducts seem to cross the cell membrane, carrying extracellular HP to intracellular targets.…”

Section: Introductionmentioning

confidence: 99%

Adenine−Hydrogen Peroxide System: DFT and MP2 Investigation

Dobado

Molina

1999

J. Phys. Chem. A

View full text Add to dashboard Cite

Theoretical calculations have been performed for different possible hydrogen bonding complexes between adenine and hydrogen peroxide (AHP). The studied complexes (1-6) were cyclic ones showing two hydrogen bonds of different strength. All of the structures have been characterized at the B3LYP/6-31G(2d,p) and MP2(full)/6-31G(2d,p) levels, yielding only real frequencies (minima) at the B3LYP/6-31G(2d,p). The binding energies have been carried out for all of the structures, taking into account the so-called BSSE and yielding for the most stable structure 6 values of -11.53 and -11.95 kcal/mol at the B3LYP and MP2 levels, respectively. BSSE-free PES calculations were also performed for several complexes. The Bader analyses were also applied to investigate the hydrogen bonding electronic properties.

show abstract

Does hydrogen peroxide exist “free” in biological systems?

Cited by 83 publications

References 32 publications

Interactions of oxygen radicals with airway epithelium.

Interactions of oxygen radicals with airway epithelium.

Oxidative RNA Damage and Neurodegeneration

Adenine−Hydrogen Peroxide System: DFT and MP2 Investigation

Contact Info

Product

Resources

About