Nitric oxide inhibition of free radical-mediated lipid peroxidation in photodynamically treated membranes and cells

Niziolek, Magdalena; Korytowski, Witold; Girotti, Albert W.

doi:10.1016/s0891-5849(03)00026-1

Cited by 37 publications

(42 citation statements)

References 37 publications

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“…The precise mechanism may be dualistic, on one hand NO generation may be an important mediator of apoptosis and is responsible for susceptibility of cancerous cells [16,17], and on the other hand, as a known scavenger of organic free radicals, would suppress photodynamic therapy [18]. Our results suggested ROS and NO level, fold that NO played a less important role in the apoptosis induced by PDT.…”

Section: Generation Of Nomentioning

confidence: 63%

Mitochondria-involved apoptosis induced by MPPa mediated photodynamic therapy

Tian

et al. 2008

Laser Phys. Lett.

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Abstract:Numerous new photosensitizers are now in various stages of trials demonstrating the broad applicability of Photodynamic therapy (PDT). However, only a handful of photosensitizers have received regulatory approval. Lack of effective photosensitizers has become a major limit for extensive application of PDT. Our previous study showed MPPa to be a good photosensitizer candidature, MPPa-PDT can lead PC-3M cell line to death mainly via apoptotic way both in vitro and in vivo, and part of the mechanism was investigated. Mitochondria may play a key role in the process, in order to further elucidate the mechanism, we investigated the level of ROS, GSH, NO, Ca 2+ , mitochondrial membrane potential, as well as cytochrome C. All in all, ROS production, depletion of GSH, and the activation of ROS downstream, such as mitochondria depolarization, cytochrome C release, were detected in our study. The results provide a mechanism by which oxidative stress provokes apoptosis of PC-3M cells.

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Section: Generation Of Nomentioning

confidence: 63%

Mitochondria-involved apoptosis induced by MPPa mediated photodynamic therapy

Tian

et al. 2008

Laser Phys. Lett.

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“…Reaction of nitric oxide with superoxide causes formation of peroxynitrite that initiates lipid peroxidation via reaction of lipids with its decomposition products hydroxyl radical and nitrogen dioxide (Brookes et al, 1998;Rubbo et al, 1994). In contrast, nitric oxide itself may directly inhibit lipid peroxidation by intercepting alkoxyl and peroxyl radical intermediates thereby terminating chain propagation reactions (Nicolescu et al, 2002;Niziolek et al, 2003;Rubbo et al, 1994).…”

Section: Inhibition Of Lipid Peroxidationmentioning

confidence: 99%

Oxidants, antioxidants and the ischemic brain

Warner

Sheng

Batinić‐Haberle

2004

Journal of Experimental Biology

540

362

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SUMMARY Despite numerous defenses, the brain is vulnerable to oxidative stress resulting from ischemia/reperfusion. Excitotoxic stimulation of superoxide and nitric oxide production leads to formation of highly reactive products,including peroxynitrite and hydroxyl radical, which are capable of damaging lipids, proteins and DNA. Use of transgenic mutants and selective pharmacological antioxidants has greatly increased understanding of the complex interplay between substrate deprivation and ischemic outcome. Recent evidence that reactive oxygen/nitrogen species play a critical role in initiation of apoptosis, mitochondrial permeability transition and poly(ADP-ribose) polymerase activation provides additional mechanisms for oxidative damage and new targets for post-ischemic therapeutic intervention. Because oxidative stress involves multiple post-ischemic cascades leading to cell death, effective prevention/treatment of ischemic brain injury is likely to require intervention at multiple effect sites.

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“…Although the protective effect of NO against apoptotic death in several models has been attributed to an increase in the expression of heme oxygenase-1, heat shock protein 70 or Bcl-2 [184 -186], this was not the case in the protection of CCRF-CEM cells from photosensitization by pre-exposure to NO [183]. The presence of NO during the photosensitization period intercepted lipid-derived radicals and protected COH-BR1 cells (human breast tumor line) from necrotic cell death, in experiments where sensitization was induced via de metabolism of added ALA to PpIX [182,187].…”

Section: Nitric Oxide and Cgmpmentioning

confidence: 99%

Intracellular signaling mechanisms in photodynamic therapy

Almeida

Manadas

Carvalho

et al. 2004

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

242

292

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In photodynamic therapy (PDT) a sensitizer, light and oxygen are used to induce death of tumor cells and in the treatment of certain noncancerous conditions. Cell death in PDT may occur by apoptosis or by necrosis, depending on the sensitizer, on the PDT dose and on the cell genotype. Some sensitizers that have been used in PDT are accumulated in the mitochondria, and this may explain their efficiency in inducing apoptotic cell death, both in vitro and in vivo. In this review we will focus on the events that characterize apoptotic death in PDT and on the intracellular signaling events that are set in motion in photosensitized cells. Activation of phospholipases, changes in ceramide metabolism, a rise in the cytosolic free Ca 2 + concentration, stimulation of nitric oxide synthase (NOS), changes in protein phosphorylation and alterations in the activity of transcription factors and on gene expression have all been observed in PDT-treated cells. Although many of these metabolic reactions contribute to the demise process, some of them may antagonize cell death. Understanding the signaling mechanisms in PDT may provide means to modulate the PDT effects at the molecular level and potentiate its antitumor effectiveness. D

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Nitric oxide inhibition of free radical-mediated lipid peroxidation in photodynamically treated membranes and cells

Cited by 37 publications

References 37 publications

Mitochondria-involved apoptosis induced by MPPa mediated photodynamic therapy

Mitochondria-involved apoptosis induced by MPPa mediated photodynamic therapy

Oxidants, antioxidants and the ischemic brain

Intracellular signaling mechanisms in photodynamic therapy

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