Nitric oxide-induced resistance to lethal photooxidative damage in a breast tumor cell line

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

doi:10.1016/j.freeradbiomed.2005.11.022

Cited by 33 publications

(30 citation statements)

References 42 publications

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“…Photodynamic treatment was shown to generate rapidly NO in various cell lines 13,14,15 . Some authors showed that NO protects cells from PDT-induced death either through inhibition of lipid peroxidation in cellular membranes 16,17 or through initiation of the cGMP-dependent signaling pathway 18 . Di Venosa et al 19 , however, did not observe any relationships between NO production and photodynamic cell injury.…”

Section: Discussionmentioning

confidence: 99%

The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

2015

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Nitric oxide (NO) is an important second messenger, involved in the implementation of various cell functions. It regulates various physiological and pathological processes such as neurotransmission, cell responses to stress, and neurodegeneration. NO synthase is a family of enzymes that synthesize NO from L-arginine. The activity of different NOS isoforms depends both on endogenous and exogenous factors. In particular, it is modulated by oxidative stress, induced by photodynamic therapy (PDT). We have studied the possible role of NOS in the regulation of survival and death of neurons and surrounding glial cells under photo-oxidative stress induced by photodynamic treatment (PDT). The crayfish stretch receptor consisting of a single identified sensory neuron enveloped by glial cells is a simple but informative model object. It was photosensitized with alumophthalocyanine photosens (10 nM) and irradiated with a laser diode (670 nm, 0.4 W/cm2). Antinecrotic and proapoptotic effects of NO on the glial cells were found using inhibitory analysis. We have shown the role of inducible NO synthase in photoinduced apoptosis and involvement of neuronal NO synthase in photoinduced necrosis of glial cells in the isolated crayfish stretch receptor. The activation of NO synthase was evaluated using NADPH-diaphorase histochemistry, a marker of neurons expressing the enzyme. The activation of NO synthase in the isolated crayfish stretch receptor was evaluated as a function of time after PDT. Photodynamic treatment induced transient increase in NO synthase activity and then slowly inhibited this enzyme.

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Section: Discussionmentioning

confidence: 99%

The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

2015

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“…Ho258 was used to detect any sustainable apoptosis and PI to confirm necrosis, which is not always discernable with Ho258 alone. Stained nuclei were counted (35,36), and the percentage of apoptotic versus necrotic cells was determined.…”

Section: Methodsmentioning

confidence: 99%

“…The following general protocol was used. Immediately after exposure to 7␣-OOH, cells were washed with PBS, incubated with RPMI medium containing 10 M DCFH-DA for 20 min at 37°C, washed again, overlaid with RPMI alone, and examined by fluorescence microscopy using 488-nm excitation and 610-nm emission (36,38). Fluorescence intensity of representative images was determined using MetaMorph TM software (36).…”

Section: Measurement Of Overall Cellularmentioning

confidence: 99%

Intracellular Dissemination of Peroxidative Stress

Kriska

Levchenko

Korytowski

et al. 2006

Journal of Biological Chemistry

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Sterol carrier protein-2 (SCP-2) plays a crucial role in the trafficking and metabolism of cholesterol and other lipids in mammalian cells. Lipid hydroperoxides generated under oxidative stress conditions are relatively long-lived intermediates that damage cell membranes and play an important role in redox signaling. We hypothesized that SCP-2-facilitated translocation of lipid hydroperoxides in oxidatively stressed cells might enhance cytolethality if highly sensitive sites are targeted and detoxification capacity is insufficient. We tested this using a clone (SC2A) of rat hepatoma cells that overexpress mature immunodetectable SCP-2. When challenged with liposomal cholesterol-7␣-hydroperoxide (7␣-OOH), SC2A cells were found to be much more sensitive to viability loss than vector control (VC) counterparts. Correspondingly, SC2A cells imported [ 14 C]7␣-OOH more rapidly. The clones were equally sensitive to tert-butyl hydroperoxide, suggesting that the 7␣-OOH effect was SCP-2-specific. Fluorescence intensity of the probes 2,7-dichlorofluorescein and C11-BODIPY increased more rapidly in SC2A than VC cells after 7␣-OOH exposure, consistent with more rapid internalization and oxidative turnover in the former. [ 14 C]7␣-OOH radioactivity accumulated much faster in SC2A mitochondria than in VC, whereas other subcellular fractions showed little rate difference. In keeping with this, 7␣-OOHstressed SC2A cells exhibited a faster loss of mitochondrial membrane potential and development of apoptosis. This is the first reported evidence that peroxidative stress damage can be selectively targeted and exacerbated by an intracellular lipid transfer protein.

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“…However, the reports on the role of NO on PDT-induced cell death are controversial. Some authors have demonstrated the protective effect of NO in photosensitized cells [54,55], whereas others stated the involvement of NO in PDT-induced apoptosis [53,56].…”

Section: No-mediated Pathwaymentioning

confidence: 99%

Protection of the Crayfish Mechanoreceptor Neuron and Glial Cells from Photooxidative Injury by Modulators of Diverse Signal Transduction Pathways

et al. 2015

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Oxidative stress is the reason of diverse neuropathological processes. Photodynamic therapy (PDT), an effective inducer of oxidative stress, is used for cancer treatment, including brain tumors. We studied the role of various signaling pathways in photodynamic injury and protection of single neurons and satellite glial cells in the isolated crayfish mechanoreceptor. It was photosensitized with alumophthalocyanine Photosens in the presence of inhibitors or activators of various signaling proteins. PDT eliminated neuronal activity and killed neurons and glial cells. Inhibitory analysis showed the involvement of protein kinases Akt, glycogen synthase kinase-3β (GSK-3β), mammalian target of rapamycin (mTOR), mitogen-activated protein kinase kinases 1 and 2 (MEK1/2), calmodulin, calmodulin-dependent kinase II (CaMKII), adenylate cyclase, and nuclear factor NF-κB in PDT-induced necrosis of neurons. Nitric oxide (NO) and glial cell-derived neurotrophic factor (GDNF) reduced neuronal necrosis. In glial cells, protein kinases Akt, calmodulin, and CaMKII; protein kinases C and G, adenylate cyclase, and p38; and nuclear transcription factor NF-κB also mediated PDT-induced necrosis. In contrast, NO and neurotrophic factors nerve growth factor (NGF) and GDNF demonstrated anti-necrotic activity. Phospholipase Cγ, protein kinase C, GSK-3β, mTOR, NF-κB, mitochondrial permeability transition pores, and NO synthase mediated PDT-induced apoptosis of glial cells, whereas protein kinase A, tyrosine phosphatases, and neurotrophic factors NGF, GDNF, and neurturin were involved in protecting glial cells from photoinduced apoptosis. Signaling pathways that control cell survival and death differed in neurons and glia. Inhibitors or activators of some signaling pathways may be used as potential protectors of neurons and glia from photooxidative stress and following death.

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Nitric oxide-induced resistance to lethal photooxidative damage in a breast tumor cell line

Cited by 33 publications

References 42 publications

The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

Intracellular Dissemination of Peroxidative Stress

Protection of the Crayfish Mechanoreceptor Neuron and Glial Cells from Photooxidative Injury by Modulators of Diverse Signal Transduction Pathways

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