Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation

Ding, Xiaofeng; Xu, Qiong; Fanguang, Liu; Zhou, Pingkun; Gu, Ying; Zeng, Jing; An, Jing; Dai, Weide; Li, Xiaosong

doi:10.1016/j.canlet.2004.07.005

Cited by 109 publications

(74 citation statements)

References 32 publications

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“…Cell death may be quantified by measuring 140 enzyme activity, 41 membrane permeability 42 or redox potentials. 43 We used a purpose-built array of 657 nm LEDs (full width at half maximum = 22 nm) for the one-photon PDT experiments, as shown in Fig. 2 (emission spectrum in Fig.…”

Section: In Vitro One-photon Pdtmentioning

confidence: 99%

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

et al. 2009

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Section: In Vitro One-photon Pdtmentioning

confidence: 99%

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

et al. 2009

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“…There is a possibility that the intracellular elevation of Ca 2ϩ in the G-Rh2-induced cells may have resulted from proteolytic degradation of protein that involves pumping cytosolic Ca 2ϩ into the endoplasmic reticulum after treatment of G-Rh2 because the elevation of Ca 2ϩ is related to endoplasmic reticulum and the degradation of protein in endoplasmic reticulum membrane is sensitive to oxidative stress (Ding et al, 2004). Elevation of Ca 2ϩ in the cytosol is likely to be linked to the perturbed mitochondrial permeability transition resulting from depolarization of the mitochondrial redox potential that consequently induces the mitochondrial release of cytochrome c and Smac.…”

Section: G-rh2-induced Ros Is Involved In Decrease Ofmentioning

confidence: 99%

Ginsenoside-Rh2-Induced Mitochondrial Depolarization and Apoptosis Are Associated with Reactive Oxygen Species- and Ca²⁺-Mediated c-Jun NH₂-Terminal Kinase 1 Activation in HeLa Cells

Ham

Jin-Hee²,

Na³

et al. 2006

J Pharmacol Exp Ther

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We show here that Ca 2ϩ and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH 2 -terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Addition of antioxidants such as N-acetyl-L-cysteine or catalase attenuates G-Rh2-induced ROS generation, JNK1 activation, and apoptosis. The overexpression of catalase down-regulates caspase-3 and JNK1 activities. G-Rh2 treatment of cells results in mitochondrial depolarization, second mitochondrial activator of caspase release, and translocation of Bax into the mitochondria, and these events are inhibited by antioxidants. Ca 2ϩ is also involved in mitochondrial depolarization during G-Rh2-induced apoptosis. These results suggest that ROS and Ca 2ϩ are important signaling intermediates leading to stress-activated protein kinase/extracellular signal-regulated kinase kinase 1/JNK1 activation and depolarization of the mitochondrial membrane potential in G-Rh2-induced apoptosis.

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“…11 The increase of free calcium ion was responsible for necrosis or apoptosis induced by photodynamic therapy. 11,18 In the present experiment with Fluo-3-AM, the concentration of intracellular calcium increased after ultrasound radiation and HMME-ultrasound treatment. The increase of Ca 2+ in the UMR-106 cells was more significant after the treatment of ultrasound and HMME together than after ultrasound radiation alone, demonstrating that HMME clearly enhanced the intracellular Ca 2+ level induced by ultrasound radiation.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, hematoporphyrin monomethyl ether (HMME), as a novel sensitizer, has been put forward in view of its advantageous physicochemical properties in China. 11,12 Our previous study has shown that HMME could effectively enhance ultrasound cytoxicity to osteosarcoma in vivo. 4 The present study aims to investigate the changes of intracellular ROS and free calcium ion in osteosarcoma cells treated by HMME and ultrasound.…”

Section: Introductionmentioning

confidence: 99%

Hematoporphyrin Monomethyl Ether Enhances the Killing of Ultrasound on Osteosarcoma Cells Involving Intracellular Reactive Oxygen Species and Calcium Ion Elevation

et al. 2010

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Objective: The present study aims to investigate the possible mechanisms of hematoporphyrin monomethyl ether (HMME) enhancing the cytotoxicity of ultrasound in osteosarcoma cells. Methods: Osteosarcoma cell line UMR-106 was treated by HMME and ultrasound radiation, with the HMME concentration kept at 20 mg/mL and ultrasound radiation for 10 seconds at the intensity of 0.5 W/cm 2 . Cell proliferation was investigated at 12, 24, 36, and 48 hours using MTT assay after ultrasound and HMME treatment. Ultrastructural morphology was observed using transmission electron microscopy (TEM). Intracellular reactive oxygen species (ROS) was measured using a flow cytometry with DCFH-DA staining and intracellular free calcium ion (Ca 2+ ) with Fluo-3-AM staining. Results: The UMR-106 cells proliferated rapidly in the sham radiation and HMME treatment alone group, but ultrasound-treated cells and HMME-ultrasound-treated cells proliferated slowly. There was a significant difference between HMME-ultrasound treatment and the controls, including ultrasound radiation, HMME treatment alone, and sham radiation (P < .05). TEM showed endoplasmic reticulum and mitochondrial swelling in the ultrasound-treated cells, and more cells presented apoptosis and necrosis after treatment with ultrasound and HMME together. Intracellular ROS and Ca 2+ in the cells increased more significantly after both ultrasound and HMME treatment than after ultrasound treatment alone. Conclusions: HMME could effectively enhance the inhibition effect of ultrasound on osteosarcoma cells. Intracellular ROS and Ca 2+ in the UMR-106 cells increased more significantly after the treatment of HMME and ultrasound together, indicating that the enhancement of HMME on ultrasound cytotoxicity to osteosarcoma cells possibly involves both intracellular ROS and Ca 2+ elevation.

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Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation

Cited by 109 publications

References 32 publications

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

Ginsenoside-Rh2-Induced Mitochondrial Depolarization and Apoptosis Are Associated with Reactive Oxygen Species- and Ca²⁺-Mediated c-Jun NH₂-Terminal Kinase 1 Activation in HeLa Cells

Hematoporphyrin Monomethyl Ether Enhances the Killing of Ultrasound on Osteosarcoma Cells Involving Intracellular Reactive Oxygen Species and Calcium Ion Elevation

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Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation

Cited by 109 publications

References 32 publications

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

One- and two-photon activated phototoxicity of conjugated porphyrin dimers with high two-photon absorption cross sections

Ginsenoside-Rh2-Induced Mitochondrial Depolarization and Apoptosis Are Associated with Reactive Oxygen Species- and Ca2+-Mediated c-Jun NH2-Terminal Kinase 1 Activation in HeLa Cells

Hematoporphyrin Monomethyl Ether Enhances the Killing of Ultrasound on Osteosarcoma Cells Involving Intracellular Reactive Oxygen Species and Calcium Ion Elevation

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Ginsenoside-Rh2-Induced Mitochondrial Depolarization and Apoptosis Are Associated with Reactive Oxygen Species- and Ca²⁺-Mediated c-Jun NH₂-Terminal Kinase 1 Activation in HeLa Cells