Electrochemical Detection of H2O2 Released from Prostate Cancer Cells Using Pt Nanoparticle-Decorated rGO–CNT Nanocomposite-Modified Screen-Printed Carbon Electrodes

In this study, we fabricated platinum nanoparticles (PtNP)-decorated, porous reduced graphene oxide (rGO)–carbon nanotube (CNT) nanocomposites on a PtNP-deposited screen-printed carbon electrode (PtNP/rGO–CNT/PtNP/SPCE) for detection of hydrogen peroxide (H2O2), which is released from prostate cancer cells LNCaP. The PtNP/rGO–CNT/PtNP/SPCE was fabricated by a simple electrochemical deposition and co-reduction method. In addition, the amperometric response of the PtNP/rGO–CNT/PtNP/SPCE electrode was evaluated through consecutive additions of H2O2 at an applied potential of 0.2 V (vs. Ag pseudo-reference electrode). As a result, the prepared PtNP/rGO–CNT/PtNP/SPCE showed good electrocatalytic activity toward H2O2 compared to bare SPCE, rGO–CNT/SPCE, PtNP/SPCE, and rGO–CNT/PtNP/SPCE. In addition, the PtNP/rGO–CNT/PtNP/SPCE electrode exhibited a sensitivity of 206 μA mM−1·cm−2 to H2O2 in a linear range of 25 to 1000 μM (R2 = 0.99). Moreover, the PtNP/rGO–CNT/PtNP/SPCE electrode was less sensitive to common interfering substances, such as ascorbic acid, uric acid, and glucose than H2O2. Finally, real-time monitoring of H2O2 released from LNCaP cells was successfully performed by this electrode. Therefore, we expect that the PtNP/rGO–CNT/PtNP/SPCE can be utilized as a promising electrochemical sensor for practical nonenzymatic detection of H2O2 in live cells or clinical analysis.

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Thermally Reduced Graphene Oxide Nanohybrids of Chiral Functional Naphthalenediimides for Prostate Cancer Cells Bioimaging

Advanced Functional Materials ◽

10.1002/adfm.201601123 ◽

2016 ◽

Vol 26 (31) ◽

pp. 5641-5657 ◽

Cited By ~ 17

Author(s):

James A. Tyson ◽

Vincenzo Mirabello ◽

David G. Calatayud ◽

Haobo Ge ◽

Gabriele Kociok-Köhn ◽

...

Keyword(s):

Prostate Cancer ◽

Graphene Oxide ◽

Cancer Cells ◽

Reduced Graphene Oxide ◽

Prostate Cancer Cells ◽

Reduced Graphene

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Salmonella–Host Cell Interactions, Changes in Host Cell Architecture, and Destruction of Prostate Tumor Cells with Genetically AlteredSalmonella

Microscopy and Microanalysis ◽

10.1017/s1431927607070833 ◽

2007 ◽

Vol 13 (5) ◽

pp. 372-383 ◽

Cited By ~ 9

Author(s):

Zhisheng Zhong ◽

Robert A. Kazmierczak ◽

Alison Dino ◽

Rula Khreis ◽

Abraham Eisenstark ◽

...

Keyword(s):

Prostate Cancer ◽

Host Cell ◽

Cancer Cells ◽

Immunofluorescence Microscopy ◽

Genetically Modified ◽

Live Cells ◽

Prostate Cancer Cells ◽

3T3 Cells ◽

Host Cell Interactions ◽

Prostate Tumor Cells

Increasingly, genetically modifiedSalmonellaare being explored as a novel treatment for cancer becauseSalmonellapreferentially replicate within tumors and destroy cancer cells without causing the septic shock that is typically associated with wild-typeS. typhimuriuminfections. However, the mechanisms by which genetically modifiedSalmonellastrains preferentially invade cancer cells have not yet been addressed in cellular detail. Here we present data that showS. typhimuriumstrains VNP20009, LT2, and CRC1674 invasion of PC-3M prostate cancer cells.S. typhimurium-infected PC-3M human prostate cancer cells were analyzed with immunofluorescence microscopy and transmission electron microscopy (TEM) at various times after inoculation. We analyzed microfilaments, microtubules, and DNA with fluorescence and immunofluorescence microscopy. 3T3 Phi-Yellow-mitochondria mouse 3T3 cells were used to study the effects ofSalmonellainfestation on mitochondria distribution in live cells. Our TEM results show gradual destruction of mitochondria within the PC-3M prostate cancer cells with complete loss of cristae at 8 h after inoculation. The fluorescence intensity in YFP-mitochondria-transfected mouse 3T3 cells decreased, which indicates loss of mitochondria structure. Interestingly, the nucleus does not appear affected bySalmonellawithin 8 h. Our data demonstrate that genetically modifiedS. typhimuriumdestroy PC-3M prostate cancer cells, perhaps by preferential destruction of mitochondria.

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