Nanoparticles In Human Cells Research Articles

Key Role of Choline Head Groups in Large Unilamellar Phospholipid Vesicles for the Interaction with and Rupture by Silica Nanoparticles.

For highly abundant silica nanomaterials, detrimental effects on proteins and phospholipids are postulated as critical molecular initiating events that involve hydrogen-bonding, hydrophobic, and/or hydrophilic interactions. Here, large unilamellar vesicles with various well-defined phospholipid compositions are used as biomimetic models to recapitulate membranolysis, a process known to be induced by silica nanoparticles in human cells. Differential analysis of the dominant phospholipids determined in membranes of alveolar lung epithelial cells demonstrates that the quaternary ammonium head groups of phosphatidylcholine and sphingomyelin play a critical and dose-dependent role in vesicle binding and rupture by amorphous colloidal silica nanoparticles. Surface modification by either protein adsorption or by covalent coupling of carboxyl groups suppresses the disintegration of these lipid vesicles, as well as membranolysis in human A549 lung epithelial cells by the silica nanoparticles. Furthermore, molecular modeling suggests a preferential affinity of silanol groups for choline head groups, which is also modulated by the pH value. Biomimetic lipid vesicles can thus be used to better understand specific phospholipid-nanoparticle interactions at the molecular level to support the rational design of safe advanced materials.

Nonresonant CARS Imaging of Porous and Solid Silicon Nanoparticles in Human Cells.

Coherent anti-Stokes Raman scattering (CARS), a nonlinear optical method for rapid visualization of biological objects, represents a progressive tool in biology and medicine to explore cells and tissue structures in living systems and biopsies. In this study, we report efficient nonresonant CARS imaging of silicon nanoparticles (SiNPs) in human cells as a proof of concept. As both bulk and porous silicon exhibit a high third-order nonlinear susceptibility, χ(3), which is responsible for the CARS intensity, it is possible to visualize the SiNPs without specific labels. Porous and solid SiNPs were obtained from layers of porous and nonporous silicon nanowires and mesoporous silicon. Electron microscopy and Raman spectroscopy showed that porous SiNPs consisted of ∼3 nm silicon nanocrystals (nc-Si) and pores, whereas solid nanoparticles comprised ∼30 nm nc-Si. All types of SiNPs were nontoxic at concentrations up to 500 μg/mL after 24 h of incubation with cells. We demonstrated that although nc-Si possesses a distinguished narrow Raman band of about 520 cm-1, it is possible to detect a high CARS signal from SiNPs in the epi-direction even in a nonresonant regime. 3D CARS images showed that all types of studied SiNPs were visualized as bright spots inside the cytoplasm of cells after 3-6 h of incubation because of the contrast provided by the high third-order nonlinear susceptibility of SiNPs, which is 1 × 104 to 1 × 105 times higher than that of water and typical biological media. Overall, CARS microscopy can provide localization of SiNPs within biological structures at the cellular level and can be a powerful tool for in vitro monitoring of silicon-based drug delivery systems or use SiNPs as labels to monitor various bioprocesses inside living cells.

Quantitative assessment of cellular uptake and differential toxic effects of HgSe nanoparticles in human cells

A comparative study of the cytotoxicity of HgSe nanoparticles and that induced by inorganic mercury and methylmercury in two cell lines.

Differential cytotoxicity of copper ferrite nanoparticles in different human cells.

Copper ferrite nanoparticles (NPs) have the potential to be applied in biomedical fields such as cell labeling and hyperthermia. However, there is a lack of information concerning the toxicity of copper ferrite NPs. We explored the cytotoxic potential of copper ferrite NPs in human lung (A549) and liver (HepG2) cells. Copper ferrite NPs were crystalline and almost spherically shaped with an average diameter of 35 nm. Copper ferrite NPs induced dose-dependent cytotoxicity in both types of cells, evident by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide and neutral red uptake assays. However, we observed a quite different susceptibility in the two kinds of cells regarding toxicity of copper ferrite NPs. Particularly, A549 cells showed higher susceptibility against copper ferrite NP exposure than those of HepG2 cells. Loss of mitochondrial membrane potential due to copper ferrite NP exposure was observed. The mRNA level as well as activity of caspase-3 enzyme was higher in cells exposed to copper ferrite NPs. Cellular redox status was disturbed as indicated by induction of reactive oxygen species (oxidant) generation and depletion of the glutathione (antioxidant) level. Moreover, cytotoxicity induced by copper ferrite NPs was efficiently prevented by N-acetylcysteine treatment, which suggests that reactive oxygen species generation might be one of the possible mechanisms of cytotoxicity caused by copper ferrite NPs. To the best of our knowledge, this is the first report showing the cytotoxic potential of copper ferrite NPs in human cells. This study warrants further investigation to explore the mechanisms of differential toxicity of copper ferrite NPs in different types of cells. Copyright © 2016 John Wiley & Sons, Ltd.

Antioxidative and cytoprotective response elicited by molybdenum nanoparticles in human cells

Nanotechnology based therapeutics can offer an alternative platform in a wide variety of biomedical applications. Here we report novel cytotoxicity preventive potential of molybdenum nanoparticles (Mo NPs) in human breast (MCF-7) and fibrosarcoma (HT-1080) cells compromised with oxidant exposure. Physicochemical properties such as size, crystallinity, purity and band gap (an optical characteristic) of Mo NPs were characterized respectively by field emission transmission electron microscopy (FETEM), X-ray diffraction (XRD), energy dispersive spectrum (EDS) and UV–vis absorption spectroscopy. The average size of crystalline Mo NPs was found to be 35nm with a band gap of 1.4eV. Potential cytotoxicity of Mo NPs was evaluated by a battery of cell viability and oxidative stress parameters. Cell viability and oxidative stress data suggested Mo NPs to be reasonably non-cytotoxic. Cytotoxic preventive and GSH restoring potential of Mo NPs was determined against cytotoxicity and oxidative stress induced by H2O2 (and ZnO NPs) in two cells. Mo NPs significantly increased GSH level in MCF-7 and HT-1080 cells, an activity that was comparable to antioxidant N-acetyl cysteine (NAC). GSH level was increased 1.56 times in MCF-7 cells and 1.25 times in HT-1080 cells by 100μg/ml of Mo NPs relative to control cells in 24h. End-point data clearly suggest that Mo NPs significantly protected cells against cytotoxicity induced by H2O2 and ZnO (NPs) (p<0.05). Our study warrants further investigation about Mo NPs that could be exploited in myriads of nanotechnology applications.

Genotoxicity of meso-2,3-dimercapto succinic acid-coated silver sulfide quantum dot

Event Abstract Back to Event Genotoxicity of meso-2,3-dimercapto succinic acid-coated silver sulfide quantum dot Deniz Özkan Vardar1*, Ibrahim Hacıoğlu2, Sevtap Aydin3, Funda Yağcı4 and A. N. Basaran3 1 Hitit University Sungurlu Vocational high Scholl, Department of Health, Türkiye 2 Koç University, Department of Materials Science and Engineering, Türkiye 3 Hacettepe University, Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Türkiye 4 Koç University, Department of Chemistry, Türkiye Nanotecnology products have been used in wide applications in chemistry, electronics, energy generation, and medicine. Despite significant interest in developing quantum dots (QDs) for biomedical applications, many researchers are convinced that QDs will never be used for the treatment of patients because of their potential toxicity. In various in vitro cell culture studies, the cytotoxic properties of some QD have been demonstrated and they have been suggested to be toxic in humans. In this study, the cytotoxic properties of Ag2S-(Meso-2,3-Dimercapto Succinic acid) nanomaterials in V79 cells (Chinese lung fibroblast cell line) were determined by MTT assay. The genotoxic effects of Ag2S-(Meso-2,3-Dimercapto Succinic acid) were evaluated by the alkaline single cell gel electrophoresis. The cells were treated with Ag2S-(Meso-2,3-Dimercapto Succinic acid) at the concentrations of 5- 2000 µg/ml. No cytotoxic effect of Ag2S-(Meso-2,3-Dimercapto Succinic acid) at all concentrations studied was observed. No significant increases in DNA damage were found at the studied concentrations when compared to negative control in V79 cells. In conclusion, further in vitro and in vivo studies are required to determine the safety doses of Ag2S-(Meso-2,3-Dimercapto Succinic acid). Acknowledgements This study was funded in part by a grant from TUBITAK (TUBITAK 3001, contract grant number: 114S861). References Ahamed, M., Karns, M., Goodson, M., Rowe, J., Hussain, S.M., Schlager, J.J., Hong, Y. 2008. “DNA damage response to different surface chemistry of silver nanoparticles in mammalian cells”, Toxicol Appl Pharmacol., 233(3), 404-10. Ahamed, M., Siddiqui, M.A., Akhtar, M.J., Ahmad, I., Pant, A.B., Alhadlaq, H.A. 2010. “Genotoxic potential of copper oxide nanoparticles in human lung epithelial cells”, Biochem Biophys Res Commun., 396(2), 578-83. AshaRani, P.V., Low Kah Mun G., Hande, M.P., Valiyaveettil, S. 2009. “Cytotoxicity and genotoxicity of silver nanoparticles in human cells”, ACS Nano., 3(2), 279-90. Chaung, W. Mi,L.J., Boorstein, R.J. 1997. “The p53 status of Chinese hamster V79 cells frequently used for studies on DNA damage and DNA repair”, Nucleic Acids Res., 25(5), 992-4. Lunov, O., Syrovets, T., Büchele, B., Jiang, X., Röcker, C., Tron, K., Nienhaus, G.U., Walther, P., Mailänder, V., Landfester, K., Simmet, T. 2010. “The effect of carboxydextran-coated superparamagnetic iron oxide nanoparticles on c-Jun N-terminal kinase-mediated apoptosis in human macrophages” Biomaterials, 31(19), 5063-7. Park, E.J., Yi, J., Chung, K.H., Ryu, D.Y., Choi, J., Park, K. 2008. “Oxidative stress and apoptosis induced by titanium dioxide nanoparticles in cultured BEAS-2B cells”, Toxicol Lett., 180(3), 222-9. Keywords: Quantum dots, MTT assay, Comet Assay, Chinese lung fibroblast cell line, Genotoxicity, Nanotoxicity Conference: ICAW 2015 - 11th International Comet Assay Workshop, Antwerpen, Belgium, 1 Sep - 4 Sep, 2015. Presentation Type: Poster Discussion Topic: Genotoxicity testing of chemicals and nanomaterials Citation: Özkan Vardar D, Hacıoğlu I, Aydin S, Yağcı F and Basaran AN (2015). Genotoxicity of meso-2,3-dimercapto succinic acid-coated silver sulfide quantum dot. Front. Genet. Conference Abstract: ICAW 2015 - 11th International Comet Assay Workshop. doi: 10.3389/conf.fgene.2015.01.00018 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 Jun 2015; Published Online: 23 Jun 2015. * Correspondence: Mrs. Deniz Özkan Vardar, Hitit University Sungurlu Vocational high Scholl, Department of Health, Çorum, 19300, Türkiye, denizozkantr@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Deniz Özkan Vardar Ibrahim Hacıoğlu Sevtap Aydin Funda Yağcı A. N Basaran Google Deniz Özkan Vardar Ibrahim Hacıoğlu Sevtap Aydin Funda Yağcı A. N Basaran Google Scholar Deniz Özkan Vardar Ibrahim Hacıoğlu Sevtap Aydin Funda Yağcı A. N Basaran PubMed Deniz Özkan Vardar Ibrahim Hacıoğlu Sevtap Aydin Funda Yağcı A. N Basaran Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. 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Targeting human dendritic cells via DEC-205 using PLGA nanoparticles leads to enhanced cross-presentation of a melanoma-associated antigen.

Targeting antigen to dendritic cells (DCs) is a powerful and novel strategy for vaccination. Priming or loading DCs with antigen controls whether subsequent immunity will develop and hence whether effective vaccination can be achieved. The goal of our present work was to increase the potency of DC-based antitumor vaccines by overcoming inherent limitations associated with antigen stability and cross-presentation. Nanoparticles prepared from the biodegradable polymer poly(lactic-co-glycolic acid) have been extensively used in clinical settings for drug delivery and are currently the subject of intensive investigation as antigen delivery vehicles for vaccine applications. Here we describe a nanoparticulate delivery system with the ability to simultaneously carry a high density of protein-based antigen while displaying a DC targeting ligand on its surface. Utilizing a targeting motif specific for the DC-associated surface ligand DEC-205, we show that targeted nanoparticles encapsulating a MART-127–35 peptide are both internalized and cross-presented with significantly higher efficiency than isotype control-coated nanoparticles in human cells. In addition, the DEC-205-labeled nanoparticles rapidly escape from the DC endosomal compartment and do not colocalize with markers of early (EEA-1) or late endosome/lysosome (LAMP-1). This indicates that encapsulated antigens delivered by nanoparticles may have direct access to the class I cytoplasmic major histocompatibility complex loading machinery, overcoming the need for “classical” cross-presentation and facilitating heightened DC stimulation of anti-tumor CD8+ T-cells. These results indicate that this delivery system provides a flexible and versatile methodology to deliver melanoma-associated antigen to DCs, with both high efficiency and heightened potency.

Differential internalization of amphotericin B – Conjugated nanoparticles in human cells and the expression of heat shock protein 70

Although a variety of nanoparticles (NPs) functionalized with amphotericin B, an antifungal agent widely used in the clinic, have been studied in the last years their cytotoxicity profile remains elusive. Here we show that human endothelial cells take up high amounts of silica nanoparticles (SNPs) conjugated with amphotericin B (AmB) (SNP-AmB) (65.4 ± 12.4 pg of Si per cell) through macropinocytosis while human fibroblasts internalize relatively low amounts (2.3 ± 0.4 pg of Si per cell) because of their low capacity for macropinocytosis. We further show that concentrations of SNP-AmB and SNP up to 400 μg/mL do not substantially affect fibroblasts. In contrast, endothelial cells are sensitive to low concentrations of NPs (above 10 μg/mL), in particular to SNP-AmB. This is because of their capacity to internalize high concentration of NPs and high sensitivity of their membrane to the effects of AmB. Low-moderate concentrations of SNP-AmB (up to 100 μg/mL) induce the production of reactive oxygen species (ROS), LDH release, high expression of pro-inflammatory cytokines and chemokines (IL-8, IL-6, G-CSF, CCL4, IL-1β and CSF2) and high expression of heat shock proteins (HSPs) at gene and protein levels. High concentrations of SNP-AmB (above 100 μg/mL) disturb membrane integrity and kill rapidly human cells (60% after 5 h). This effect is higher in SNP-AmB than in SNP.

Intracellular trafficking pathway of layered double hydroxide nanoparticles in human cells: Size-dependent cellular delivery

Layered double hydroxide (LDH) nanoparticles are promising candidates as delivery carriers, since they have low toxicity and can intercalate anionic drugs or genes in the interlayer spaces of two dimensional lattices. However, little information is available about their intracellular fate and trafficking pathway in human cells, which is important to improve delivery efficiency and predict toxicity potential. From the immunofluorescence and confocal microscopic studies to evaluate intracellular colocalization of fluorescein isothiocyanate-labeled nanoparticles (50 and 100nm) with specific compartments, we found that the cellular uptake reached a maximum level at 0.5h and gradually decreased over time. The present nanoparticles were highly colocalized with early endosomes within the first 0.5h and largely found in an exocytic organelle, the Golgi apparatus over a period of 1–24h. Most of 100nm could escape a typical endo-lysosomal degradation, while 50nm followed an endosome–lysosome pathway as well as exocytosis one with the same degree. A model for the intracellular trafficking of LDH nanoparticles depending on particle size is proposed on the basis of quantitative analysis data.

CuO Nanoparticle Interaction with Human Epithelial Cells: Cellular Uptake, Location, Export, and Genotoxicity

The toxicity of CuO nanoparticles (NPs) to human lung epithelial (A549) cells was investigated in this study. CuO NPs (10-100 mg/L) had significant toxicity to A549 cells, whereas CuO bulk particles (BPs) showed much lower toxicity (24 h IC(50), 58 and 15 mg/L for CuO BPs and NPs, respectively). Transmission electron microscopic analysis demonstrated CuO NP entry into A549 cells and organelles, including lysosomes, mitochondria, and nucleus. Endocytosis was the primary pathway of CuO NPs uptake. CuO NPs (15 mg/L) induced mitochondrial depolarization, possibly mediated by reactive oxygen species (ROS) generation. Intracellular CuO NPs first generate ROS, which subsequently induces the expression of p38 and p53 and ultimately causes DNA damage (Comet assay). We confirm for the first time that the primary cytotoxic response is oxidative stress rather than DNA damage. A fraction of the CuO NPs was exported to the extracellular environment. In this study, centrifugal ultrafiltration tubes were successfully employed to determine the dissolved Cu(2+) from CuO NPs in the cell medium. Dissolved Cu(2+) ions contributed less than half of the total toxicity caused by CuO NPs, including ROS generation and DNA damage. This study provided useful data for understanding transport and toxicity of metal oxide NPs in human cells.

Differential regulation of intracellular factors mediating cell cycle, DNA repair and inflammation following exposure to silver nanoparticles in human cells

BackgroundInvestigating the cellular and molecular signatures in eukaryotic cells following exposure to nanoparticles will further our understanding on the mechanisms mediating nanoparticle induced effects. This study illustrates the molecular effects of silver nanoparticles (Ag-np) in normal human lung cells, IMR-90 and human brain cancer cells, U251 with emphasis on gene expression, induction of inflammatory mediators and the interaction of Ag-np with cytosolic proteins.ResultsWe report that silver nanoparticles are capable of adsorbing cytosolic proteins on their surface that may influence the function of intracellular factors. Gene and protein expression profiles of Ag-np exposed cells revealed up regulation of many DNA damage response genes such as Gadd 45 in both the cell types and ATR in cancer cells. Moreover, down regulation of genes necessary for cell cycle progression (cyclin B and cyclin E) and DNA damage response/repair (XRCC1 and 3, FEN1, RAD51C, RPA1) was observed in both the cell lines. Double strand DNA damage was observed in a dose dependant manner as evidenced in γH2AX foci assay. There was a down regulation of p53 and PCNA in treated cells. Cancer cells in particular showed a concentration dependant increase in phosphorylated p53 accompanied by the cleavage of caspase 3 and PARP. Our results demonstrate the involvement of NFκB and MAP kinase pathway in response to Ag-np exposure. Up regulation of pro-inflammatory cytokines such as interleukins (IL-8, IL-6), macrophage colony stimulating factor, macrophage inflammatory protein in fibroblasts following Ag-np exposure were also observed.ConclusionIn summary, Ag-np can modulate gene expression and protein functions in IMR-90 cells and U251 cells, leading to defective DNA repair, proliferation arrest and inflammatory response. The observed changes could also be due to its capability to adsorb cytosolic proteins on its surface.

Cellular uptake, evolution, and excretion of silica nanoparticles in human cells

A systematic study on the interaction of silica nanoparticles (NPs) with human cells has been carried out in the present work. Endocytosis and exocytosis are identified as major pathways for NPs entering, and exiting the cells, respectively. Most of the NPs are found to be enclosed in membrane bounded organelles, which are fairly stable (against rupture) as very few NPs are released into the cytoplasm. The nanoparticle-cell interaction is a dynamic process, and the amount of NPs inside the cells is affected by both the amount and morphology (degree of aggregation) of NPs in the medium. These interaction characteristics determine the low cytotoxicity of SiO(2) NPs at low feeding concentration.

Intracellular Synchrotron Nanoimaging and DNA Damage/Genotoxicity Screening of Novel Lanthanide-Coated Nanovectors

In cancer therapy, research has focused on the development of nanocarriers that can aid diagnosis, deliver therapeutic agents and monitor treatment progress. This study introduces high-resolution synchrotron x-ray fluorescence microscopy (SR-XFM) to investigate intracellular localization of novel lanthanide-coated nanoparticles in human cells and their genotoxicity screening after internalization. Noble metal nanoparticles coated with cerium and luminescent europium complexes have been developed as platforms for bioimaging and potential biodelivery applications. The intracellular distribution after internalization has been analyzed by ultrasensitive SR-XFM and genotoxicity evaluated using γ-H2AX DNA damage foci phosphorylation assay. We demonstrate the unprecedented capability of SR-XFM for extremely sensitive nanoimaging and intracellular elemental distribution analysis of noble metal nanoparticles in cells. Furthermore, we show that, depending on the charge of the coating complex and the presence of the DNA cargo, the internalization of functionalized nanoparticles by human fibroblasts can cause elevated levels of DNA damage detected by histone H2AX phosphorylation. The variable genotoxic impact of newly designed nanovectors emphasizes the need for careful and comprehensive testing of biological responses of all new nanoconstructs intended for future clinical applications. This can be greatly facilitated by SR-XFM nanoimaging of nanoparticles in cells at very low concentrations.

Oxidative Stress Mediates the Effects of Raman‐Active Gold Nanoparticles in Human Cells

Polyethylene glycol (PEG)ylated Raman-active gold nanoparticles (PEG-R-AuNPs) consist of an interchangeable Raman organic molecule layer held onto a gold nanocore by a silica shell. PEG-R-AuNPs have been shown preclinically to increase the sensitivity and specificity of Raman spectroscopy, with picomolar sensitivity and multiplexing capabilities. Although clinical trials are being designed to use functionalized PEG-R-AuNPs in various applications (e.g., to target dysplastic bowel lesions during colonoscopy), the effects of these nanoparticles on human cells remain unknown. The occurrence and mechanisms underlying any potential cytotoxicity induced by these nanoparticles (0-1000 PEG-R-AuNPs/cell) are investigated in immortalized human HeLa and HepG2 cell lines at several time points (0-48 h) after exposure. Using fluorometric assays, cell viability (MTT), reactive oxygen species (ROS) generation (dichlorofluorescein diacetate), protein oxidation (protein carbonyl content), and total cellular antioxidant concentrations the concentrations (metmyoblobin-induced oxidation of ABTS) are assessed. Analysis of lipid oxidation using an enzyme immunoassay (8-isoprostane concentrations), gene expression of antioxidant enzymes using quantitative reverse transcription polymerase chain reactions, and the intracellular location of PEG-R-AuNPs using transmission electron microscopy is also undertaken. PEG-R-AuNPs cause no cytotoxicity in either HeLa or HepG2 cells in the acute setting as ROS generation is balanced by antioxidant enzyme upregulation. Following prolonged exposures (48 h) at relatively high concentrations (1000 PEG-R-AuNPs/cell), nanoparticles are found within vesicles inside cells. Under these conditions, a minimal amount of cytotoxicity is seen in both cell lines owing to increases in cellular oxidative stress, most likely due to ROS overwhelming the antioxidant defenses. Evidence of oxidative stress-induced damage includes increased lipid and protein oxidation. Although further in vivo toxicity studies are necessary, these initial encouraging results show that PEG-R-AuNPs cause minimal toxicity in human cells in the acute setting, which bodes well for potential future applications of these nanoparticles in living subjects.

Growth of Gold Nanoparticles in Human Cells

Gold nanoparticles of 20-100 nm diameter were synthesized within HEK-293 (human embryonic kidney), HeLa (human cervical cancer), SiHa (human cervical cancer), and SKNSH (human neuroblastoma) cells. Incubation of 1 mM tetrachloroaurate solution, prepared in phosphate buffered saline (PBS), pH 7.4, with human cells grown to approximately 80% confluency yielded systematic growth of nanoparticles over a period of 96 h. The cells, stained due to nanoparticle growth, were adherent to the bottom of the wells of the tissue culture plates, with their morphology preserved, indicating that the cell membrane was intact. Transmission electron microscopy of ultrathin sections showed the presence of nanoparticles within the cytoplasm and in the nucleus, the latter being much smaller in dimension. Scanning near field microscopic images confirmed the growth of large particles within the cytoplasm. Normal cells gave UV-visible signatures of higher intensity than the cancer cells. Differences in the cellular metabolism of cancer and noncancer cells were manifested, presumably in their ability to carry out the reduction process.