Handbook of Vitamin C Research

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168Borut Poljsak and John G. IonescuFigure 8. Nickel content of 20 breast cancer and 8 control human biopsies.Figure 9. Chromium content of 20 breast cancer and 8 control human biopsies.Antioxidants can modify cellular oxidative balance resulting in proliferation stimulation(increased viability) or protect damaged cells from oxidative-stress induced suicide(apoptosis), and thereby accelerate cancer progression in higher eucaryotes. Antioxidants cansometimes suppress apoptosis, and sometimes facilitate it (Hampton and Orrenius 1998;Clement and Pervais 1999, Halliwell 2000). Apoptosis is accompanied by an intracellularshift towards increased oxidation, but too much oxidation will stop apoptosis by oxidising
Pro-Oxidant vs. Antioxidant Effects of Vitamin C 169and inactivating the caspase enzymes (Hampton and Orrenius 1998). On the other hand, lowquantities of reactive oxygen species often stimulate cell proliferation (Burdon 1995). Inaddition, when an inappropriate pro-oxidant activity develops in normal cells, the reactiveoxygen metabolites generated could damage the DNA and cellular membranes. The initiationof programmed cell death in tumor cells could result in the loss of malignant cellularintegrity. In contrast, (reducing agents) antioxidants that quench free radicals or reactiveoxygen products in transforming tumor cells may allow these selected cells to proliferate,enhance DNA repair and become therapeutically more resistant to treatment. Cancer cells areknown to accumulate large amounts of antioxidants, such as glutathione, which, in turn,render these cells resistant to classic anticancer therapies (Luisini 2001, Yeh 2006).According to Schwartz (1996) when an antioxidant activity occurs in transformed cells anenhanced growth may result. The result of this modification of the tumor population wouldbe the inadvertent enhanced survival and selection of tumor cell clones.Increasing cellular viability with ascorbic acid pretreatment in Cr(VI)-induced toxicitywas reported by Poljsak et al. (2002; 2005) in yeast cells. This might not always bebeneficial. Chromium-induced growth-arrest and apoptosis are at the molecular decisionpoint between chromium toxicity and chromium carcinogenesis (Singh et al., 1998; Carlisle etal., 2000). When normal growing cells come in contact with carcinogenic forms of chromium,they may respond by undergoing growth arrest, apoptosis and necrosis. A population ofgenetically damaged cells may also emerge, which exhibits either intrinsic or inducedresistance to apoptosis (Carlisle et al., 2000). Such cells may be predisposed to neoplasia as aresult of their altered growth/death ratio, disrupted cell cycle control, or genomic instability.This, however, raises the question of whether ascorbic acid-decreased Cr(VI) toxicity mayactually increase the incidence of cancer (in higher eukaryotes) by allowing the inappropriatesurvival of genetically damaged cells. Besides, cells have their own endogenous antioxidants(superoxid dismutase , catalase, glutathion) and the addition of one single syntheticantioxidant could interfere with the complex antioxidant (redox) network and decrease theactivity of endogenous defense. Because vitamin C is essential for collagen maturation andstabilization, it has been suggested that ascorbic acid may reduce tumor spreading bypotentiating the stability of the extracellular matrix, especially since neoplastic invasionexhibits similar pathological manifestations as vitamin C deficiency (Gonzales et al., 2005).Unfortunately, the effects of vitamin C deficiency on metastasis caused by reduced collagenstabilization have not yet been examined in vivo due to the lack of appropriate animal models(Li and Schellhorn 2007). Though not fully understood, there are two opposing views on therole of the collagen-stabilizing function of vitamin C on tumor growth. First, by stabilizingcollagen, ascorbic acid fortifies the extracellular matrix and stromal structures, leading tobetter confinement of neoplastic cells to their primary sites and preventing tumor growth andmetastasis (Gonzales et al., 2005). Second, the same function may also facilitate theformation of new blood vessels, providing the prerequisite for malignant tumor growth(Telang et al., 2007). The interplay of these effects in vivo, especially under pharmacologicallevels of vitamin C, is far from clear (Li and Schellhorn 2007). In addition to angiogenesis,cancer cells can also modify their energy metabolic pathways to adapt to the low oxygenmicroenvironment in the interior of a solid tumor (Leo et al., 2004; Vaupel 2004). This isachieved by activation of hypoxia-responsive gene expression networks controlled by
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ContentsPrefaceChapter IChapter IIC
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PrefaceThe 6-carbon lactone known a
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Prefaceixbalance of antioxidant and
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Prefacexiprovided or is contradicto
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PrefacexiiiChapter IX - Background:
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Prefacexvdetoxification defence sys
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Prefacexviiprogressed faster than i
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2Kelsey H. Fisher-Wellman and Richa
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10Kelsey H. Fisher-Wellman and Rich
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In: Handbook of Vitamin C Research
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Human Specific Vitamin C Metabolism
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mgmgmgHuman Specific Vitamin C Meta
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88Ana I. Haza, Almudena García and
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90Figure 1.Ana I. Haza, Almudena Ga
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94Figure 3.Ana I. Haza, Almudena Ga
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100Ana I. Haza, Almudena García an
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Page 149 and 150: Vitamin C: Dietary Requirements, Di
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Page 206 and 207: 186Magdalena Stevanović and Dragan
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Molecular Bases of the Cellular Han
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Vitamin C: Daily Requirements, Diet
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262Alan M. Preston, Luis Vázquez Q
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Percent of Study Group Selecting Di
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The Role of Vitamin C in Human Repr
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300Mustafa NazıroğluKeywords: Vit
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302Mustafa NazıroğluNO is synthes
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304Mustafa Nazıroğlu‗recycling
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306Mustafa Nazıroğluagents, such
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308Mustafa NazıroğluFuture Direct
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310Mustafa Nazıroğlu[21] Basu, TK
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312Mustafa Nazıroğlu[59] Cengiz M
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314Samar Al Sayegh Petkovšek and B
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(mgg -1 )320Samar Al Sayegh Petkov
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330Antonio J. López-Farré, José
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Vitamin C in the Treatment of Endot
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Vitamin C Intake by Japanese Patien
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Reciprocal Effects of Ascorbate on
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378Akihito Ishigamicontrols (12,13)
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380Akihito IshigamiFigure 3. Vitami
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382Akihito IshigamiFuture of the SM
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The Importance of Food Processing o
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IndexAA , 249abdominal cramps, 243a
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Index 391atherosclerotic plaque, 23
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Index 393catalase, 6, 13, 169, 181,
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Index 395cyclooxygenase-2, 337, 341
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Index 397endometrium, 286, 294endon
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Index 399GCS, 18gel, x, 87, 92, 121
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Index 401hyperglycaemia, 223hypergl
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Index 403kinetics, 71, 120, 124, 14
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Index 405metastases, 182metastasis,
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Index 407nitrate, 14, 88, 179, 234,
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Index 409phosphodiesterase, 344, 35
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Index 411recovery, vii, 1, 5, 7, 8,
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Index 413steady state, 63, 76, 78st
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Index 415UV, 156, 191, 201, 204, 22
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