Platelet ascorbic acid levels in normal subjects and in disease

Lloyd, John Uri; Davis, Peter S.; Emery, H.; Lander, Harry

doi:10.1136/jcp.25.6.478

Cited by 24 publications

(9 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Millimolar concentrations of ascorbate can be achieved intracellularly by carrier-mediated mechanisms (Table 2). There is no detectable level of DHA in cells as intracellular DHA is readily reduced by an array of biological reductants and enzyme systems [55,56]. …”

Section: Biosynthesis and Uptakementioning

confidence: 99%

Ascorbic acid: Chemistry, biology and the treatment of cancer

Cullen

Buettner

2012

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

765

901

View full text Add to dashboard Cite

Section: Biosynthesis and Uptakementioning

confidence: 99%

Ascorbic acid: Chemistry, biology and the treatment of cancer

Cullen

Buettner

2012

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

765

901

View full text Add to dashboard Cite

“…For instance, as opposed to the normal cells, the cancer cells are often deficient in catalase [71], and/or superoxide dismutase [72], and/or glutathione peroxidase [73]. This selectivity of combined vitamins C and K 3 action on cancer cells may be conditioned by the ability of cancer cells to accumulate vitamin C [74,75]. Such a selective activity was confirmed by the fact that cell death was observed only in the cancer cells, whereas no toxicity or morphological alteration was observed during the histological examination of the main organs of CK 3 -treated mice [16,63,64].…”

Section: Cancer Growth Inhibition By Vitamin Ck 3 Treatmentmentioning

confidence: 99%

Potential Therapeutic Application of the Association of Vitamins C and K3 in Cancer Treatment

Calderón¹,

Cadrobbi

Marques

et al. 2002

CMC

View full text Add to dashboard Cite

The decision of stressed cells to die or to survive is made by integrating signals at different levels through multiple check points. However, initiation and continued progression toward cell death by apoptosis in cancer cells may be blocked by mutation of the tumor suppressor p53 or overexpression of members of the bcl-2 family of proteins. The existence of such mechanisms indicates that cancer cells lose the controls regulating their cell cycle. Therefore, the activation of their programmed cell death appears as a major therapeutic target. Oxidative stress can stimulate growth, trigger apoptosis, or cause necrosis depending upon the dose and the exposure time of the oxidizing agent. A large body of evidence supports the idea that oxidative stress induced by redox cycling of vitamins C and K(3) in association surpasses cancer cellular defense systems and results in cell death. The molecular mechanisms underlying such a process are, however, still unknown. Indeed, several types of cell death may be produced, namely autoschizis, apoptosis and necrosis. Combined vitamin C and K(3) administration in vitro and in vivo produced tumor growth inhibition and increased the life-span of tumor-bearing mice. CK(3)-treatment selectively potentiated tumor chemotherapy, produced sensitization of tumors resistant to some drugs, potentiated cancer radiotherapy and caused inhibition of the development of cancer metastases without inducing toxicity in the host. We propose the association of vitamins C and K(3) as an adjuvant cancer therapy which may be introduced into human cancer therapy without any change in the classical anticancer protocols, and without any supplementary risk for patients.

show abstract

“…Free-radical analytical 126 system 4 technology has been shown to offer a quick, simple, precise, 127 and reliable method for assessing the oxidative status in dairy cows 128 [14] and in horses [15]. Such technology is particularly useful in the and inflammatory parameters is usually not found or is only weak, and 157 the induction of proinflammatory activities caused by AOPPs seems to 158 be more intense [25,26], suggesting that oxidative stress is more closely 159 linked to inflammation and acute-phase reactions than to the advanced 160 glycation process and its end products. [29].…”

mentioning

confidence: 99%