Research: BLASZCZAK and COLLEAGUES,  

Listed in Issue 281

Abstract

BLASZCZAK and COLLEAGUES,   1 Radiobiology Lab, The Greater Poland Cancer Centre, Garbary, 61-866 Poznan, Poland. w.z.blaszczak@gmail.com ; 2 Radiobiology Lab, The Greater Poland Cancer Centre, Garbary, 61-866 Poznan, Poland. wbarczak@ump.edu.pl ; 3 Department of Head and Neck Surgery, Poznan University of Medical Sciences, The Greater Poland Cancer Centre, Garbary, 61-866 Poznan, Poland. wbarczak@ump.edu.pl ;       4 Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, 60-355 Poznan, Poland. juliamasternak@wp.pl ;5 Centre for Orthodontic Mini-implants at the Department and Clinic of Maxillofacial Orthopedics and Orthodontics, Poznan University of Medical Sciences, 60-812 Poznan, Poland. pkopczynski@orto1.net ; 6 Department of Pathology and Laboratory Medicine, Brown University, Providence, RI 02912, USA. anatoly_zhitkovich@brown.edu; 7 Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, 60-355 Poznan, Poland. blazejr@ump.edu.pl reviewed the published literature regarding how vitamin C alters aspects of cancer cell metabolism which may promote activity of specific drugs.

 

Background

Ascorbic acid (vitamin C) has been gaining attention as a potential treatment for human malignancies. Various experimental studies have shown the ability of pharmacological doses of vitamin C alone or in combinations with clinically used drugs to exert beneficial effects in various models of human cancers.

Methodology

Cytotoxicity of high doses of vitamin C in cancer cells appears to be related to excessive reactive oxygen species generation and the resulting suppression of the energy production via glycolysis.

Results

A hallmark of cancer cells is a strongly upregulated aerobic glycolysis, which elevates its relative importance as a source of ATP (Adenosine 5'-triphosphate). Aerobic glycolysis is maintained by a highly increased uptake of glucose, which is made possible by the upregulated expression of its transporters, such as GLUT-1, GLUT-3, and GLUT-4. These proteins can also transport the oxidized form of vitamin C, dehydroascorbate, permitting its preferential uptake by cancer cells with the subsequent depletion of critical cellular reducers as a result of ascorbate formation. Ascorbate also has a potential to affect other aspects of cancer cell metabolism due to its ability to promote reduction of iron(III) to iron(II) in numerous cellular metalloenzymes. Among iron-dependent dioxygenases, important targets for stimulation by vitamin C in cancer include prolyl hydroxylases targeting the hypoxia-inducible factors HIF-1/HIF-2 and histone and DNA demethylases.

Conclusion

Altered metabolism of cancer cells by vitamin C can be beneficial by itself and promote activity of specific drugs.

References

Wiktoria Blaszczak  1 , Wojciech Barczak  2   3 , Julia Masternak  4 , Przemysław Kopczyński  5 , Anatoly Zhitkovich  6 , Błażej Rubiś  7. Vitamin C as a Modulator of the Response to Cancer Therapy Molecules ;24(3):453. https://doi.org/10.3390/molecules24030453. Jan 28 2019.

ICAN Skyscraper

Scientific and Medical Network 2

Royal Rajasthan Cycle 2021

Amazon Wilderness Trek 2022

Cycle Kilimanjaro to the Coast 2022

top of the page