Ascorbic acid modulates pathogenecity markers of Candida albicans

Khan L.A.1*, Ojha R.2, Manzoor N.3
1Department of Biosciences, Faculty of Natural Sciences
2Research Scholar, Department of Biosciences, Jamia Millia Islamia (Central University), New Delhi, India.
3Assistant Professor, Department of Biosciences, Jamia Millia Islamia (Central University), New Delhi, India.
* Corresponding Author : luqmank5@rediffmail.com

Received : -     Accepted : -     Published : 15-06-2009
Volume : 1     Issue : 1       Pages : 19 - 24
Int J Microbiol Res 1.1 (2009):19-24
DOI : http://dx.doi.org/10.9735/0975-5276.1.1.19-24

Keywords : Candida albicans, ascorbic acid, proteinase, oxidative stress, cytotoxicity, hyphal transition
Conflict of Interest : None declared
Acknowledgements/Funding : The current study was supported by UGC India, grant no: 33-223/2007 to Dr. L.A. Khan and Dr. N. Manzoor. Authors wish to thank Amber Khan and Aijaz Ahmad for their cooperation and support

Cite - MLA : Khan L.A., et al "Ascorbic acid modulates pathogenecity markers of Candida albicans." International Journal of Microbiology Research 1.1 (2009):19-24. http://dx.doi.org/10.9735/0975-5276.1.1.19-24

Cite - APA : Khan L.A., Ojha R., Manzoor N. (2009). Ascorbic acid modulates pathogenecity markers of Candida albicans. International Journal of Microbiology Research, 1 (1), 19-24. http://dx.doi.org/10.9735/0975-5276.1.1.19-24

Cite - Chicago : Khan L.A., Ojha R., and Manzoor N. "Ascorbic acid modulates pathogenecity markers of Candida albicans." International Journal of Microbiology Research 1, no. 1 (2009):19-24. http://dx.doi.org/10.9735/0975-5276.1.1.19-24

Copyright : © 2009, Khan L.A., et al, Published by Bioinfo Publications. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Abstract

Candida albicans is an opportunistic commensal of the human gastrointestinal tract and vaginal mucosa, causing opportunistic fungal infections in an immunocompromised patient. In the present study we have investigated the effect of ascorbic acid on growth and its several pathogenicity markers. Turbidometric measurement for growth; proteinase assay, WST-1 cell cytotoxicity assay, colony count method and inverted microscopy were performed to check pathogenecity markers of C. albicans ATCC 10261 strain. 150 mg/ml concentration of ascorbic acid arrests cell growth. It was observed that higher ascorbate level of 250 mg/ml reduces proteinase secretion (an important mechanism suggestive of virulence in Candida) exhibited by mean precipitation zone value of 2.375 which is remarkably less than that of Control cells (value 4.125). At higher concentration of ascorbic acid increases cell cytotoxcity (79.71 percent inhibition at 150 mg/ml) and decreases percent viability under oxidative stress (98 percent reduction at 250 mg/ml concentration). Transition studies showed cessation of germ tube induction and hyphae formation at lower concentrations (15 mg onwards) of ascorbic acid. Results indicate that higher ascorbic acid level somehow decreases pathogenic attribute of Candida albicans, while yeast to hyphal studies show an exception, were lower concentration was effective in inhibiting hyphae formation. Thus ascorbic acid exhibits its pro-oxidant nature in present in-vitro studies.

References

[1] Odds F.C. (1988) Candida and candidosis. 2nd ed. Bailliere-Tindall. London  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[2] Cathcart R.F., (1981 Medical Hypotheses, 7, 1359-1376  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[3] Paillaud E., Merlier I., Dupeyron C. Scherman E. Poupon J. and Bories P.N. (2004) Br J Nut, 92(5), 861-7  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[4] Yaohui W.,Thomas A., Oran K. Stephen C. Steven C. and Rumsey. (1997) Proc. Natl. Acad. Sci. USA, 94, 13816–13819  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[5] Yaohui W.,Thomas A., Oran K. Stephen C. Steven C. and Rumsey. (1997) Proc. Natl. Acad. Sci. USA, 94, 13816–13819  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[6] Brajtburg J., Elberg S., Kobayashi G.S. and Medoff G. (1989) J Antimicrob Chemother, 24(3), 333-7  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[7] Mailland, Federico. (Jan 2005). European Patent. EP1500394  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[8] Rita de C.M., Marlise I.K., Magda B.G. Janaina A.O.R. Reginaldo B.G. and Jose F.H (2006) Brazilian Journal of Microbiology, 37, 26-32  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[9] Padmashree C.G.R., Akiko N., Gena Y. Won and Neta D. (2006) Molecular Biology of the Cell, (17), 4364–4378  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[10] Huh W.K., Lee B.H., Kim S.T. Kim Y.R. Rhie G.E. and Baek Y.W. (1998) Mol Microbiol, 30, 895–903  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[11] Anitra C.C. and Balz F. (1999) Am J Clin Nutr, 69 (6), 1086-1107.  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[12] Hube B. (1998) Rev.Iberoam. Micol, 15, 68- 71.  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[13] De Bernardis F., Sullivan P.A and Cassone A. (2001) Med Mycol, 39, 303–313  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[14] Hube B.and J. Naglik (2001) Microbiology, 147, 1997–2005.  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[15] Victor H.G., Juan Carlos V.and David W.G. (2001) J Biol Chem, 276 (44), 40955– 40961  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[16] Johnsen A.R., Bendixen K. and Karlson U. (2002) Appl Environ Microbiol, 68, 2683–2689  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[17] McCluskey C., Quinn J.P. and McGrath J.W. (2005) Microb Ecol, 49,379–387  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[18] Kuhn D.M., Balkis M., Chandra J. Mukherjee P.K. and Ghannoum M. (2003) J Clin Microbiol, 41, 506–508  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[19] Meletiadis J., Mouton J.W., Meis F., Bouman B.A. Donnelly J.P. and Verweij P.E. (2001) J Clin Microbiol, 39, 3402– 3408  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[20] Wiederhold N.P., Kontoyiannis D.P., Prince R. and Lewis R.E (2005) Antimicrob Agents Chemother, 49, 5146–5148  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[21] Zhou W.C. and Zhou H.Y. (2006) Chin J Pharm, 37,125–133  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[22] Wen P., Chen L. and Guo Y.F. (2007) J Microbiol, 27:104–106  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[23] Levine M., Conry-Cantilena C., Wang Y. Welch R.W. Washko P.W. and Dhariwal K.R. (1996) Proc.Natl. Acad.Sci. USA,93, 3704-3709.  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus  

[24] Gold H.S. and Moellering R.C.J. (1996) N.Engl.J.Med, 335, 1445-1453  
» CrossRef   » Google Scholar   » PubMed   » DOAJ   » CAS   » Scopus