Metronidazole induces programmed cell death in the protozoan parasite Blastocystis hominis

Microbiology ◽  
2004 ◽  
Vol 150 (1) ◽  
pp. 33-43 ◽  
Author(s):  
A. M. A. Nasirudeen ◽  
Yap Eu Hian ◽  
Mulkit Singh ◽  
Kevin S. W. Tan
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Protozoan Parasite ◽  
Blastocystis Hominis

Do Blastocystis hominis colony forms undergo programmed cell death?

2001 ◽  
Vol 87 (5) ◽  
pp. 362-367 ◽  
Author(s):  
Kevin S. W. Tan ◽  
J. Howe ◽  
E.H. Yap ◽  
M. Singh
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Blastocystis Hominis

Blastocystis hominis : evidence for caspase-3-like activity in cells undergoing programmed cell death

2001 ◽  
Vol 87 (7) ◽  
pp. 559-565 ◽  
Author(s):  
Nasirudeen A. ◽  
Singh M. ◽  
Yap E. ◽  
Tan K.
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Caspase 3 ◽  
Blastocystis Hominis ◽  
In Cells

scholarly journals Characterization of Metacaspases with Trypsin-Like Activity and Their Putative Role in Programmed Cell Death in the Protozoan Parasite Leishmania

2007 ◽  
Vol 6 (10) ◽  
pp. 1745-1757 ◽  
Author(s):  
Nancy Lee ◽  
Sreenivas Gannavaram ◽  
Angamuthu Selvapandiyan ◽  
Alain Debrabant
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Leishmania Donovani ◽  
Protozoan Parasite ◽  
Protein Band ◽  
Mrna Levels ◽  
Enzymatic Assays ◽  
Rich Domain ◽  
Axenic Amastigotes

ABSTRACT In this report, we have characterized two metacaspases of Leishmania donovani, L. donovani metacaspase-1 (LdMC1) and LdMC2. These two proteins show 98% homology with each other, and both contain a characteristic C-terminal proline-rich domain. Both genes are transcribed in promastigotes and axenic amastigotes of L. donovani; however, LdMC1 shows increased mRNA levels in axenic amastigotes. An anti-LdMC antibody was obtained and showed reactivity with a single ∼42-kDa protein band in both promastigote and axenic amastigote parasite whole-cell lysates by Western blotting. Pulse-chase experiments suggest that LdMCs are not synthesized as proenzymes, and immunofluorescence studies show that LdMCs are associated with the acidocalcisome compartments of L. donovani. Enzymatic assays of immunoprecipitated LdMCs show that native LdMCs efficiently cleave trypsin substrates and are unable to cleave caspase-specific substrates. Consistently, LdMC activity is insensitive to caspase inhibitors and is efficiently inhibited by trypsin inhibitors, such as leupeptin, antipain, and N α-tosyl-l-lysine-chloromethyl ketone (TLCK). In addition, our results show that LdMC activity was induced in parasites treated with hydrogen peroxide, a known trigger of programmed cell death (PCD) in Leishmania and that parasites overexpressing metacaspases are more sensitive to hydrogen peroxide-induced PCD. These findings suggest that Leishmania metacaspases are not responsible for the caspase-like activities reported in this organism and suggest a possible role for LdMCs as effector molecules in Leishmania PCD.

scholarly journals Programmed cell death in the unicellular protozoan parasite Leishmania

2002 ◽  
Vol 9 (1) ◽  
pp. 53-64 ◽  
Author(s):  
N Lee ◽  
S Bertholet ◽  
A Debrabant ◽  
J Muller ◽  
R Duncan ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Protozoan Parasite ◽  
Parasite Leishmania

scholarly journals Staurosporine-induced programmed cell death in Blastocystis occurs independently of caspases and cathepsins and is augmented by calpain inhibition

Microbiology ◽  
2010 ◽  
Vol 156 (5) ◽  
pp. 1284-1293 ◽  
Author(s):  
Jing Yin ◽  
Josephine Howe ◽  
Kevin S. W. Tan
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Mammalian Cells ◽  
Membrane Integrity ◽  
Protozoan Parasite ◽  
Cysteine Protease Inhibitor ◽  
Nuclear Condensation ◽  
Induced Apoptosis ◽  
Mitochondrial Transition Pore

Previous studies have shown that the protozoan parasite Blastocystis exhibits apoptotic features with caspase-like activity upon exposure to a cytotoxic monoclonal antibody or the anti-parasitic drug metronidazole. The present study reports that staurosporine (STS), a common apoptosis inducer in mammalian cells, also induces cytoplasmic and nuclear features of apoptosis in Blastocystis, including cell shrinkage, phosphatidylserine (PS) externalization, maintenance of plasma membrane integrity, extensive cytoplasmic vacuolation, nuclear condensation and DNA fragmentation. STS-induced PS exposure and DNA fragmentation were abolished by the mitochondrial transition pore blocker cyclosporine A and significantly inhibited by the broad-range cysteine protease inhibitor iodoacetamide. Interestingly, the apoptosis phenotype was insensitive to inhibitors of caspases and cathepsins B and L, while calpain-specific inhibitors augmented the STS-induced apoptosis response. While the identities of the proteases responsible for STS-induced apoptosis warrant further investigation, these findings demonstrate that programmed cell death in Blastocystis is complex and regulated by multiple mediators.

scholarly journals Cell Death after Photodynamic Therapy Treatment in Unicellular Protozoan Parasite Tritrichomonas foetus

2020 ◽  
Author(s):  
Newton Soares da Silva ◽  
Aline Margraf Ferreira ◽  
Carolina Weigert Galvão ◽  
Rafael Mazer Etto ◽  
Cristina Pacheco Soares
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Programmed Cell Death ◽  
Protozoan Parasite ◽  
Future Research ◽  
Tritrichomonas Foetus ◽  
Cellular Death ◽  
Nuclear Abnormalities ◽  
Cell Changes ◽  
Therapy Treatment

Programmed cell death in T. foetus does not seem to make sense at first sight; however, different mechanisms of cellular death in this unicellular organism have been observed. This review summarizes the available data related to programmed cell death already published for the cattle parasite T. foetus and attempts to clarify some crucial points to understand this mechanism found in non-mitochondriates parasites, as well as assist in future research. Important results with different treatments showed that the T. foetus can choose among different pathways how to initiate cell death. Thus, a major challenge for cellular death research remains the identification of the molecular cell death machinery of this protist, such as caspases pathway, nuclear abnormalities, morphology cell changes, cellular death in this parasite and the prospects in the future research. Although, the possibility of the existence of different pathways to cell death in trichomonads is discussed and a model for possible executioners pathways during T. foetus cell death is proposed.

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