Adhesion Molecules-28

Advances and Experimental-3

Aging-9

Agricultural Biotechnology-37

Angiogenesis-29

Antisense-4

Apoptosis-49

Atherosclerosis-12

Autoimmunity-69

Bacterial Virulence-18

Bioinformatics-13

BioMaterials-18

Biosurfactants-1

Biotechnology-99

Cancer Genetics-25

Cancer Metastasis-19

Cell Biology-16

Cell Cycle-34

Cell Metabolism-327

Channels and Transporters-79

Chaperones-11

Circadian Rhythms-13

Coagulation-14

Cytokines/Growth Factors-52

Development-223

DNA-56

DNA Surveillance and Repair-42

Drug Design-17

Endocrine-66

Evolution-33

Extracellular Matrix-30

Gastroenterology-52

Gene Expression-178

Gene Therapy-53

Heart-61

Heat Shock Proteins-19

Hematology-11

Immunology-93

Infectious Disease-71

Ischemia-Reperfusion-33

Leptin and Leptin Antagonists-1

Medical-20

MHC-17

Mitochondria-17

Molecular Biology-15

Molecular Complexes and Signaling-1

Nanomedicine-30

Neurodegenerative Disease-72

Neuropharmacology-112

Neuroscience-38

Nucleus-15

Oncogenes-8

Oncology-87

Parasitic Disease-12

Pharmacogenomics-14

Prebiotic Evolution-2

Protein-12

Reproductive Biology-59

RNA-152

Signal Transduction-186

Stem Cells-80

Surgery-37

T-Cell Activation-12

Tissue Engineering-116

Transplant-51

Vaccines-82

Viruses-85

Chapter category: Apoptosis

Cell Death in Trichomonads

Chapter authors:
Marlene Benchimol

Programmed cell death (PCD) is not confined to mammals and is extremely widespread, possibly universal, in multicellular animals. It is now evident that PCD also occurs in single-celled organisms and it is an important feature of host-pathogen relationships. Protists are capable of eliciting an apoptotic response in several circumstances. Studies are in course in order to establish whether these organisms share some or all of the effectors and regulators common to multicellular PCD or have evolved their own divergent pathways. Trichomonads are amitochondrial protists that inhabit different ecological niches. Among them Tritrichomonas foetus, a cattle parasite and Trichomonas vaginalis, a human parasite, are the most important because they cause trichomoniasis, a sexually transmitted disease. They do not possess mitochondria, but harbor another type of membrane-bounded organelle, an unusual anaerobic energy-producing organelle called hydrogenosome. Studies of cell death in trichomonads are under way in order to establish whether the hydrogenosome could represent an alternative to mitochondria whether these organisms possess all caspase activities and which conditions lead trichomonads to cell death. In these organisms the known “mitochondrial cell death machinery” is supposed to be distinct from mitochondrial eukaryotes. The presence of a cell death program in trichomonads suggests the existence either of a dependent or independent caspase-like execution pathway in such organisms. Dramatic changes in trichomonad morphology are observed when the cells are under stress, such as after drug treatment and nutrient depletion. These changes include intense plasma membrane and nuclear envelope blebbing, nucleus fragmentation, an abnormal number of oversized vacuoles and altered hydrogenosomes. DNA fragmentation, exposure of phosphatidylserine (PS) in the outer leaflet of the plasma membrane, hydrogenosomal membrane potential dissipation, are features observed in apoptotic cells. Trichomonads also present autophagic processes, observed when altered hydrogenosomes, misshapen flagella, abnormal cellular elements and tubulin precipitates are located in autophagic vacuoles, which are limited by a double or multiple concentric membrane. In all stress situations, trichomonads form pseudocysts, cells with internalized flagella. Different forms of cell death, such as apoptosis, autophagy and necrosis have been shown to exist in trichomonads and so the possibility of the existence of different pathways to cell death in trichomonads is raised.

Marlene Benchimol
Rua Jornalista Orlando Dantas

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