Inhibition by superoxide dismutase and catalase of the damage of isolated Leishmania mexicana amazonensis by phenazine methosulfate

Nabi, Zeenat F.; Rabinovitch, M.

doi:10.1016/0166-6851(84)90028-8

Cited by 17 publications

(5 citation statements)

References 11 publications

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“…It is well established that reactive oxygen species (ROS) generated by antiparasitic agents or macrophages can induce cell death in intracellular parasites (Mauel et al 1984;Nabi and Rabinovitch 1984) and are therefore important regulators of protozoal infection (Schirmer et al 1987;Solbach and Laskay 2000). The in vitro effects of ROS are also well documented in a variety of unicellular eukaryotes and also in mammalian cells (Madeo et al 1999;Ridgley et al 1999;Vollgraf et al 1999;Li et al 2000;Das et al 2001).…”

Section: Introductionmentioning

confidence: 94%

Hydrogen peroxide induces caspase activation and programmed cell death in the amitochondrial Tritrichomonas foetus

Mariante

Guimarães

Linden

et al. 2003

Histochemistry and Cell Biology

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Tritrichomonas foetus is an amitochondrial parasite protist which lacks typical eukaryote organelles such as mitochondria and peroxisomes, but possesses the hydrogenosome, a double-membrane-bound organelle that produces ATP. The cell death of amitochondrial organisms is poorly studied. In the present work, the cytotoxic effects of hydrogen peroxide on T. foetus and its participation on cell death were analyzed. We took advantage of several microscopy techniques, including videomicroscopy, light microscopy immunocytochemistry for detection of caspase activation, and scanning and transmission electron microscopy. We report here that in T. foetus: (1) H(2)O(2) leads to loss of motility and induces cell death, (2) the dying cells exhibit some characteristics similar to those found during the death of other organisms, and (3) a caspase-like protein seems to be activated during the death process. Thus, we propose that, although T. foetus does not present mitochondria nor any known pathways of cell death, it is likely that it bears mechanisms of cell demise. T. foetus exhibits morphological and physiological alterations in response to H(2)O(2) treatment. The hydrogenosome, a unique organelle which is supposed to share a common ancestral origin with mitochondria and has an important role in oxidative responses in trichomonads, is a candidate for participating in this event.

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Section: Introductionmentioning

confidence: 94%

Hydrogen peroxide induces caspase activation and programmed cell death in the amitochondrial Tritrichomonas foetus

Mariante

Guimarães

Linden

et al. 2003

Histochemistry and Cell Biology

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“…Upon transmission to the mammalian host as bloodstream-infective promastigotes, they are engulfed by the macrophages where they reside intracellularly as non-flagellated amastigotes (21). At the time of engulfment of the promastigotes by the macrophages, ROS is generated by the host cell in an attempt to kill the parasites (22). ROS is also generated by anti-leishmanial drugs targeting ⌬ m of amastigotes to kill them (23).…”

mentioning

confidence: 99%

Increase in Cytosolic Ca2+ Levels through the Activation of Non-selective Cation Channels Induced by Oxidative Stress Causes Mitochondrial Depolarization Leading to Apoptosis-like Death in Leishmania donovaniPromastigotes

Mukherjee

Sudhandiran

et al. 2002

Journal of Biological Chemistry

190

167

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Reactive oxygen species are important regulators of protozoal infection. Promastigotes of Leishmania donovani, the causative agent of Kala-azar, undergo an apoptosis-like death upon exposure to H 2 O 2 . The present study shows that upon activation of death response by H 2 O 2 , a dose-and time-dependent loss of mitochondrial membrane potential occurs. This loss is accompanied by a depletion of cellular glutathione, but cardiolipin content or thiol oxidation status remains unchanged. ATP levels are reduced within the first 60 min of exposure as a result of mitochondrial membrane potential loss. A tight link exists between changes in cytosolic Ca 2؉ homeostasis and collapse of the mitochondrial membrane potential, but the dissipation of the potential is independent of elevation of cytosolic Na ؉ and mitochondrial Ca 2؉ . Partial inhibition of cytosolic Ca 2؉ increase achieved by chelating extracellular or intracellular Ca 2؉ by the use of appropriate agents resulted in significant rescue of the fall of the mitochondrial membrane potential and apoptosis-like death. It is further demonstrated that the increase in cytosolic Ca 2؉ is an additive result of release of Ca 2؉ from intracellular stores as well as by influx of extracellular Ca 2؉ through flufenamic acid-sensitive non-selective cation channels; contribution of the latter was larger. Mitochondrial changes do not involve opening of the mitochondrial transition pore as cyclosporin A is unable to prevent mitochondrial membrane potential loss. An antioxidant like Nacetylcysteine is able to inhibit the fall of the mitochondrial membrane potential and prevent apoptosis-like death. Together, these findings show the importance of non-selective cation channels in regulating the response of L. donovani promastigotes to oxidative stress that triggers downstream signaling cascades leading to apoptosis-like death.Mitochondria are pivotal in controlling cell life and death (1). Maintenance of proper mitochondrial transmembrane potential (⌬ m ) 1 is essential for the survival of the cell as it drives the synthesis of ATP and maintains oxidative phosphorylation (2). Recently, the study of mitochondrial potential has become a focus of apoptosis regulation as many investigations demonstrate a major functional impact of mitochondrial alterations on apoptosis (2). Apoptosis is a process of cell death in which the cells undergo nuclear and cytoplasmic shrinkage; the chromatin is condensed and partitioned into multiple fragments, and finally the cells are broken into multiple membrane-bound bodies. In a number of experimental systems, disruption of ⌬ m constitutes a constant early event of the apoptotic process that precedes nuclear disintegration (3-5). For example, in thymocytes or tumor necrosis factor-stimulated U937 cells (3, 6), thymocytes or imexon-treated myeloma cells (5, 7), and PC-12 cells (8), a loss of ⌬ m occur as an early change associated with apoptosis. Lymphocytes with low ⌬ m show irreversible commitment to apoptosis in comparison to cells with high ⌬ m that do...

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“…Future research is needed to determine if the mechanisms of action are similar to what has been described in fungi and bacteria. Indeed, one study by Nabi and Rabinovitch (1984) suggests that ROS are important for PMS-mediated killing of L. m. amazonensis.…”

Section: Phenazines In Bacterial-fungal Interactionsmentioning

confidence: 97%

The Yin and Yang of Phenazine Physiology

Grahl

Kern

Newman

et al. 2013

Microbial Phenazines

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Microorganisms are seldom solitary. They are surrounded by both clonal cells and other members of the local microbial community, and they often exist in, on, or in close proximity to multi-cellular host organisms like plants and humans. Whether in vivo during infection or in situ in the nutrient rich rhizosphere, microorganisms affect each other and the host. Phenazines, a class of secondary metabolites secreted by diverse bacteria, are best known for their antibiotic properties and have been shown to affect a broad spectrum of organisms ranging from bacteria over fungi, plants, nematodes, parasites, and humans. However, phenazines are also involved in numerous aspects of bacterial physiology like survival, iron acquisition, signaling, and biofilm formation in ways that have the potential to increase the fitness of both the phenazine-producing strain and non-producers alike. The overarching theme of this chapter is that phenazines can be beneficial or detrimental to organisms, depending on the milieu and one's perspective. In this chapter, we will highlight specific examples to discuss the yin and yang of phenazine physiology.

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Inhibition by superoxide dismutase and catalase of the damage of isolated Leishmania mexicana amazonensis by phenazine methosulfate

Cited by 17 publications

References 11 publications

Hydrogen peroxide induces caspase activation and programmed cell death in the amitochondrial Tritrichomonas foetus

Hydrogen peroxide induces caspase activation and programmed cell death in the amitochondrial Tritrichomonas foetus

Increase in Cytosolic Ca2+ Levels through the Activation of Non-selective Cation Channels Induced by Oxidative Stress Causes Mitochondrial Depolarization Leading to Apoptosis-like Death in Leishmania donovaniPromastigotes

The Yin and Yang of Phenazine Physiology

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