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Antiprotozoal Effects of Wild Plants
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Ethnopharmacology of Wild Plants, 2021
Muhammad Subbayyal Akram, Rao Zahid Abbas, José L. Martinez
Lycorine was isolated from Hippeastrum santacatarina and belongs to family Amaryllidaceae which are the native plant of Brazil (Giordani et al. 2008). Lycorine is one of the most common Amaryllidaceae alkaloids found in H. santacatarina. The T. vaginalis in the peak growth culture was exposed to lycorine at 250 1M, which halted growth of parasite as compared to untreated growth culture. Analysis indicates the arrest in cell cycle of T. vaginalis at the G1 phase after 6 hours of treatment and lycorine also has significant potential to halt the cell cycle of T. vaginalis in the G2/M phase after 24 hours as the cells in the G2/M phase increased in the culture, from 47.37% to 62.31%, which are treated by it (Giordani et al. 2011). This cell cycle arrest confirms the DNA damage of cells and it tries to repair the damage (Weirnet and Hartwell 1990). Lycorine induces alteration in the original shape of trophozoites, depression can be observed on its surface, the endoplasmic reticulum of parasitic cell become undisrupted, and cytoplasmic degeneration and abnormal shape of nucleus were accrued after 24 hours. Lycorine causes paraptosis of T. vaginalis when used with a concentration of 2.5 to 1000 1M (Giordani et al. 2011).
Antileukemic Treatment Targeted at Apoptosis Regulators
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Simone Fulda, Klaus-Michael Debatin
Although caspases are crucial for cell death execution in many systems, caspase-independent apoptosis as well as nonapoptotic modes of cell death have also to be considered. For example, necrosis, autophagy, paraptosis, or some forms of cell death that cannot be easily classified at present have been described (20). Although the signaling pathways and molecules involved in these alternative forms of cell death have not yet exactly been defined, non-caspase proteases such as calpains or cathepsins may be involved (21). The relative contribution of these diverse cell death mechanisms under various conditions both in vitro and in vivo in malignant cells of the hematopoietic system will be an area of future studies.
Eosinophil exocytosis in a poorly differentiated tubular gastric adenocarcinoma: case report
Published in Ultrastructural Pathology, 2022
Rosario Caruso, Eleonora Irato, Luciana Rigoli
Eosinophils may eliminate target tumor cells in vitro by releasing cytotoxic proteins, such as granzyme A, cationic proteins (major basic protein, eosinophil cationic protein, eosinophil-derived neurotoxin, and eosinophil peroxidase), and multiple cytokines including TNF, IFN, and IL-18, and 33.9,10,30,31 Accordingly, our ultrastructural study shows that eosinophils are in intimate contact with undamaged or dying tumor cells. These tumor cells exhibited various degrees of cell injury ranging from mitochondrial swelling, dilation of the nuclear envelope up to cytoplasmic vacuoles, and nuclear chromatin condensation, but without margination of chromatin. These morphological changes are similar to those reported in paraptosis, a non-apoptotic form of programmed cell death, characterized by a vacuolization process that starts with dilatation of the endoplasmic reticulum and the mitochondria.32 Electron microscope is a useful tool to identify various types of cell death.33 Paraptosis can be distinguished from other types of cell deaths such as apoptosis, autophagic cell death, as well as necrosis, according to ultrastructural morphologies such as chromatin condensation and margination (present in apoptosis), accumulation of autophagic vacuoles containing intracellular content (as observable in autophagic cell death), cytoplasmic swelling, and rupture of plasma membrane (necrosis).33
Ginger extract activates caspase independent paraptosis in cancer cells via ER stress, mitochondrial dysfunction, AIF translocation and DNA damage
Published in Nutrition and Cancer, 2021
Divya Nedungadi, Anupama Binoy, Vivek Vinod, Muralidharan Vanuopadath, Sudarslal Sadasivan Nair, Bipin G. Nair, Nandita Mishra
The most prevalent chemotherapy against cancer target the classical apoptosis pathway to curb the uncontrolled division of cells (1). In spite of this, the cancer cells develop resistance to the treatments and keeps proliferating (2). Triple negative breast cancer cells (like MDA-MB-231) lack the therapeutic targets such as estrogen, progesterone and herceptin-2 receptor, owing to which they are classified as the most aggressive and difficult to treat cancer (3). The non small lung cancer cells (like A549) also constitute a major percent of lung tumors which are not amenable to therapy (4). Chemotherapy which is the commonly used mode of treatment triggers apoptotic pathways which are overcome by the heterogeneous cancer cells. Thus alternative approaches which induce non-apoptotic death pathways are sought to circumvent this situation. In recent times, we see the emergence of non-apoptotic cell death pathways which could aid in the effective treatment of cancer cells (5). Paraptosis is a caspase independent death pathway without the hallmark features of apoptosis like DNA fragmentation, caspase activation etc. (6). Cytoplasmic vacuolation due to endoplasmic reticulum (ER) and mitochondrial swelling followed by cell death is the distinctive feature of paraptosis (7–10).
Modulation of Biological Activities in Glioblastoma Mediated by Curcumin
Published in Nutrition and Cancer, 2019
Teresa Trotta, Maria A. Panaro, Elona Prifti, Chiara Porro
Paraptosis is a type of programed cell death that occurs in some stages of the development, and as a response to exposure to natural compounds both in vivo and in vitro models (75). It does not require caspase activation nor involve DNA fragmentation, but sometimes it is activated by protein kinases and/or protein synthesis (76). Paraptosis can take place in glaucoma (77) and neurodegenerative diseases (78). A recent study shows that after exposure to 50 µM of Curcumin for 24 h, the human glioblastoma cell line, A172 cells, display altered Endoplasmic Reticulum (ER) morphology, over expression of ERSR genes and altered expression of ER-related miRNAs, in particular half of miRNAs are downregulated (miR-27a, miR-21,miR-151-3p, miR-27b, miR-222, and miR 125a-5p) and the other half are upregulated (miR-133a, miR-181a, miR-223, miR-449, miR-30a-5p, and miR-1290). The miRNAs regulated by Curcumin participated in AKT-Insulin and p53-BCL2 pathways and decreased AKT protein levels, so Curcumin exerts its cell-death properties by affecting the integrity of the reticulum and leading to paraptosis in the glioblastoma cells (79).