Bromfenvinphos induced suicidal death of human erythrocytes

Officioso, Arbace; Manna, Caterina; Alzoubi, Kousi; Läng, Florian

doi:10.1016/j.pestbp.2015.07.007

Cited by 36 publications

(4 citation statements)

References 75 publications

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“…Signaling contributing to stimulation of eryptosis includes activated caspases, stimulated activity of casein kinase 1 α , Janus‐activated kinase JAK3, protein kinase C, and p38 kinase, as well as impaired activity of AMP activated kinase AMPK, cGMP‐dependent protein kinase, mitogen‐activated kinase and stress‐activated kinase MSK, PAK2 kinase, and sorafenib/sunitinib sensitive kinases . Eryptosis is triggered by a wide variety of xenobiotics and enhanced eryptosis is observed in several clinical conditions including dehydration, hyperphosphatemia, chronic kidney disease (CKD), hemolytic‐uremic syndrome, diabetes, hepatic failure, malignancy, sepsis, sickle‐cell disease, beta‐thalassemia, Hb‐C and G6PD‐deficiency, as well as Wilsons disease …”

Section: Introductionmentioning

confidence: 99%

Ceranib‐2‐induced suicidal erythrocyte death

Signoretto

Zierle

Bhuyan

et al. 2016

Cell Biochemistry & Function

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Ceramide is known to trigger apoptosis of nucleated cells and eryptosis of erythrocytes. Eryptosis is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Besides ceramide, stimulators of eryptosis include increase of cytosolic Ca(2+) -activity ([Ca(2+) ]i ) and oxidative stress. Ceramide is degraded by acid ceramidase and inhibition of the enzyme similarly triggers apoptosis. The present study explored, whether ceramidase inhibitor Ceranib-2 induces eryptosis. Flow cytometry was employed to quantify phosphatidylserine-exposure at the cell surface from annexin-V-binding, cell volume from forward scatter, [Ca(2+) ]i from Fluo3-fluorescence, reactive oxygen species (ROS) from DCF dependent fluorescence, and ceramide abundance utilizing specific antibodies. Hemolysis was estimated from hemoglobin concentration in the supernatant. A 48 h exposure of human erythrocytes to Ceranib-2 significantly increased the percentage of annexin-V-binding cells (≥50 μM) and the percentage of hemolytic cells (≥10 μM) without significantly modifying forward scatter. Ceranib-2 significantly increased Fluo3-fluorescence, DCF fluorescence and ceramide abundance. The effect of Ceranib-2 on annexin-V-binding was not significantly blunted by removal of extracellular Ca(2+) . Ceranib-2 triggers phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to increase of ceramide abundance and induction of oxidative stress, but not dependent on Ca(2+) entry. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Introductionmentioning

confidence: 99%

Ceranib‐2‐induced suicidal erythrocyte death

Signoretto

Zierle

Bhuyan

et al. 2016

Cell Biochemistry & Function

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“…In addition, our results determined that atrazine Gesaprim ® caused blebbing in the erythrocytes of L. spectabilis. The apoptosis of the erythrocytes could be due to the following alterations: a decrease in ATP [32], the activation of caspases [33], alteration of phosphatidylserine [34,35], increased calcium, and the formation of reactive oxygen species (ROS) [36,37]. Studies on exposed fish to xenobiotics have found that caspase 3 can be considered a universal indicator of erythrocyte apoptosis [35,36].…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic Effects of the Atrazine Herbicide on Erythrocytes and Liver Damage in Lithobates spectabilis

Méndez-Tepepa,

Hernández-Pérez,

Juárez-Santacruz

et al. 2023

Fishes

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In Mexico, atrazine is one of the herbicides most widely authorized and used in different irrigation districts. Atrazine is a herbicide that contaminates aquatic systems. Previous studies have shown that atrazine causes damage to red blood cells and liver tissue in different aquatic species, including abnormalities in melanomacrophages. However, more information on amphibians is needed, since most of these studies have been done on fish. Furthermore, no study has determined the effect of atrazine on species native to Mexico. Therefore, in this study, we asked what the effects of atrazine are on the erythrocytes and melanomacrophages of the liver in the male frog (Lithobates spectabilis). In the present study, we analyzed (1) the cytotoxicity of atrazine using the micronucleus test, (2) the area of melanomacrophage centers and the presence of melanin, and (3) the characterization of liver damage using histological techniques. Our results show that atrazine is cytotoxic to erythrocytes, increases the area of and melanin presence in melanomacrophage centers, and causes liver damage in male L. spectabilis. Therefore, hepatotoxicity and cytotoxicity are indicators of environmental stress. We suggest monitoring Mexico’s aquatic systems and further analyzing atrazine effects and other pollutants on native species.

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“…Erythrocytes from newborns are highly sensitive to oxidative stress leading to rapid eryptosis and subsequent clearance of those erythrocytes following birth . Eryptosis is triggered by complement, hyperosmotic shock, energy depletion, oxidative stress, cellular K + loss, hyperthermia and a wide variety of xenobiotics including diverse cytostatic drugs (see below).…”

Section: Introductionmentioning

confidence: 99%

Suicidal death of erythrocytes in cancer and its chemotherapy: A potential target in the treatment of tumor‐associated anemia

Lang

Bissinger

Qadri

et al. 2017

Intl Journal of Cancer

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In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis characterized by cell shrinkage and cell membrane scrambling. Eryptotic erythrocytes are rapidly cleared from circulating blood and may adhere to the vascular wall. Stimulation of eryptosis thus impairs microcirculation and leads to anemia as soon as the loss of erythrocytes cannot be fully compensated by enhanced erythropoiesis. Signaling stimulating eryptosis includes increase of cytosolic Ca -activity, ceramide, caspases, calpain, p38-kinase, protein-kinase C, Janus-activated kinase 3, casein-kinase 1α, and cyclin-dependent kinase 4. Eryptosis is inhibited by AMP-activated kinase, p21-activated kinase 2, cGMP-dependent protein-kinase, mitogen- and stress-activated kinase, and sorafenib- and sunitinib-sensitive tyrosine-kinases. Eryptosis is triggered by complement, hyperosmotic shock, energy-depletion, oxidative stress, multiple xenobiotics including diverse cytostatic drugs, diabetes, hepatic failure, iron-deficiency, chronic kidney disease, hemolytic-uremic-syndrome, fever, systemic lupus erythematosus, infections, sepsis, sickle cell anemia, thalassemia, glucose-6-phosphate-dehydrogenase deficiency, and Wilson´s disease. Compelling evidence points to a decisive role of eryptosis in anemia of malignancy. As shown for lung cancer, eryptosis inducing plasma components accumulate in cancer patients and trigger oxidative stress and ceramide. The tumor-induced eryptosis leads to anemia despite increased erythropoiesis. The stimulation of eryptosis in malignancy is compounded by cytostatic treatment, as a large number of cytostatic agents trigger eryptosis. Inhibiting eryptosis may be a useful strategy in reducing tumor-induced anemia and impaired microcirculation. Inhibitors of eryptosis may, however, be harmful, if they similarly interfere with death of tumor cells. Clearly, additional experimental effort is required to achieve killing of tumor cells with simultaneous avoidance of stimulated eryptosis.

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Bromfenvinphos induced suicidal death of human erythrocytes

Cited by 36 publications

References 75 publications

Ceranib‐2‐induced suicidal erythrocyte death

Ceranib‐2‐induced suicidal erythrocyte death

Cytotoxic Effects of the Atrazine Herbicide on Erythrocytes and Liver Damage in Lithobates spectabilis

Suicidal death of erythrocytes in cancer and its chemotherapy: A potential target in the treatment of tumor‐associated anemia

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