Trifluoperazine-Induced Suicidal Erythrocyte Death and S-Nitrosylation Inhibition, Reversed by the Nitric Oxide Donor Sodium Nitroprusside | Zendy

Mehrdad Ghashghaeinia | Zendy; Mauro C. Wesseling | Zendy; Elena Ramos | Zendy; Polina PetkovaKirova | Zendy; Sabrina Waibel | Zendy; Elisabeth Lang | Zendy; Rosi Bissinger | Zendy; Kossai Alzoubi | Zendy; Baerbel Edelmann | Zendy; Zohreh Hosseinzadeh | Zendy; Peter Dreischer | Zendy; Azam Shahvaroughi-Farahani | Zendy; Ulrich Mrowietz | Zendy; Martin Köberle | Zendy; Lars Kaestner | Zendy; Ingolf Bernhardt | Zendy; Antonio Martı́nez-Ruiz | Zendy; Thomas Wieder | Zendy; Florian Läng | Zendy

Open Access

Trifluoperazine-Induced Suicidal Erythrocyte Death and S-Nitrosylation Inhibition, Reversed by the Nitric Oxide Donor Sodium Nitroprusside

Author(s) -

Mehrdad Ghashghaeinia,

Mauro C. Wesseling,

Elena Ramos,

Polina PetkovaKirova,

Sabrina Waibel,

Elisabeth Lang,

Rosi Bissinger,

Kossai Alzoubi,

Baerbel Edelmann,

Zohreh Hosseinzadeh,

Peter Dreischer,

Azam Shahvaroughi-Farahani,

Ulrich Mrowietz,

Martin Köberle,

Lars Kaestner,

Ingolf Bernhardt,

Antonio Martı́nez-Ruiz,

Thomas Wieder,

Florian Läng

Publication year - 2017

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000479838

Subject(s) - sodium nitroprusside , nitric oxide , trifluoperazine , chemistry , pharmacology , s nitrosylation , nitrosylation , medicine , biophysics , biochemistry , biology , calmodulin , calcium , enzyme , cysteine

The high potency antipsychotic drug trifluoperazine (10-[3-(4-methyl-1-piperazinyl)-propyl]-2-(trifluoromethyl)-(10)H-phenothiazine dihydrochloride; TFP) may either counteract or promote suicidal cell death or apoptosis. Similar to apoptosis, erythrocytes may enter eryptosis, characterized by phosphatidylserine exposure at the cell surface and cell shrinkage. Eryptosis can be stimulated by an increase in cytoplasmic Ca2+ concentration ([Ca2+]i) and inhibited by nitric oxide (NO). We explored whether TFP treatment of erythrocytes induces phosphatidylserine exposure, cell shrinkage, and calcium influx, whether it impairs S-nitrosylation and whether these effects are inhibited by NO.

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