Cytotoxic effects of imipramine on platelets

David J. Goode; Herbert Y. Meltzer

doi:10.1016/0006-2952(74)90186-5

Cytotoxic effects of imipramine on platelets

David J. Goode^*, Herbert Y. Meltzer

^*Corresponding author for this work

Psychiatry and Behavioral Sciences

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Incubation for 30 min at 30° with 1 mM imipramine, chlorpromazine or phencyclidine produced increases in creatine phosphokinase (CPK) activity of rat platelet-rich plasma (PRP). Increases in lactic dehydrogenase (LDH) activity of human PRP were produced by imipramine at 0.5 mM. Ouabain, diphenylhydantoin, calcium chloride, EDTA and thrombin did not affect CPK activity of rat PRP. None of the dugs tested except 10 mM diphenylhydantoin affected CPK or LDH activity in platelet-poor plasma. Increases in enzyme activity of PRP produced by 1 mM imipramine were associated with a decrease in platelet count. The increases were independent of temperature of incubation from 0° to 30° and were maximal after a 5-min incubation. The release of LDH and CPK caused by the above drugs is not related to platelet aggregation or the platelet release reaction. The increases in LDH and CPK activity in PRP appear to be the result of platelet destruction or damage to the platelet plasma membrane with release of these enzymes.

Original language	English (US)
Pages (from-to)	2629-2635
Number of pages	7
Journal	Biochemical Pharmacology
Volume	23
Issue number	18
DOIs	https://doi.org/10.1016/0006-2952(74)90186-5
State	Published - Sep 15 1974

Funding

The present study was designed to investigate the effects of CPZ and imipramine on the release of CPK from rat platelets and lactic dehydrogenase (LDH) from human platelets in vitro. Both enzymes are mainly soluble in the cytoplasm rather than present in organelles. After determining that both drugs could promote release of these enzymes from platelets, the mechanism of the imipramine-induced release of CPK and LDH from platelets was further studied by comparison of its action with agents which promote platelet aggregation and the platelet release reaction, as well * This work was supported by State of Illinois 231-12-RD and USPHS MH 16-1271 Dr. Goode is a recipient of a fellowship from the Foundations Fund for Research in Psychiatry. Dr. Meltzer is the recipient of Research Scientist Development Award MH 47,808. 2629

ASJC Scopus subject areas

Biochemistry
Pharmacology

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10.1016/0006-2952(74)90186-5

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title = "Cytotoxic effects of imipramine on platelets",

abstract = "Incubation for 30 min at 30° with 1 mM imipramine, chlorpromazine or phencyclidine produced increases in creatine phosphokinase (CPK) activity of rat platelet-rich plasma (PRP). Increases in lactic dehydrogenase (LDH) activity of human PRP were produced by imipramine at 0.5 mM. Ouabain, diphenylhydantoin, calcium chloride, EDTA and thrombin did not affect CPK activity of rat PRP. None of the dugs tested except 10 mM diphenylhydantoin affected CPK or LDH activity in platelet-poor plasma. Increases in enzyme activity of PRP produced by 1 mM imipramine were associated with a decrease in platelet count. The increases were independent of temperature of incubation from 0° to 30° and were maximal after a 5-min incubation. The release of LDH and CPK caused by the above drugs is not related to platelet aggregation or the platelet release reaction. The increases in LDH and CPK activity in PRP appear to be the result of platelet destruction or damage to the platelet plasma membrane with release of these enzymes.",

author = "Goode, \{David J.\} and Meltzer, \{Herbert Y.\}",

note = "Funding Information: The present study was designed to investigate the effects of CPZ and imipramine on the release of CPK from rat platelets and lactic dehydrogenase (LDH) from human platelets in vitro. Both enzymes are mainly soluble in the cytoplasm rather than present in organelles. After determining that both drugs could promote release of these enzymes from platelets, the mechanism of the imipramine-induced release of CPK and LDH from platelets was further studied by comparison of its action with agents which promote platelet aggregation and the platelet release reaction, as well * This work was supported by State of Illinois 231-12-RD and USPHS MH 16-1271 Dr. Goode is a recipient of a fellowship from the Foundations Fund for Research in Psychiatry. Dr. Meltzer is the recipient of Research Scientist Development Award MH 47,808. 2629",

year = "1974",

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day = "15",

doi = "10.1016/0006-2952(74)90186-5",

language = "English (US)",

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T1 - Cytotoxic effects of imipramine on platelets

AU - Goode, David J.

AU - Meltzer, Herbert Y.

N1 - Funding Information: The present study was designed to investigate the effects of CPZ and imipramine on the release of CPK from rat platelets and lactic dehydrogenase (LDH) from human platelets in vitro. Both enzymes are mainly soluble in the cytoplasm rather than present in organelles. After determining that both drugs could promote release of these enzymes from platelets, the mechanism of the imipramine-induced release of CPK and LDH from platelets was further studied by comparison of its action with agents which promote platelet aggregation and the platelet release reaction, as well * This work was supported by State of Illinois 231-12-RD and USPHS MH 16-1271 Dr. Goode is a recipient of a fellowship from the Foundations Fund for Research in Psychiatry. Dr. Meltzer is the recipient of Research Scientist Development Award MH 47,808. 2629

PY - 1974/9/15

Y1 - 1974/9/15

N2 - Incubation for 30 min at 30° with 1 mM imipramine, chlorpromazine or phencyclidine produced increases in creatine phosphokinase (CPK) activity of rat platelet-rich plasma (PRP). Increases in lactic dehydrogenase (LDH) activity of human PRP were produced by imipramine at 0.5 mM. Ouabain, diphenylhydantoin, calcium chloride, EDTA and thrombin did not affect CPK activity of rat PRP. None of the dugs tested except 10 mM diphenylhydantoin affected CPK or LDH activity in platelet-poor plasma. Increases in enzyme activity of PRP produced by 1 mM imipramine were associated with a decrease in platelet count. The increases were independent of temperature of incubation from 0° to 30° and were maximal after a 5-min incubation. The release of LDH and CPK caused by the above drugs is not related to platelet aggregation or the platelet release reaction. The increases in LDH and CPK activity in PRP appear to be the result of platelet destruction or damage to the platelet plasma membrane with release of these enzymes.

AB - Incubation for 30 min at 30° with 1 mM imipramine, chlorpromazine or phencyclidine produced increases in creatine phosphokinase (CPK) activity of rat platelet-rich plasma (PRP). Increases in lactic dehydrogenase (LDH) activity of human PRP were produced by imipramine at 0.5 mM. Ouabain, diphenylhydantoin, calcium chloride, EDTA and thrombin did not affect CPK activity of rat PRP. None of the dugs tested except 10 mM diphenylhydantoin affected CPK or LDH activity in platelet-poor plasma. Increases in enzyme activity of PRP produced by 1 mM imipramine were associated with a decrease in platelet count. The increases were independent of temperature of incubation from 0° to 30° and were maximal after a 5-min incubation. The release of LDH and CPK caused by the above drugs is not related to platelet aggregation or the platelet release reaction. The increases in LDH and CPK activity in PRP appear to be the result of platelet destruction or damage to the platelet plasma membrane with release of these enzymes.

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Cytotoxic effects of imipramine on platelets

Abstract

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