Lipid peroxidation, phosphoinositide turnover and protein kinase C activation in human platelets treated with anthracyclines and their complexes with Fe(III)

Ornella Parolini, P. Banfi, C. Lanzi, R. A. Gambetta

Risultato della ricerca: Contributo in rivistaArticolo in rivista

7 Citazioni (Scopus)

Abstract

The effects of the antitumor drugs daunorubicin, doxorubicin and their complexes with Fe(III) on phosphoinositide hydrolysis, lipid peroxidation and protein kinase C (PKC) activation were measured in intact human platelets. Doxorubicin and the Fe(III) complexes of both doxorubicin and daunorubicin quickly induced lipid peroxidation [as measured by the thiobarbituric acid (TBA) assay], phosphorylation of the 40 K substance of PKC, and increased levels of phosphatidic acid and inositol phosphates. Fe(III) alone or complexed to acetohydroxamic acid induced high levels of TBA-reactive material but did not affect either PKC activation or phosphoinositide turnover. In contrast, daunorubicin, which was ineffective per se, inhibited all these doxorubicin- and anthracyclines/Fe(III)-induced biochemical events. We suggest that phosphoinositide hydrolysis determined by anthracyclines, and consequently PKC activation, could be due to lipid peroxidation, thus triggering the activity of phospholipase C.
Lingua originaleEnglish
pagine (da-a)1521-1527
Numero di pagine7
RivistaBiochemical Pharmacology
Volume43
DOI
Stato di pubblicazionePubblicato - 1992

Keywords

  • Blood Platelets
  • Daunorubicin
  • Diglycerides
  • Doxorubicin
  • Enzyme Activation
  • Ferric Compounds
  • Humans
  • Inositol Phosphates
  • Lipid Peroxidation
  • Neomycin
  • Phosphatidic Acids
  • Phosphatidylinositols
  • Phosphorylation
  • Protein Kinase C

Fingerprint Entra nei temi di ricerca di 'Lipid peroxidation, phosphoinositide turnover and protein kinase C activation in human platelets treated with anthracyclines and their complexes with Fe(III)'. Insieme formano una fingerprint unica.

Cita questo