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AMIODARONE PHOTOTOXICITY TO HUMAN ERYTHROCYTES AND LYMPHOCYTES
Author(s) -
HASAN Tayyaba,
E. Kochevar Irene,
Abdulah Dorina
Publication year - 1984
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1984.tb04642.x
Subject(s) - phototoxicity , catalase , hemolysis , chemistry , sodium azide , superoxide dismutase , hydrogen peroxide , erythrocyte fragility , superoxide , red blood cell , in vivo , pharmacology , oxygen , biochemistry , antioxidant , in vitro , biology , immunology , enzyme , microbiology and biotechnology , organic chemistry
Amiodarone (AD) therapy for cardiac arrhythmia frequently leads to cutaneous phototoxicity. Amiodarone and its metabolite, desethylamiodarone (DEA), photosensitized hemolysis of red blood cells (RBC) and were phototoxic to lymphocytes. Hemolysis photosensitized by 3.3 μ M AD was partially oxygen dependent and was partially quenched 5 m M sodium azide, 50 m M mannitol, superoxide dismutase (251 U/me e ) and catalase (1500 U/m e ), but was unaffected when H 2 O was replaced by D 2 O. These results suggest that membrane damage may be important in the in vivo phototoxicity to AD, that both oxygen dependent and oxygen independent mechanisms may operate, and that active oxygen species such as O 2 and hydrogen peroxide may be involved. Photohemolysis was more rapid in the presence of DEA than of AD. However, this may be due to the greater fragility of the cell membrane in the presence of DEA. The greater phototoxicity of DEA than AD towards lymphocytes was not due to greater membrane fragility.
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