Apoptosis-accommodating effect of nitric oxide in photodynamically stressed tumor cells. Photochem Photobiol 2010;86(3):681-6
Date
03/25/2010Pubmed ID
20331521DOI
10.1111/j.1751-1097.2010.00712.xScopus ID
2-s2.0-77951837144 (requires institutional sign-in at Scopus site) 7 CitationsAbstract
Using a 5-aminolevulinic acid (ALA)-photodynamic therapy model, we have discovered a new effect of nitric oxide (NO)-the ability to accommodate apoptosis. When sensitized by disseminated ALA-generated protoporphyrin IX, COH-BR1 tumor cells in glucose-containing medium died mainly by necrosis with a low level of apoptosis. Introduced before light at a nontoxic concentration, the NO donor SPNO inhibited necrosis, but supported apoptosis such that the latter became predominant in the remaining cell death. Accompanying this was a large increase in caspase-3/7 activation. SPNO-supported apoptosis was more pronounced when glucose-deprived cells were compared with glucose-replenished, SPNO-treated counterparts. SPNO plus glucose also suppressed plasma membrane-damaging lipid peroxidation and loss of cellular ATP under photostress. The NO effect is attributed to membrane protection with maintenance of sufficient glycolytic ATP to sustain apoptosis.
Author List
Niziolek-Kierecka M, Pilat A, Korytowski W, Girotti AWAuthor
Albert W. Girotti PhD Adjunct Professor in the Biochemistry department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Adenosine TriphosphateAminolevulinic Acid
Apoptosis
Cell Line, Tumor
Cell Membrane
Glucose
Glycolysis
Humans
Lipid Peroxidation
Necrosis
Nitric Oxide
Nitric Oxide Donors
Photochemotherapy
Photosensitizing Agents
Protoporphyrins
