NDLI: Reactive oxygen species induce signals that lead to apoptotic DNA degradation in primary CD4+ T cells

Content Provider	Springer Nature Link
Author	Pajusto, M. Toivonen, T. H. Tarkkanen, J. Jokitalo, E. Mattila, P. S.
Copyright Year	2005
Abstract	Reactive oxygen species are toxic to cells but they may also have active roles in transducing apoptotic events. To study the role of reactive oxygen species in growth factor depletion induced apoptosis of human primary CD4+ T cells, we used a synthetic manganese porphyrin superoxide dismutase mimetic to detoxify superoxide anions formed during apoptosis. Apoptosis of primary CD4+ T cells was characterized by generation of superoxide anions, plasma membrane phosphatidyl-serine translocation, loss of mitochondrial membrane potential, activation of caspase 3, condensation of chromatin, as well as DNA degradation. The detoxification of superoxide anions did not influence plasma membrane phosphatidyl-serine translocation, or chromatin condensation, and only marginally inhibited the loss of mitochondrial membrane potential and the formation of DNA strand breaks. In contrast, the detoxification of superoxide anions significantly reduced caspase 3 activity and almost completely inhibited the apoptotic decrease in total cellular DNA content as measured by propidium iodide staining. Our results indicate that reactive oxygen anions induce signals leading to efficient DNA degradation after the initial formation of DNA strand breaks. Thus, reactive oxygen anions have active roles in signaling that lead to the apoptotic events.
Starting Page	1433
Ending Page	1443
Page Count	11
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	10
Issue Number	6
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2005-10-03
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	apoptosis DNA fragmentation free radicals reactive oxygen species superoxide anions T cells Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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