Comparative study of apoptosis induced by H(2)O(2) and NO: limitation of apoptosis induced by NO due to slower recovery of activity of NO-modified caspase.
Both H(2)O(2) and NO can act as apoptogens, triggering apoptosis in many cells. They are also well known inhibitors of caspases, essential enzymes in apoptosis. The differences between these two agents as apoptosis inducers and how caspases mediate apoptosis with these inhibitory agents is still unclear. Consistent with the previous reports, these two agents induced apoptosis accompanied by caspase activation with limitation of all apoptotic events for NO. It was found that NO-modified caspase-3 showed a slower recovery of its activity in the presence of the reducing agents compared to that of H(2)O(2) modification. This is one possible cause of the limited apoptosis in the case of NO.
Kim
Ja-Eun
JE
Research Center for Proteineous Materials (RCPM) and Department of Bio-Materials Engineering, Chosun University, Gwangju 501-759, Korea and Department of Chemistry, Yonsei University, Wonju, Korea.
Seok
Heeyoung
H
Karki
Pratap
P
Lee
Jung Sup
JS
Shin
Song Yub
SY
Cho
Byungyun
B
Park
Il-Seon
IS
D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D019169:Jurkat Cells; D009569:Nitric Oxide / Q000494:pharmacology*
D061945:Caspase Inhibitors; D009569:Nitric Oxide; D045304:Cytochromes c; D006861:Hydrogen Peroxide; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases