Abstract:
PURPOSE:γ-rays (IR) cause an increase in intracellular calcium [Ca(2+)], alters contractility and triggers apoptosis via the activation of protein kinase C in intestinal guinea pig smooth muscle cells. The present study investigated the role of the mitochondria in these processes and characterized proteins involved in IR-induced apoptosis. MATERIALS AND METHODS:Intestinal smooth muscle cells were exposed to 10-50 Gy from a (60)Co γ-source. Reactive oxygen species (ROS) levels were measured by colourimetry with a fluorescente probe. Protein expression was analyzed by immunoblotting and immunofluorescence. RESULTS:Apoptosis was inhibited by glutathione, possible by inhibiting the generation or scavenging ROS. Apoptosis was mediated by the mitochondria releasing cytochrome c leading to caspase 3 activation. IR increased the expression of the cyclins A, B2 and E and led to unbalanced cellular growth in an absorption dose-dependent manner. However, radiation did not induce alterations in the mitochondrial ultrastructure or in transmembrane electric potential. In contrast, IR increased the nuclear expression of cytoplasmic proteins and cyclins A and E. CONCLUSION:Smooth muscle cells subjected to IR undergo mitochondrial-mediated apoptosis that involves oncoproteins activation and preserves mitochondrial structure. IR also cause alterations in the expression and localization of both pro- and anti-apoptotic proteins.
journal_name
Int J Radiat Bioljournal_title
International journal of radiation biologyauthors
Claro S,Oshiro ME,Mortara RA,Paredes-Gamero EJ,Pereira GJ,Smaili SS,Ferreira ATdoi
10.3109/09553002.2014.911988subject
Has Abstractpub_date
2014-10-01 00:00:00pages
914-27issue
10eissn
0955-3002issn
1362-3095journal_volume
90pub_type
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journal_title:International journal of radiation biology
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