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Prolonged swimming promotes cellular oxidative stress and p66Shc phosphorylation but does not induce oxidative stress in mitochondria in the rat heart.
MedLine Citation:
PMID:  25287525     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
ABSTRACT Exercise-induced changes in p66Shc-dependent signaling pathway are still not fully understood. The p66Shc protein is one of the key players in cell signaling, particularly in response to oxidative stress. Therefore, the aim of this study was to investigate the effect of prolonged swimming on the phosphorylation of p66Shc as well as the induction of mitochondrial and cellular oxidative stress in rat hearts. Male Wistar rats were divided into a sedentary control group and an exercise group. The exercised rats swam for 3 hours and were burdened with an additional 3% of their body weight. After the cessation of exercise, their hearts were removed immediately for experiments. The exercise protocol caused increased levels of the following oxidative stress parameters in cardiac cells: DNA damage, protein carbonyls and lipid dienes. There was also increased phosphorylation of p66Shc without any alterations in Akt and ERK kinases. Changes in the ferritin L levels and the L to H subunit ratio were also observed in the exercised hearts compared to the control hearts. Despite increased phosphorylation of p66Shc, there was no significant increase observed for either mitochondrial H2O2 release or mitochondrial oxidative stress markers. Regardless of the changes in phosphorylation of p66Shc, the antioxidant enzyme activities (SOD, Cat) and anti-apoptotic (Bcl2), and pro-apoptotic (Bax) protein levels were not affected by prolonged swimming. Further studies are required to investigate whether p66Shc phosphorylation is beneficial or negative for cardiac cells after exercise cessation.
Authors:
Wieslaw Ziolkowski; Damian Jozef Flis; Malgorzata Halon; Dhivya Vadhana Ms; Robert Antoni Olek; Manuel Carloni; Jedrzej Antosiewicz; Jan Jacek Kaczor; Rosita Gabbianelli
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-10-7
Journal Detail:
Title:  Free radical research     Volume:  -     ISSN:  1029-2470     ISO Abbreviation:  Free Radic. Res.     Publication Date:  2014 Oct 
Date Detail:
Created Date:  2014-10-7     Completed Date:  -     Revised Date:  2014-10-8    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  1-31     Citation Subset:  -    
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