Paraoxonase and Oxidative Stress Changes in Left and Right Ventricles of Exhaustively Exercised Rats

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Date

2021

Journal Title

Journal ISSN

Volume Title

Publisher

Canadian Science Publishing

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Green Open Access

No

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Abstract

Exhaustive exercise can cause subclinical inflammation to the heart, as it is an oxidative tissue that works continuously. The effect of exhaustive exercise on left and right ventricles (LVs, RVs) may be different. It is claimed that paraoxonase-1 (PON1), an antioxidant enzyme, has a cardioprotective effect on oxidative stress. Rats were separated as non-exercised controls (Con), those euthanized immediately after (E-0) and 24 h after exhaustive exercise (E-24). Cardiac troponin-I (cTnI), total antioxidant status (TAS), total oxidant status (TOS), PON1 activities, and histological findings in LV and RV of the exhausted rats were evaluated. TAS and PON1 levels were lower in LVs compared with RVs of all groups. TOS levels were high in LVs compared with RVs of all groups. In LVs, TAS levels decreased significantly in the E-0 group while PON1 activity decreased in E-0 and E-24 groups compared with controls. In LVs, TOS levels decreased significantly in E-0 and E-24 groups, but in RVs a decrease was seen only in the E-0 group. cTnI levels increased significantly in the E-0 group and decreased to control levels in the E-24 group. Considering the histological and biochemical findings, exhaustive exercise affected the heart to the maximum during and just after exhaustion, and LV was influenced more than RV.

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Keywords

exhaustive exercise, inflammation, paraoxonase-1, left ventricle, right ventricle, Male, Oxidative Stress, Aryldialkylphosphatase, Heart Ventricles, Physical Conditioning, Animal, Troponin I, Animals, Rats, Wistar, Antioxidants, 796, Rats

Fields of Science

03 medical and health sciences, 0302 clinical medicine

Citation

WoS Q

Q4

Scopus Q

Q3
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OpenCitations Citation Count
2

Source

Canadian Journal of Physiology and Pharmacology

Volume

99

Issue

7

Start Page

752

End Page

759

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CrossRef : 2

Scopus : 2

PubMed : 1

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2

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2

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3

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