Home General Physiology and Biophysics 2013 General Physiology and Biophysics Vol.32, No.3, p.415–420, 2013

Journal info


Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
6 times per year

Aims and Scope
Editorial Info
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.32, No.3, p.415–420, 2013

Title: Effect of aging on formation of reactive oxygen species by mitochondria of rat heart
Author: Stanislav Kuka, Zuzana Tatarkova, Peter Racay, Jan Lehotsky, Dusan Dobrota, Peter Kaplan

Abstract: Mitochondrial electron transport chain is thought to be a major source of reactive oxygen species (ROS) during aging. However, this view is supported mainly by accumulation of mitochondrial oxidative damage with age and the exact sites of ROS formation remains unknown. In the present study, we measured rate of ROS formation using 2’,7’-dichlorofluorescein (DCF) probe in cardiac mitochondria from adult (6-month-old), old (15-month-old) and senescent (26-month-old) rats. In mitochondria oxidizing complex II substrate, succinate, the rate of ROS formation progressively increased with age. In the presence of complex I inhibitor rotenone or complex III inhibitor antimycin A, the rate ROS formation significantly decreased, but even the combination of inhibitors could not fully prevent generation of ROS. Age-dependent increase of ROS formation was accompanied by a loss of thiol groups, tryptophan degradation and increased lipid peroxidation. These data suggest that in addition to complex I and complex II other mitochondrial sites can contribute to accelerated ROS generation and oxidative damage during aging.

Keywords: Aging — Heart — Mitochondria — ROS — Oxidative stress
Year: 2013, Volume: 32, Issue: 3 Page From: 415, Page To: 420
doi:10.4149/gpb_2013049


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.