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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


OXIDATIVE STRESS AND MYOCARDIUM, PLASMA ANTIOXIDANT STATUS IN AGED RATS
Abstract number: PW03-18

Sivonova1 M., Tatarkova1 Z., Dobrota1 D., Pavlikova1 M., Kaplan1 P.

1Dept. Med. Biochem., Comenius Univ., Jessenius Faculty of Medicine,Martin, Slovakia

Aims: 

To provide better insight into the role of oxidative stress during aging, we studied the relationship between the antioxidant potential of plasma and heart homogenate and several oxidative stress parameters, the macromolecules damage (lipid peroxidation, uric acid, total sulfhydryl group content and oxidative damage to DNA), in young (6 months), old (15 months) and senescent (26 months) male Wistar rats.

Methods: 

The antioxidant capacity of heart homogenate and plasma was determined by R-phycoerythrin based TRAP method. The content of total sulfhydryl groups and degree of lipid peroxidation in plasma and heart homogenate was determined spectrophotometricaly. DNA single strand breaks were measured using alkaline comet assay.

Results: 

The antioxidant capacity was significantly decreased in plasma and myocardium of old and senescent rats, whereas plasma level of uric acid was elevated in 26 months old rats. Age-related decline in plasma and heart antioxidant capacity was accompanied by a significant loss in total sulfhydryl group content, increased lipid peroxidation and higher DNA damage in lymphocytes. Correlations between TRAP and oxidative damage to lipids, proteins and DNA suggest that the decline in antioxidant status may play an important role in age-related accumulation of cell damage caused by reactive oxygen species.

Conclusions: 

Our study demonstrates an age-related decrease in the total antioxidant capacity of rat plasma and myocardium and provides the indication that this decrease may be involved in the mechanisms of free radical-induced damage to lipids, proteins and DNA during aging.

Supported by grants UK/38/2005, VEGA 1/2263/05 and APVT-51-027404.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PW03-18

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