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XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

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Lectures<br />

oxidaTIve STrESS aND HEart aGING.<br />

Zuzana Tatarková, Eva Babušíková, Stanislav Kuka, Ján Lehotský, Peter Račay,<br />

Dušan Dobrota and Peter Kaplán<br />

Department of medical biochemistry JLF UK Martin<br />

Aging plays in our life uniquely role and oxidative stress (OS) is considered by many<br />

authors as a major factor in this process. The causes and consequences of aging involve<br />

the interaction of many processes. Mitochondria are the main sources of ROS (reactive<br />

oxygen species) during normal metabolism. ROS production by mitochondria is important<br />

because it underlies oxidative damage in a lot of pathologies and is characterized<br />

by destruction of structural integrity of membrane, leading to a decrease in membrane<br />

fluidity and enzyme activities. Therefore, the objective of our study was to determine<br />

the specific relationship between heart aging and changes in the level of OS, lipid peroxidation<br />

and OS-sensitive enzymes activities. We used three different age groups (6-,<br />

15- and 26-months old rats) which represented adult, old and senescence. The activities<br />

of all respiratory enzymes significantly decreased with the highest activity losses (37%)<br />

in complex IV. Inhibition of citric acid cycle enzymes, a-KGDH and SDH in the hearts of<br />

senescent rats, is also due to reaction of ROS with the thiol groups of these proteins. For<br />

this reason we studied total thiol group content, which decreases by 30%. The whole aging<br />

process was associated with elevation in basal levels of lipid peroxidation-end products,<br />

MDA and HNE. Cells are continually challenged by conditions that cause acute or chronic<br />

stress and there are many antioxidant mechanisms that cope with this situation. Activity<br />

of the Mn-SOD was together with cytosolic CuZn-SOD continuously depressed with age,<br />

but mitochondria creates higher level of MnSOD protein, which possibly could help to<br />

another antioxidant enzymes fight against OS. In all this reasons, OS in mitochondria<br />

may drive myocardial aging. But there are still many processes that we need investigate.<br />

Acknowledgements: This work was supported by grants VEGA 1/0027/08, VEGA 1/0049/09,<br />

VVCE-0064-07.<br />

<strong>XXII</strong>. Biochemistry Congress, Martin<br />

101

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