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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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Posters<br />

95.<br />

METYLNICOTINAMIDE AND DNA OXIDATION DAMAGE IN raTS WITH<br />

STREPTOZOTOCINE INDUCED DIABETES MELLITUS<br />

Zuzana Országhová 1 , Zuzana Paduchová 1 , Ingrid Žitňanová 1 , Cezary Watala 2 ,<br />

Jana Muchová 1 and Zdeňka Ďuračková 1<br />

1<br />

Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry,<br />

Medical School, Comenius University, Bratislava, Slovakia;<br />

2<br />

Department of Haemostasis and Haemostatic Disorders,<br />

Medical University of Lodz, Poland<br />

Increased oxidative and glycooxidative stresses contribute to the development and progression<br />

of diabetes-associated complications. Under conditions of DM many important<br />

biomolecules including DNA, lipids or proteins are affected. N(1)methylnicotin-amide<br />

chloride (MNA), which is a derivative of nicotinamide, is an intensively studied agent<br />

possessing remarkable anti-inflammatory as well as antidiabetic properties. This effect is<br />

associated with scavenging of reactive forms of oxygen, in particular superoxide radical<br />

anion and hydroxyl radical. In this study we have studied the level of oxidative damage to<br />

DNA in lymphocytes and liver tissue as well as markers of glycation (AGEs) and oxidation<br />

(carbonyls) damage of proteins in streptozotocine induced diabetic rats. Administration<br />

of MNA in dose 200 mg/kg of weight during 7 weeks significantly decreased DNA damage<br />

in lymphocytes and level of protein carbonyls. All doses of MNA decreased DNA damage<br />

in liver tissue. Advanced glycation of proteins were not affected with MNA. Our results<br />

show possible beneficial protective role of MNA against oxidative stress and damage of<br />

important biomolecules under the conditions of DM.<br />

Acknowledgement: This study was partially supported by MVTS and VEGA grants.<br />

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

219

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