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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 />

56.<br />

EffECT OF PAMAM G4 DENDRIMER ON LIVER MITOCHONDRIA<br />

OXIDATIVE PHOSPHORYLATION AND METABOLIC CONTROL IN<br />

EXPERIMENTAL DIABETES<br />

Oľga Vančová 1 , Oľga Uličná 1 , Katarína Šebeková 2 ,<br />

Magdalena Labieniec 3 and Cezary Watala 3<br />

1<br />

Pharmacobiochemical laboratory 3rd Dept of Int Medicine LFUK Bratislava,<br />

2<br />

Department of Preventive and Clinical Medicine SZU Bratislava, 3 Department of<br />

Haemostasis and Haemostatic Dis Med Univ of Lodz, Poland<br />

Prolonged exposure to hyperglycaemia causes non-enzymatic glycation of proteins and<br />

can lead to production of reactive oxygen species.<br />

Polyamidoamine dendrimer PAMAM G4, a strong nucleophilic molecule with 64 free<br />

primary amino groups at its surface appears as an effective scavenger of excessive<br />

glucose in diabetes.<br />

The aim was to study the ability of PAMAM G4 to lower the concentration of plasma<br />

glucose, to suppress long-term parameters of hyperglycaemia and to improve oxidative<br />

phosphorylation in the liver mitochondria.<br />

Experimental diabetes mellitus was evoked by an injection of streptozotocin in male Wistar<br />

rats. After 7 days half the rats were administered PAMAM 64 i.p. daily. After 8 weeks the<br />

concentration of glucose, the end-products of advanced glycation and the end-products<br />

of advanced protein oxidation in plasma and glycated haemoglobin in blood were determined.<br />

Liver tissue was used for mitochondria isolation and parameters of oxidative<br />

phosphorylation were measured using volt-amper method with a Clark oxygen electrode.<br />

Our results, for the first time in vivo experiment, show that PAMAM G4, regardless of<br />

its known cytotoxicity, significantly reduced hyperglycaemia and all the measured longterm<br />

markers of hyperglycaemia in diabetic rats. This positive effect is not sufficient to<br />

restore the impaired mitochondrial function in experimental diabetes.<br />

Acknowledgement: Supported by grant VEGA 1/0328/10.<br />

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

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