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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 />

122.<br />

EnvirONMENTal POLLUTaNTS as faCTOrs MODULaTING THE<br />

INflaMMaTOry rESPONSE aND fUNCTIONS of LUNG CELLS<br />

Lenka Umannová 1,2 , Miroslav Machala 2 , Alois Kozubík 1 and Jan Vondráček 1,2<br />

1<br />

Laboratory of Cytokinetics, Institute of Biophysics, ASCR v.v.i., 612 65 Brno,<br />

Czech Republic<br />

2<br />

Veterinary Research Institute v.v.i., 621 00 Brno, Czech Republic<br />

Chronic inflammation plays a central role in pathogenesis of lung cancer or chronic obstructive<br />

pulmonary disease, which belong among leading causes of death. Air pollution<br />

represents a significant risk factor for lung cancer incidence. The polluted atmosphere<br />

contains various matrices with carcinogenic potential including vehicle exhaust, side-stream<br />

tobacco smoke, coal combustion effluents and transient metals. In the present study, we<br />

analyzed mutual deregulation of enzymes involved both in xenobiotic metabolism and<br />

inflammatory responses, caused by environmental pollutant and important tobacco smoke<br />

constituent benzo[a]pyrene (BaP) and TNF-a in rat lung RLE-6TN alveolar type II cell line.<br />

Our results show that BaP modulates the expression/activity of enzymes induced by<br />

TNF-a that are involved in inflammatory responses such as prostaglandin-endoperoxide<br />

synthase 2 (COX-2) or inducible nitric oxide synthase (iNOS), leading to enhanced release<br />

of their products such as prostaglandin E2. Moreover, BaP increases expression of inflammatory<br />

cytokines induced by TNF-a in target cells. Important role in increased expression<br />

may play oxidative stress and activation of p38 mitogen activated protein kinases. These<br />

results demonstrate that environmental pollutants affect signaling pathways related to<br />

inflammatory response and may thus contribute to deregulated inflammation and lung<br />

epithelial damage.<br />

Acknowledgement: Supported by the Czech Ministry of Agriculture, grant No. MZe<br />

0002716202.<br />

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

247

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