Thioredoxin overexpression shows a cardioprotection against the redox metabolism alterations initiated by air pollution exposure.

MAGNANI, NATALIA; GARCÉS, MARIANA; PEREZ, VIRGINIA; MARCHINI, TIMOTEO; CALABRO, VALERIA; MARGIOTTIELLO, DANIEL; CACERES, LOURDES; D'ANNUNZIO, VERONICA; ALVAREZ, SILVIA; GELPI, RICARDO; EVELSON, PABLO

Congreso virtual

Congreso; LXV Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica; 2020

Sociedad Argentina de Investigación Clínica

Epidemiological studies showed correlations between daily changes in particulate matter (PM) concentration with cardiovascular diseases such as heart failure. PM-initiated reactive O2 species leading to oxidative damage initiates adverse mechanisms. Thioredoxin-1 (Trx1) through redox homeostasis regulation have shown an ischemia/reperfusion injury cadioprotection, reducing the infarct size. Therefore, the aim of the present project was to further assess the Trx1 protection against the cardiopulmonary toxicity initiated by Residual Oil Fly Ashes (ROFA) exposure, used as a PM inhalation model. Wild type (WT) and overexpressing Trx-1 (TRX) transgenic mice were Intranasally instilled with a ROFA suspension (1 mg/kg) or saline. Heart tissue redox metabolism and cardiac function were evaluated 3h after treatment. Trx-1 overexpression was able to revert the tissue O2 consumption decreased observed after ROFA exposure (p