Heart mitocondrial function in rats with thyroid disorder and hipovolemia

OGONOWSKY NS; PUCHULU MB; BALASZCZUK AM; ZAOBORNYJ T; ZOTTA E; RUKAVINA MIKUSIC IA; VALDEZ LB; FELLET AL

Buenos Aires

Congreso; Reunion Conjunta de Sociedades de Biociencia; 2017

SAIC, SAIB, SAI, SAA, SABiologia, SABiofisica, SAFE, SAFIS, SAH, SAP

Cardiovascular system regulation would be crucial in pathologicalsituations such as hypovolemia. The actions of thyroid hormoneswould be relevant during this condition considering its actions oncellular respiration and mitochondrial function. The aim of the presentwork was to examine the effect of thyroid state on rat heart mitochondriafunction during hypovolemia. Sprague-Dawley rats aged2 months old treated with T3 (hyper, 20 μg/100 g body weight) or0.02% methimazole (hypo, w/v) during 28 days. Hypovolemic statewas induced by a loss of 20% of blood volume during 2 minutes.Hearts were removed for mitochondria isolation and determinationof O2 uptake, enzyme activity of complex I and protein levels (mt-NOS, akt T and akt P). The malate-glutamate-supported state 3respiration decreased and increased in hypo and Hyper rats. Hemorrhagedid not change this parameter. Malate-glutamate-supportedstate 4 did not change. No differences in succinate-supported state4 and 3 respiration were observed in all groups. Hypothyroidismincreased nNOS protein levels. This protein levels did not changein Hyper animals. Withdrawal decreased and increased nNOS proteinlevels in hypo and Hyper rats, respectively. Hyper increasedcomplex I activity and hemorrhage did not change this activity. Nodifferences were observed between Eut and hypo rats. Hemorrhageonly increased complex I activity in hypo group. Thyroid disorders increasedaktT protein levels. Hemorrhage did not change this parameter.Hyper increased akt P protein levels meanwhile hemorrhageinduced a decreased of this protein levels. In hypothyroidism thelowest NO production would be responsible for increasing cellularrespiration and guaranteeing the supply of oxygen to the tissues.The opposite would happen in the hyperthyroid where high levelsof NO try to decrease the oxygen consumption as in the euthyroid.Alterations of complex I activity as well as AKT pathway could mediatethese effects.