Book of Abstracts - New Frontiers 2022

Abstracts of oral presentations

ACUTE STRESS-INDUCED ALTERATIONS IN EXPRESSIONS OF GENES INVOLVED IN IRON METABOLISM IN THE HEARTS AND LIVERS OF NORMOTENSIVE RATS I. Bernatova 1 , M. Kluknavsky 1 , A. Micurova 1 , P. Balis 1 , M. Skratek 2 , M. Okuliarova 3 , S. Liskova 1,4 , J. Manka 2 1 Institute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, Bratislava, Slovakia; 2 Institute of Measurement Science, Slovak Academy of Sciences, Bratislava, Slovakia; 3 Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia; 4 Institute of Pharmacology and Clinical Pharmacology, Faculty of Medicine, Comenius University, Bratislava, Slovakia Iron is essential in many metabolic processes and chronic stress was shown to alter iron homeostasis. Stress is also considered to be an etiological factor in the development of cardiovascular diseases and metabolic disorders. In addition, there is also a crosstalk between the heart and liver: liver disorders trigger cardiovascular complications (and vice versa) with a significant clinical impact. We investigated if mild repeated acute stress alters the expressions of certain genes involved in iron homeostasis, nitric oxide and superoxide productions as well as the content of iron-containing compounds in the hearts and livers of Wistar-Kyoto rats. Acute stress was induced by three sessions of 5-sec air jet (AJ, at 20, 50 and 130 min) during the 140-min experiment. Changes in relative iron content were determined using SQUID magnetometry (1 T hysteresis curve measured at -271.15 oC). Gene expressions of nuclear factor erythroid 2-related factor 2 (NRF2), inducible and endothelial nitric oxide synthase (iNOS, eNOS), superoxide dismutase 1 and 2 (SOD 1, SOD2), glutathione peroxidase 4 (GPx4), hepcidin (HAMP), ferroportin (FPT), divalent metal transporter 1 (DMT1), ferritin heavy chain 1 (FTH1), transferrin (TF) and transferrin receptor 1 (TFR1) were determined by qRT-PCR. Mean arterial pressure (MAP) was determined in the carotid artery continuously. AJ elevated MAP significantly during each session by about 50% vs. pre-stress levels. AJ also elevated plasma corticosterone and relative content of iron-containing compounds in the liver but not in the left heart ventricle (LHV). AJ failed to affect NO and superoxide productions in both tissues investigated. In the liver, expressions of NRF2, PPAR-gamma, iNOS, FTH1 and FPT were significantly elevated vs. controls. In the LHV, only FTH1 and SOD1 expressions were elevated, without the changes in expressions of the remaining abovementioned genes. There was significant positive correlation between the saturation magnetization and FTH1 expression in the liver but not in the LHV. In conclusion, repeated, relatively mild, acute stress increased FTH1 expression in the LHV and liver while relative content of iron-containing compounds was elevated only in the liver. The results suggest rapid effect of acute psycho-emotional stress on iron accumulation in the liver that may provide the link between stress and liver diseases that may consequently result in cardiac function disturbances.

Keywords: iron metabolism, stress, nitric oxide, heart, liver

Funding:This study was supported by the grants VEGA 2/0157/21 and APVV-16-0263.

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