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Article Citation - WoS: 2Citation - Scopus: 2Paraoxonase and Oxidative Stress Changes in Left and Right Ventricles of Exhaustively Exercised Rats(Canadian Science Publishing, 2021) Sarikaya, Badegul; Runa, Metin; Dayanir, Duygu; Gunduztepe, Yasemin; Pinar, LamiaExhaustive exercise can cause subclinical inflammation to the heart, as it is an oxidative tissue that works continuously. The effect of exhaustive exercise on left and right ventricles (LVs, RVs) may be different. It is claimed that paraoxonase-1 (PON1), an antioxidant enzyme, has a cardioprotective effect on oxidative stress. Rats were separated as non-exercised controls (Con), those euthanized immediately after (E-0) and 24 h after exhaustive exercise (E-24). Cardiac troponin-I (cTnI), total antioxidant status (TAS), total oxidant status (TOS), PON1 activities, and histological findings in LV and RV of the exhausted rats were evaluated. TAS and PON1 levels were lower in LVs compared with RVs of all groups. TOS levels were high in LVs compared with RVs of all groups. In LVs, TAS levels decreased significantly in the E-0 group while PON1 activity decreased in E-0 and E-24 groups compared with controls. In LVs, TOS levels decreased significantly in E-0 and E-24 groups, but in RVs a decrease was seen only in the E-0 group. cTnI levels increased significantly in the E-0 group and decreased to control levels in the E-24 group. Considering the histological and biochemical findings, exhaustive exercise affected the heart to the maximum during and just after exhaustion, and LV was influenced more than RV.Erratum Erratum: Correction: Cardiac Hypertrophy Caused by Hyperthyroidism in Rats: the Role of ATF-6 and Trpc1channels (Canadian Journal of Physiology and Pharmacology (2021) 99 11 Doi: 10.1139/Cjpp-2021-0260)(Canadian Science Publishing, 2024) Aykanat, N.E.B.; Şahin, E.; Kacar, S.; Bağcı, R.; Karakaya, Ş.; Burukoǧlu, D.B.; Şahintürk, V.In the originally published article, the grant number was listed incorrectly in the funding statement. The correct funding information is as follows: “This present study was funded by the Eskisehir Osmangazi University (ESOGU) Science Foundation Grant No. 2018-1109”. The original article has been corrected. © 2024 The Author(s).Article Citation - WoS: 12Citation - Scopus: 10Cardiac Hypertrophy Caused by Hyperthyroidism in Rats: the Role of Atf-6 and Trpc1 Channels(Canadian Science Publishing, 2021) Aykanat, Nuriye Ezgi Bektur; Sahin, Erhan; Kacar, Sedat; Bagci, Ridvan; Karakaya, Serife; Donmez, Dilek Burukoglu; Sahinturk, VarolHyperthyroidism influences the development of cardiac hypertrophy. Transient receptor potential canonical channels (TRPCs) and endoplasmic reticulum(ER) stress are regarded as critical pathways in cardiac hypertrophy. Hence, we aimed to identify the TRPCs associated with ER stress in hyperthyroidism-induced cardiac hypertrophy. Twenty adult Wistar albino male rats were used in the study. The control group was fed with standard food and tap water. The group with hyperthyroidism was also fed with standard rat food, along with tap water that contained 12 mg/L of thyroxine (T4) for 4 weeks. At the end of the fourth week, the serum-free triiodothyronine (T3), T4, and thyroid-stimulating hormone (TSH) levels of the groups were measured. The left ventricle of each rat was used for histochemistry, immunohistochemistry, Western blot, total antioxidant capacity (TAC), and total oxidant status (TOS) analysis. As per our results, activating transcription factor 6 (ATF-6), inositol-requiring kinase 1 (IRE-1), and TRPC1, which play a significant role in cardiac hypertrophy caused by hyperthyroidism, showed increased activation. Moreover, TOS and serum-free T3 levels increased, while TAC and TSH levels decreased. With the help of the literature review in our study, we could, for the first time, indicate that the increased activation of ATF-6, IRE-1, and TRPC1-induced deterioration of the Ca2+ ion balance leads to hypertrophy in hyperthyroidism due to heart failure.
