Akri̇lami̇de Maruz Kalan Siçanlarin Kalp Dokusu Üzeri̇nde Selenyumun Koruyucu Rolü

Abstract

Objective: Acrylamide (ACR) is a harmful organic reactive compound widely used in different industrial fields. Selenium (SEL) is a trace element that takes part in some chemical and enzymatic reactions in both animals and human organisms and can cause some disorders in many systems such as the cardiovascular system in case of deficiency. The aim of this study is to investigate whether SEL has a protective effect on cardiac tissue in experimentally induced ACR toxicity in rats.
 Material and Methods: A total of 28 rats were randomly and equally divided into four groups: Control, SEL, ACR, SEL + ACR. At the end of the study, cardiac markers such as creatine kinase MB (CKMB), lactate dehydrogenase (LDH) and ischemia-modified albumin (IMA) from blood samples were measured. Oxidative stress markers such as total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) in heart tissue were analyzed. In addition, inducible nitric oxide synthase iNOS activities were determined in heart sections using immunohistochemical methods.
 Results: The ACR + SEL group showed a significant decrease in TOS, OSI, CKMB, LDH, IMA levels and significant increase in TAS level compared to the ACR group. In histopathological and immunohistochemical evaluation of the heart sections; Disorganization in cardiac muscle fibers, increased connective tissue between muscle fibers and irregular eosinophilia in muscle fibers were detected in ACR group. A decrease in histopathological findings was observed in the SEL treated group compared to the ACR group. iNOS immunoreactivities; Moderate marking was observed in the ACR group sections, while poor marking was observed in the treatment group.
 Conclusion: We determined that ACR caused damage to the heart tissue of rats through various metabolic pathways and that these damages were reversed in the groups given the SEL.

Cardioprotective Effects of Rutin and Mesenchymal Stem Cells on Acetaminophen Induced Cardiac Enzymatic Damage in Rats

“…every 72h for 21 days and left without any treatment for 30 and 60 days as compared to NC group. Similar findings were achieved by [2,28,29,27]. The increase in cystolic LDH activity by PARA may be because of the intracellular collection of Ca 2+ , which results in initiation of phosphofructo-kinase and anaerobic glycolysis prompting lactate formation [29].…”

“…PARA passes through many organs through the circulatory system and causes toxic effects by reacting with DNA and various enzymes [27]. The results in this work showed that PARA caused a highly significant increase (P < 0.05) found in CK-MB and LDH levels in treated rats that given PARA at a dose of (750 mg/kg b.w.)…”

“…Besides, [30] suggested that the increased of the LDH activity may be due to a cellular damage and leaked of the enzyme from the tissues into the blood. In addition, increased significantly in the CK-MB and LDH levels markers of cardiac damage for the damaged heart tissue [27]. Also, [31] said the serum LDH considered as a prognostic marker for the investigation of tissues injury.…”