Browsing by Author "Krstic, Danijela (57199836500)"

Various studies have shown that the serum concentration of folic acid is inversely related to the serum homocysteine concentration. In addition, data suggest that increases in serum homocysteine levels decrease the activity of acetyl cholinesterase (AChE). The aim of this study was to investigate the effects of acute folic acid treatment on AChE activity in the brain, heart and the blood of a rat. We used male Wistar rats, with a body mass of 250-300 g divided into two categories: a control group given placebo (1 ml 0.9% NaCl, i.p. n1=6) and an experimental group treated with folic acid (1 ml 0.011 μmol/g per body mass, pH 7.4, i.p., n2=6). Sixty minutes after the treatment, the rats were decapitated. The brain and the heart were removed, and blood was taken. The brain and heart were homogenised in phosphate buffer pH 8 (1 ml buff er/20 mg tissue). Th e homogenised tissues and blood were used as a substrate for the spectrophotometric analysis, and enzyme activity was measured in vitro by the Ellman method. Rats treated with folic acid showed significantly reduced AChE activity in the brain and blood compared to the control group (38% and 82%, respectively). We did not observe a significant difference between the enzyme activity in the blood of treated versus untreated rats. In conclusion, this study shows that acute treatment with folic acid decreases the AChE activity in the brain and heart of rats without affecting the AChE activity in the blood.

Limited data exist in the literature regarding the effects of homocysteine thiolactone on the activity of the acetylcholinesterase (AChE) in the blood, and practically no data exist regarding the influence of homocysteine thiolactone on the enzyme in the brain and heart. Taking into consideration the importance of hyperhomocysteinemia in clinical practice, it has been thought to be of particular interest to examine the effect of homocysteine thiolactone on the activity of AChE in the rat's blood, brain and heart. In this study, male Wistar rats (weighing 250-300g) were used, and they were divided into two groups; one served as a control group and receieved a placebo (1 ml 0.9 % NaCl, i.p.), while the other group received a homocysteine thiolactone solution (5.5 mmol/kg b.m., i.p.). An hour after the administration, the rats were euthanized by decapitation, heir tissues were harvested, buffered, and homogenized in a phosphate buffer (pH 8). The concentration in the tissue homogenates was 20 mg of tissue per 1 ml of buffer. The buffered and homogenized parts of the tissues were used as substrates for spectrophotometric measurements. The AChE activity was then measured by the Ellman method. Statistical analysis was conducted using a one-way ANOVA test, and the intergroup comparisons were performed using a Bonfferoni test. The results showed a significant reduction in AChE activity in all tissues obtained from the animals treated with homocysteine thiolactone compared to the enzyme activity of the control group. In addition, the results also showed that the blood enzyme activity inhibition was the lowest (12%), while the enzyme activity was slightly higher in the brain (27.8%) and heart specimens (86.3%). It was concluded that homocysteine thiolactone significantly inhibited AChE activity in the heart and brain tissue, but not in the blood of the rat.

Background/Aim: Hyperhomocysteinaemia is linked to higher level of acetylcholinesterase (AChE) in brain, but there is insufficient information on influence of homocysteine (Hcy) and gasotransmitters on cardiac AChE. Thus, the aim of this study was to evaluate the influence of certain gasotransmitter inhibitors in Hcy-induced changes on rat cardiac AChE activity. Methods: Research was performed on 72 male Wistar albino rats distributed into 6 groups: 1) Control group - saline (1 ml 0.9% NaCl ip); 2) DL-Hcy (8 mmol/kg ip DL homocysteine (DL-Hcy); 3) L-NAME (10 mg/kg ip Nω-Nitro-L-arginine methyl ester (L-NAME), inhibitor of NO production); 4) DL-PAG (50 mg/kg ip DL-propar- gylglycine (DL-PAG), inhibitor of H2S production); 5) DL-Hcy+L-NAME (8 mmol/ kg ip DL-Hcy + 10 mg/kg ip L-NAME); and 6) DL-Hcy+DL-PAG (8 mmol/kg ip DL-Hcy + 50 mg/kg ip DL-PAG). All tested substances were administered in a single dose, intraperitoneally, 60 minutes before animals’ sacrifice. AChE activity was measured in the rats’ cardiac tissue homogenate. Results: Administration of Hcy and L-NAME induced significant decrease in AChE activity compared with control condition. Administration of DL-PAG, DL-Hcy+L- NAME and DL-Hcy+DL-PAG did not change AChE activity compared with the control group. Conclusion: The effects of acute Hcy administration on the cardiac AChE activity are partially mediated via interaction with tested gasotransmitters. © 2019, Faculty of Medicine, University of Banja Luka. All rights reserved.

Background: The importance of homocysteine (Hcy) is increasingly recognized in last few decades as an independent risk factor for atherosclerosis and thrombosis, but there is lack of data referring to influence of Hcy on plasma oxidative stress parameters as well as the role of gasotransmitters in these effects. Therefore, this study aim was to assess the role of gasotransmitter inhibitors in Hcy-induced effects on plasma oxidative stress in rats. Material and Methods: Study involved 96 male Wistar albino rats divided into 8 groups: 1) Control group - saline (1ml 0.9% NaCl i.p.,); 2) DL-Hcy (8 mmol/kg i.p. DL homocysteine (DL-Hcy); 3) L-NAME (10 mg/kg i.p. Nω-Nitro-L-arginine methyl ester (L-NAME), inhibitor of NO production); 4) ZnPPR IX (30 mol/kg i.p. protoporphyrin IX zinc (ZnPPR IX), inhibitor of CO production); 5) DL-PAG (50 mg//kg i.p. DL-propargylglycine (DL-PAG), inhibitor of H2S production); 6) DL-Hcy+L-NAME (8 mmol/kgi.p. DL-Hcy + 10 mg/kg i.p. L-NAME); 7) DL-Hcy+ZnPPR IX (8 mmol/kgi.p. DL-Hcy + 30 mol/kg i.p. Zn PPR IX), and 8) DL-Hcy+DL-PAG (8 mmol/kg i.p. DL-Hcy + 50 mg//kg i.p. DL-PAG). In all experimental groups, tested substances were administered in a single dose, intraperitoneally, 60 minutes before animals’ euthanasia. In the collected blood samples malondialdehyde concentration, catalase, glutathione peroxidase and superoxide dismutase activity were measured. Results: Applied substances induced rapid and strong increase of plasma antioxidant enzymatic activity probably as a compensatory response to its pro-oxidant influence. Conclusion: The effects of Hcy on the activity of plasma antioxidant enzymes are in part mediated via interaction with gasotransmitters. © 2019 Djuric et al.