Please use this identifier to cite or link to this item:
|Title:||Vitamin B complex mitigates cardiac dysfunction in high-methionine diet-induced hyperhomocysteinemia|
|Authors:||Jeremic, Jovana |
Nikolic Turnic T.
Djuric, Dragan M.
|Journal:||Clinical and Experimental Pharmacology and Physiology|
|Abstract:||© 2018 John Wiley & Sons Australia, Ltd This research is designed to test the hypothesis that elevated homocysteine (Hcy) levels in vivo, caused by a deficit in vitamin B complex, promote changes in cardiac function and redox status that lead to heart failure. In order to conduct the study, we used adult male Wistar albino rats (n = 30; 4 weeks old; 100 ± 15 g body weight). Hyperhomocysteinaemia (HHcy) in these animals was achieved by dietary manipulation. For 4 weeks, the animals were fed with a standard rodent chow (control, CF), a diet enriched in methionine with no deficiency in B vitamins (i.e., folic acid, B6 and B12) (HMNV) or a diet enriched in methionine and deficient in B vitamins (HMLV). After 28 days of dietary manipulation, all animals were killed. The rat hearts were isolated and retrogradely perfused according to the Langendorff technique at a gradually increasing perfusion pressure. We found a negative correlation between elevated serum Hcy and total body and heart weight. The maximum rate of left ventricular pressure development was significantly increased in the HMNV group compared with in the other groups. Systolic left ventricular pressure was significantly changed in all groups. HHcy induces remodelling of the cardiac tissues, as moderate HHcy is associated with more prominent interstitial and perivascular fibrosis. Our results suggest that a high methionine diet without vitamin B complex causes profound negative effects associated with HHcy.|
|Appears in Collections:||Faculty of Medical Sciences, Kragujevac|
|[ Google Scholar ]|
Files in This Item:
|29.86 kB||Adobe PDF|
View/Open Request a copy
Items in SCIDAR are protected by copyright, with all rights reserved, unless otherwise indicated.