Experimental alimentary obesity: apoptosis, antioxidant system, macro- and microelements in the liver
DOI:
https://doi.org/10.11603/mcch.2410-681X.2015.v17.i4.5680Keywords:
alimentary obesity, apoptosis, antioxidant protection, trace elements.Abstract
The results of the study of the mechanism of liver injury of experimental alimentary obesity are provided. It was established that in 14 days the experiment activates superoxide dismutase and catalase, which are directly related to the level of zinc (r=0.77; p<0.05) and copper (r=0.64; p<0.05), which outside the active site of the enzyme Cu/Zn-SOD, providing regulation of the initiation stage peroxidation of chain oxidation. After 28 days of experiment functional capacity of antioxidant system is exhausted, as evidenced by decreased activity of SOD and catalase, the relationship with traсe elements is lost. Violation of trace elements metabolism after 28 days of experimental model in the rats are characterized by increased levels of copper, reduced zinc, magnesium and chromium in liver tissue, compare to the control (p<0.05). Also, apoptotic death of macrophages is present in the liver, which is 2.9 times higher than the control values, and depending on the level of zinc in liver tissue (p<0.05).
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