The changes of activity of effector caspase cascade components in case of alimentary obesity in rats

Abstract

Abstract:Objective: The prevalence of obesity is rising in a global fashion, placing this population at higher risk for type 2 diabetes mellitus and cardiovascular disease. Current strategies for treatment of obesity are largely unsuccessful over the long term, since weight loss, even when achieved initially, is often followed by weight regain. More knowledge about the molecular and cellular mechanisms governing adipose tissue accumulation is needed to develop more effective preventative and therapeutic approaches to obesity. Materials and Methods: This study was conducted to investigate the macro-and microelements contents in the blood of experimental animals and assess their influence on the level of apoptotic cell death of blood leukocyte suspension in case of alimentary obesity, which was modelled on male, non-liner, white rats of around 3 months. Annexin V binding assays were performed by flow cytometry, the atomic absorption spectrophotometer was used to quantify micro-and macro-element contents.Results and Discussion: It was established a significant increase in leptin concentration at almost the same level of adiponectin. Experimental obesity was characterized by 2.1 times increasing of Annex+ cells percentage, while the level of PI+ cells remained within the control values. It was established the increasing of total calcium level, which exceeded by approximately 25.0 % of the control data. The same trend was marked on changes of ionized calcium level (p<0.05). So, alimentary obesity in rats is accompanied by the increasing of total and ionized calcium contents and decreasing of iron, magnesium and zinc contents. The combination of the dysmetabolism of investigated bioelements with the maximum effect of zinc affects the apoptotic cells' death at obesity. Conclusion: Changing of activity of effector caspase cascade components, including caspase -3 in case of diet-induced alimentary obesity, causes implementing of blood suspension leukocyte cells' death by apoptosis, and the initiation of apoptosis in this case depends on the body mass index and leptin concentration. The study showed that the combination of the dysmetabolism of investigated bioelements with the maximum effect of zinc affects the apoptotic cells' death at obesity.

Вивчення Ефектів Поєднаної Дії Харчових Добавок

“…Кількість харчових добавок, які застосовують у виробництві харчових продуктів у різних країнах, досягає сьогодні п'ятисот, не враховуючи комбінованих добавок, ароматизаторів. На території України поширені такі харчові добавки: Е621 -мононатрієва сіль глутамінової кислоти (16 %), Е260 -оцтова кислота (15 %), Е211 -натрій бензоат (15 %), E330 -лимонна кислота (39 %), Е1442 -гідроксипропілдикрохмальфосфат (15 %), тоді як найпоширенішими харчовими добавками у Європі є: Е471 -моногліцериди і дигліцериди жирних кислот (13 %), Е412 -гуарова камідь (13 %), Е1442 -гідроксипропілдикрохмальфосфат (13 %), E330 -лимонна кислота (37 %), Е621 -мононатрієва сіль глутамінової кислоти (12 %), Е407 -карагінан і його солі (12 %) [1,2].…”

The influence of thyroid hormones on mitochondrial mechanisms of blood neutrophils’ apoptosis in case of experimental periodontitis

“…Apoptosis involves a cascade of complex events, from external apoptotic signals, activating specific receptor complexes, to the execution of apoptosis, by activation of proteases and endonucleases. The commitment to apoptosis depends on the balance between proapoptotic and antiapoptotic signaling components within cells [13][14] . Hyperproduction of ROS and oxidative stress may result in a pathological transformation of mitochondria -the opening of the mitochondrial permeability transition pore and induction of cell death [15][16][17] .…”

Features of leukocytes’ apoptosis and emoxypine succinate efficacy in case of combined trauma of the chest and both thighs in rats

“…Structural and functional alteration of mitochondria plays an important role in the pathogenesis of many diseases, since mitochondria, as a semiautonomous organelle in cells, apart from containing their own genetic material, play an important role in energy metabolism, oxidation-reduction balance and calcium homeostasis, pathways of mitochondriamediated or receptor-independent apoptosis, provide mechanisms of signal transduction in the control of nuclear function [1][2][3][4][5][6] . The molecular mechanisms of apoptosis involve several pathways and activation of caspases, a family of cysteine proteases, represents a common event for several pro-apoptotic stimuli 7 . Regarding on the characterisation of the events upstream from caspase activation, mitochondrial damage has been reported to trigger this process.…”