ANALYSIS OF A PATHOMORPHOSIS OF ALIMENTARY DEFICIT OF MAGNESIUM IN UTERUS AND OVARY WITH DIFFERENT SALTS OF MAGNESIUM

Abstract

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Purpose of the work was to reveal the morphofunctional patterns of changes in uterus and ovary in conditions of induced pathomorphosis of magnesium deficit. Materials and methods of the study: modeling of an alimentary deficit of magnesium was carried out using a special magnesium-deficient diet, a similar diet, offered by MP Biomedicals Company (USA). The experimental groups included: 1st intact female rats, 2nd female rats which were on a magnesium-deficient diet for 12 weeks, the group of an induced pathomorphosis from 9th to 12th week was given with alimentary magnesium as magnesium sulphate (group 3), magnesium aspartate (group 4), magnesium taurinat (group 5), magnesium chloride (group 6) at dose 50 mg/kg of body weight perorally After the pathoanatomical, morphometric, and statistical analyses the most signified changes in the alimentary deficiency of magnesium were caused by the processes of atrophy and impaired microcirculation with predominantly epithelial lesions of ovarian and endometrial structures. Desmoplastic process with the affection of the spiral arteries walls and smooth myocytes atrophy plays a leading role in the myometrium. We noted an adaptive amplification of cytoplasmic expression of TRPM6, TRPM7, decrease of expression of Bcl-2 and increase of expression of Bax-positive cells, which characterizes the predominance of apoptosis processes and desmoplastic changes over the compensatory and adaptive processes in the uterus and ovaries. In the setting of the induced pathomorphosis alimentary magnesium deficiency we noted a positive dynamics of morphometric parameters. The most favorable effect was observed in the group of correction with magnesium taurinate. The sizes of the exocrinocytes of endometrium glands, thickness of the endometrium and myometrium, thickness of the vessel walls of the myometrium became normal, but at the same time, there was a hypertrophy of a single layer of columnar epithelium and the exocrinocytes of the endometrium glands, the volume part of the glands of the endometrium did not changed significantly, in respect of the performance groups of animals with alimentary magnesium deficiency. These changes support the preservation of dystrophic and atrophic changes in the uterus and ovaries. After the pathomorphosis of alimentary magnesium deficiency induced by other salts of magnesium we noted a less signified positive dynamics, which indicates the increase in metabolic capacities of ovarian tissues of the uterus and ovaries, which is confirmed by the normalization of a fewer morphometric parameters and the preservation of more signified degenerative and atrophic changes in the uterus and ovaries. Conclusions: thus, we can conclude that in pathomorphosis of the alimentary magnesium deficiency induced by magnesium salts partial regression of atrophic changes takes place as well as restoration of a number of morphological parameters of the parenchyma of uterus and ovaries, while maintaining an inverse dependence between the expressiveness of desmoplastic processes and compensatory hyperplasia, which shows the implementation of reparative regeneration processes on a substitution level.