Aim: To assess, under experimental conditions of cellular dehydration of varying severity, the nature of structural changes in the nephron and the dynamics of reparative processes during the recovery period.
Materials and Methods: The study was conducted on 110 young male Wistar rats, divided into two groups. The first group (30 rats) remained intact, while the second group (80 rats) was adapted to dehydration. Adaptation was achieved through alternating a low-mineral diet with 1.5% hypertonic sodium chloride solution (for two days) and a standard vivarium diet (for one day) over 42 days. Cellular dehydration in the second group was induced by administering 1.5% hypertonic sodium chloride solution along with dried oats and crackers. The degree of dehydration was determined based on the water deficit. In the next stage of the experiment, animals were returned to a normal diet, and readaptation changes were assessed at 1, 3, 6, and 12 weeks after the cessation of the dehydrating factor. The morphological state of the kidney structures was examined using microscopic, electron-microscopic, morphometric, and statistical methods.
Results: As a result of exposure dehydrating factor, the renal parenchyma shows functional tension in the glomeruli and tubular epithelial cells due to the increased load on the kidney. Changes of podocyte pedicels affect the size of filtration slits that regulate glomerular filter permeability. The first indicators of disorders in the glomerular-tubular system are the basal membranes in the composition of capillaries and epithelium. Even in mild dehydration, as the dehydrating factor increases, the basal membrane thickens, loses its three-layer structural organization, becomes homogeneous and osmiophilic. Gradually, podocytes and endothelial cells of capillaries are damaged, undergoing dystrophy. The process of readaptation after rehydration of the previously dehydrated organism involves a complex of morphological changes following cellular dehydration, aimed at restoring lost or weakened functions of cells and tissues, their adaptive-compensatory changes, which ensure adaptation to certain conditions. Structural transformations of cells during readaptation may manifest in the enhanced stabilization of cell membranes and the resistance of tissues to intensive influences. Previous adaptation under dehydration leads to the mitigation of the dehydrating factor’s impact, manifested in a lower severity of structural-metabolic disturbances and increased energy exchange.
Conclusions: The structural components of the nephron immediately respond to disturbances in the body’s water-electrolyte balance by changing their structural organization. These changes are significant in severe cellular dehydration, and their restoration requires a long period of time.

Aim: To investigate the effect of succinic acid on the humoral component of the immune system in rats.
Materials and Methods: The study was conducted on two groups of mature non-linear white rats (males) of similar weight (200-270 g, aged 6-8 months),with 5 animals in each group. The control group was fed a standard diet with free access to water throughout the experiment. Rats in the experimental group were subcutaneously injected with a 0,1% solution of succinic acid in a liposomal emulsion at a dose of 20 cm³ for five days. The state of the humoral component of the immune system was assessed by measuring serum immunoglobulins A, M, and G using solid-phase enzyme-linked immunosorbent assay. Circulating immune complexes were determined in a 40% solution of polyethylene glycol.
Results: Under the influence of succinic acid in liposomal emulsion the content of class A immunoglobulins increased by 44,0% (p<0.01) compared to rats in the control group. The activation of class A immunoglobulin synthesis points to the provision of local immunity of the mucous membranes in the rat’s body. The content of class M immunoglobulins increased by 61,0% (p<0.001) compared to the control group rats. This high activity of class M immunoglobulins indicates their rapid activation in the body of rats in response to primary contact with succinic acid in liposomal emulsion. The content of class G immunoglobulins increased by 36,0% (p<0.05) compared to the control group rats. No clinical deviations from physiological norms were observed in the rats after the use of succinic acid in liposomal emulsion. After the use of succinic acid in liposomal emulsion in the experimental group of rats, the concentration of CICs increased by 15,0% (p<0.05) compared to the control group rats. In our case, the increase in CIC levels is not correlated with clinical manifestations but is a consequence of increased levels of class M and G immunoglobulins.
Conclusions: The succinic acid in liposomal emulsion activates the production of class A, M, G immunoglobulins, circulating immune complexes, it prevents
the development of secondary immunodeficiency and has a positive impact on the humoral branch of the immune system in rats.