Aim. To identify changes in cognitive function performance and endogenous oxytocin levels in various brain regions and biological fluids in mice with an experimental model of Alzheimer’s disease, chronic zinc acetate intoxication, and their combined effects. Materials and methods. CD-1 mice (n = 32). Chronic zinc acetate intoxication was modeled by administering Zn(CH3CO2)2 (Zn2+ concentration: 5 mg/L) as drinking water for 3 months; the control group received pure water. Alzheimer’s disease was modeled via intrahippocampal β-amyloid injection; the control group received phosphate-buffered saline. Associative memory was assessed using conditioned freezing testing. Oxytocin levels in brain regions and biological fluids were measured via ELISA. Results. Chronic zinc acetate intoxication and its combined effect with β-amyloid led to increased oxytocin levels in the hippocampus, entorhinal cortex, hypothalamic-pituitary region, and cerebrospinal fluid. β-Amyloid exposure either had no effect on oxytocin levels or caused a decrease (amygdala, blood plasma). Conditioned reflex formation and contextual memory were impaired in all experimental groups. Fear-associated memory in mice with the Alzheimer’s model combined with chronic zinc acetate intoxication did not differ from controls. Exposure to β-amyloid alone worsened fear-associated memory. Oxytocin levels in the amygdala correlated with changes in the mice’s ability to form fear memory. Conclusion. Chronic zinc acetate intoxication and its combination with β-amyloid increase oxytocin levels in nearly all examined brain regions and cerebrospinal fluid, likely as a compensatory response to Zn2+ neurotoxicity. Acute β-amyloid exposure did not cause significant changes. Thus, chronic zinc acetate exposure is the primary factor elevating oxytocin levels in the brain and biofluids. Increased oxytocin levels may contribute to the restoration of cognitive functions.

Aim. The aim of this article is to provide a comprehensive review of the pathogenetic mechanisms underlying the development of acute adrenal crisis (AAC) in children, with an emphasis on recent experimental and clinical findings. Materials and Methods. A comprehensive literature search was conducted using MEDLINE, Embase, Scopus, Cochrane, PubMed, Google Scholar and Elibrary databases, as well as through citation tracking of studies published between 2019 and June 2025. A total of 40 national and international publications were analyzed, including clinical, experimental, and genomic studies, as well as systematic reviews and meta-analyses focused on the pathogenesis of adrenal insufficiency and adrenal crisis in pediatric populations. Results. The classical pathogenesis of AAC is associated with cortisol and aldosterone deficiency, leading to severe metabolic and hemodynamic disturbances. However, in recent years, a new concept of the multifactorial nature of this syndrome has emerged, encompassing systemic, molecular, immune, and microbiota-related components. Key etiological forms have been analyzed, including congenital adrenal hyperplasia, glucocorticoid-induced adrenal insufficiency, and autoimmune adrenalitis. Data are presented on the involvement of pro-inflammatory cytokines (IL-6, TNF-α), mitochondrial dysfunction, altered expression of ACTH receptors (MC2R, MRAP), and epigenetic modifications (NR0B1, CYP21A2). Particular attention is given to sepsis-induced adrenal dysfunction, endothelial impairment, and the influence of the gut–adrenal axis on crisis development. Conclusion. The current understanding of AAC pathogenesis extends beyond the classical hormonal deficiency model and includes complex interactions among inflammatory, mitochondrial, immune, genetic, and microbiota-related mechanisms. The importance of early diagnosis, molecular stratification, and personalized treatment strategies is emphasized. These findings highlight the need to revise current approaches to prevention and management in pediatric practice, with a focus on targeted and multidisciplinary therapeutic interventions.