Radiotherapy is one of the risk factors for radiation-induced premature ovarian failure and infertility in cancer patients. The development of methods for ovarian radioprotection remains relevant. Moreover, electrons are a little-studied and promising method of radiation with the least toxic effect on normal tissues. The assessment of intracellular mechanisms regulating the protective effects of leukocyte-poor platelet-rich plasma in a model of radiation-induced premature ovarian failure caused by electron irradiation. Wistar rats were divided into four groups, namely a control group, irradiation group (electron exposure), irradiation + leukocyte-poor platelet-rich plasma group, and only leukocyte-poor platelet-rich plasma group. Fragments of ovaries were removed and hormonal, oxidant, histological, and morphometric studies were carried out. The cell cycle of ovarian follicles and the inflammatory and vascular response were assessed using immunohistochemistry. The activity of MAPK, ERK, and PI3K pathways was also assessed using the RT-qPCR. We found that electron irradiation causes a decrease in the functional activity of the ovaries and the death of follicular cells through apoptosis. The administration of LP-PRP led to a partial restoration of the cytokine balance. In addition, minor ovarian damage and mild inflammation were observed in this group. Leukocyte-poor platelet-rich plasma components have anti-inflammatory, angiogenetic, and radioprotective effects, reducing the activation of the NOX4, caspase and cytokine cascades, and inflammatory response severity through the MAPK/p38/JNK signaling pathway. This leads to the induction of endogenous antioxidant protection, the repair of post-radiation follicular damage, and slowing down the development of radiation-induced premature ovarian failure after electron irradiation.

Background: Macrophages are key components of the tumor microenvironment and play a critical role in melanoma progression. However, the dynamics of different macrophage subsets, particularly CD68⁺ and CD163⁺ populations, in relation to tumor thickness and stage remain insufficiently characterized. Objective: This study aimed to quantitatively assess intratumoral and peritumoral CD68⁺ and CD163⁺ macrophages in cutaneous melanoma and to investigate their associations with Breslow thickness, pT stage, and AJCC stage. Methods: We conducted a retrospective cohort study of 126 patients with cutaneous melanoma (AJCC stages IA–IIID). Tumor samples were examined histologically and immunohistochemically for CD68⁺ and CD163⁺ macrophages, and quantitative analysis was performed in intratumoral and peritumoral regions. Results: This study included 126 patients with cutaneous melanoma, ranging in stage from IA to IIID. Histopathological analysis revealed that melanoma tissues were primarily composed of irregular clusters of atypical melanocytic cells infiltrating the dermis and subcutaneous fat. Immunohistochemical staining identified CD68⁺ and CD163⁺ macrophages both within the tumor and in the surrounding stroma. Macrophage infiltration significantly increased with tumor thickness (Breslow) and progression to more advanced stages. Specifically, at Breslow thickness 4.0 mm. CD163⁺ macrophages showed similar trends, with a rise from 15.6 ± 2.8 cells at 4.0 mm in the intratumoral zone. Additionally, macrophage density was higher in tumors with ulceration, and both CD68⁺ and CD163⁺ macrophage numbers increased progressively with tumor stage, particularly in advanced stages. The number of CD68⁺ macrophages at stage IA in the intratumoral zone was 21.6 ± 3.1 cells and increased to 56.4 ± 6.8 cells at stage IIID, while CD163⁺ macrophages rose from 13.8 ± 3.2 cells at stage IA to 36.4 ± 4.6 cells at stage IIID. This suggests that macrophage infiltration, particularly CD163⁺ cells, correlates with melanoma progression. Conclusions: Our findings highlight distinct spatial and phenotypic patterns of macrophage infiltration in melanoma progression. The prominent increase in CD68⁺ and CD163⁺macrophages suggests their important role in tumor-associated immunomodulation. Further studies are warranted to elucidate macrophage polarization states and their prognostic and therapeutic implications in melanoma.

Leukocyte-poor platelet-rich plasma (LP-PRP) has a potential influence on tissue regeneration by stimulating proliferation and differentiation of progenitor cells.The aim of this work is morphologi...

Background and purpose: With the emergence of linear accelerators in radiotherapy, it becomes necessary to accurately select new dosing regimens. The purpose of this study was to assess the morphological changes of spermatogenesis after radiation exposure. Materials and methods: Male Wistar rats (n = 40) were subjected to targeted ionizing radiation on a pulsed electron accelerator “NOVAC-11” with doses of 2, 8 and 12 Gy. Spermatogenesis was assessed a week later using light microscopy and immunohistochemical method (antibodies to Ki-67, Bcl-2, p53, Caspase 3). Results: A decrease in the number of normal germ cells was seen in all experimental groups, while radioresistant Sertoli and Leydig cells were barely affected. The most serious damage to the tubules and germ cells was observed in 8 and 12 Gy irradiation groups. IHC analysis of testes after irradiation showed a shift in the proliferative-apoptotic balance toward apoptosis of germ cells: a decrease in the expression levels of Ki-67 and Bcl-2, an increase in p53-positive and caspase 3-positive cells by the end of the experiment. Conclusion: Dose-dependent progressive pathomorphological changes in histoarchitectonics of the testes are traced, and a decrease in the number of germ cells is seen on the seventh day after irradiation with a pulsed electron accelerator “NOVAC-11”.

BACKGROUND: Radiation hepatitis with the development of radiation-induced acute liver failure is considered one of the most serious complications of radiotherapy for malignant neoplasms of the liver, abdominal organs, or whole body irradiation. However, the exact mechanisms of radiation-induced liver cell death have not been fully elucidated, and therefore the study of changes in the proliferative-apoptotic ratio in liver structures remains relevant, and pre-irradiation administration of ascorbic acid can potentially protect them from the effects of electron irradiation. AIM: Assessment of proliferation and apoptosis of hepatocytes after administration of ascorbic acid in a model of radiation hepatitis. MATERIALS AND METHODS: Wistar rats (Rattus Wistar; n=40) were divided into four experimental groups: I — control (n=10); II (n=10) — fractional irradiation with electrons in a total irradiation dose of 30 Gy; III (n=10) — administration of ascorbic acid before electron irradiation; IV (n=10) — administration of ascorbic acid. Animals of all groups were removed from the experiment a week after the last fraction. Morphological and immunohistochemical (with antibodies to Ki-67 and caspase-3) studies were carried out. RESULTS: A week after electron irradiation, a sharp decrease in the proportion of Ki-67-positive hepatocytes in combination with an increase in immunolabeling with antibodies to caspase-3 was observed in group II. During the administration of ascorbic acid in group III, less pronounced depth and range of liver damage was noted, confirmed by morphological and immunohistochemical methods (less pronounced decrease in the level of Ki-67 expression and an increase in the proportion of caspase-positive hepatocytes compared to the control) methods. CONCLUSIONS: An immunohistochemical study of proliferation and apoptosis of hepatocytes revealed that a week after fractional electron irradiation in total irradiation dose 30 Gy, there is a decrease in mitotic activity and an increase in cell death, and pre-irradiation administration of ascorbic acid helped level out the detected changes, which indicates its protective effect.

Kidney disease has emerged as a significant global health issue, projected to become the fifth-leading cause of years of life lost by 2040. The kidneys, being highly radiosensitive, are vulnerable to damage from various forms of radiation, including gamma (γ) and X-rays. However, the effects of electron radiation on renal tissues remain poorly understood. Given the localized energy deposition of electron beams, this study seeks to investigate the dose-dependent morphological and molecular changes in the kidneys following electron irradiation, aiming to address the gap in knowledge regarding its impact on renal structures. The primary aim of this study is to conduct a detailed morphological and molecular analysis of the kidneys following localized electron irradiation at different doses, to better understand the dose-dependent effects on renal tissue structure and function in an experimental model. Male Wistar rats (n = 75) were divided into five groups, including a control group and four experimental groups receiving 2, 4, 6, or 8 Gray (Gy) of localized electron irradiation to the kidneys. Biochemical markers of inflammation (interleukin-1 beta [IL-1β], interleukin-6 [IL-6], interleukin-10 [IL-10], tumor necrosis factor-alpha [TNF-α]) and oxidative stress (malondialdehyde [MDA], superoxide dismutase [SOD], glutathione [GSH]) were measured, and morphological changes were assessed using histological and immunohistochemical techniques (TUNEL assay, caspase-3). The study revealed a significant dose-dependent increase in oxidative stress, inflammation, and renal tissue damage. Higher doses of irradiation resulted in increased apoptosis, early stages of fibrosis (at high doses), and morphological changes in renal tissue. This study highlights the dose-dependent effects of electrons on renal structures, emphasizing the need for careful consideration of the dosage in clinical use to minimize adverse effects on renal function.