In toxicity studies on laboratory animals, a priority task is to establish reliable toxicometric characteristics of compounds, including threshold, effective (ED), and lethal (LD) doses, in accordance with the objectives of the experiment. In the case of inhalation exposure to a toxicant, there are difficulties in calculating absorbed doses, which are related both to the influence of the physical and chemical properties of the toxicant and to the species-specific characteristics of the biological test subjects used in the study. This feature poses a challenge in the interspecies extrapolation of inhalation doses to humans, making it difficult to plan and conduct further experiments. This study aims to review the domestic and foreign literature on the interspecies extrapolation of inhalation doses. The main databases used for searching scientific publications were PubMed, Google Scholar, and Web of Science. The study provides an analysis of the key biological determinants that influence the efficacy of toxicants, including anatomical and morphological features, physiological parameters, and pathological changes in laboratory animals. Additionally, the study highlights the main physical and chemical properties of compounds that affect the interaction of the system with the xenobiotic. Special attention is given to aerosol generation parameters, which are essential for assessing the risks of toxicant exposure on biological subjects. Based on the analysis, the most optimal method for calculating absorbed doses is proposed, taking into account the specific features of the respiratory systems of living organisms during experimental studies. Furthermore, key approaches for extrapolating inhalation doses to humans are outlined, including the allometric approach, the use of interspecies and dosimetric coefficients, and the physiologically based pharmacokinetic model (PBPK).

Authors’ contribution:
Popov N.S. – the concept and design of the study, collection of material, writing a text;
Konshakov Yu.O. – the concept and design of the study, editing;
Ustinova T.M. – collection of material;
Vengerovich N.G. – editing.
All co-authors – are responsible for the integrity of all parts of the manuscript and approval of the manuscript final version.

Conflict of interest. The authors declare no apparent and potential conflicts of interest in relation to the publication of this article.

Funding. The study had no sponsorship.

Received: May 25, 2025 / Revised: June 27, 2025 / Accepted: March 27, 2026 / Published: April 30, 2026

This review article summarizes current knowledge on the endocrine-disrupting effects of chloroacetanilide herbicides – compounds widely employed in agriculture for the control of annual grasses and certain dicotyledonous weeds. Exposure to these xenobiotic has been associated with a range of adverse health outcomes in both adult and developing organisms. To assess their endocrine toxicity, the authors performed a comprehensive analysis of toxicological data retrieved from major international and national scientific databases, including FAO/WHO, EXTOXNET, EPA, EFSA, EMBASE, Global Health, Scopus, Web of Science, MedLine, PubMed, eLibrary, CyberLeninka, and Springer Nature Link.

The reviewed evidence indicates that chloroacetanilides exert multimodal effects on the endocrine system, targeting the hypothalamic-pituitary-adrenal (HPA), hypothalamic-pituitary-gonadal (HPG), and hypothalamic-pituitary-thyroid (HPT) axes. These compounds interfere with the synthesis of steroid and thyroid hormones through both direct interaction with hormone receptors and modulation of enzymes involved in hormone biosynthesis and metabolism. Specifically, dose-dependent suppression of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion has been demonstrated, along with competitive binding of acetochlor, metolachlor, and their metabolites to androgen receptors. In addition, estrogenic activity has been observed, evidenced by the induction of vitellogenin synthesis and upregulation of aromatase (cyp19a1a) gene expression in aquatic species, suggesting disruption of endogenous estrogen regulation. With respect to the HPT axis, the primary effect is a reduction in thyroxine (T₄) levels, likely mediated through inhibition of type 2 deiodinase – the enzyme responsible for peripheral conversion of T₄ to triiodothyronine (T₃). Notably, these effects were most pronounced following exposure to S-enantiomers.

Authors’ contribution:
Sinitskaya T.A. – scientific supervision, study concept and design, editing;
Khamidulina Kh.Kh. – scientific consulting, editing;
Poroshin M.A. – material collection and writing.
All co-authors are responsible for the integrity of all parts of the manuscript and approval of the manuscript final version.

Conflict of interest. The authors declare no obvious or potential conflicts of interest in connection with the publication of this article.

Funding. The study had no sponsorship.

Received: March 24, 2026 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Lead is considered to be a ubiquitous poison that pollutes both industrial and residential areas. Exposure to lead and its compounds has a negative impact on developing and mature organisms, potentially leading to cardiovascular changes.

Material and methods. The experiment was conducted on outbred male albino rats aged 3 to 4 weeks (24 rats, mean body weight: 41.96 ± 1.59 g) and 12 months (27 rats, mean body weight: 439.26 ± 5.77 g). Lead acetate trihydrate (Pb(CH₃COO)₂ ∙ 3H₂O) was administered intraperitoneally thrice a week for 6 weeks at the doses of 5.50, 11.00, and 22.88 mg/kg b.w. Sterile saline solution was administered to control animals. The hemodynamic parameters measured included systolic, diastolic, and mean arterial pressure (SAP, DAP, and MAP), heart rate (HR) during pressure measurement, tail artery blood flow, and tail vein blood volume.

Results. We observed a statistical decrease in SAP in the adult rats administered 11.00 mg/kg b.w. of lead acetate. Pulse pressure also decreased significantly following moderate and high exposures in the adult rats and high exposure in the young rodents. HR decreased significantly only in the adult group. The tail artery blood flow dropped only in the young rats following the exposure doses of 11.0 and 22.88 mg/kg b.w. The tail vein blood volume decreased in both young (11.0 and 22.88 mg/kg b.w.) and adult (5.50; 11.00 and 22.88 mg/kg b.w.) animals compared to the controls.

Limitations. All animals were of the same sex.

Conclusion. Lead acetate had a negative impact on both young and adult rats. A dose-dependent effect was observed for tail artery blood volume only. Presumably, the mechanism of toxic effects of lead on hemodynamics may be associated with oxidative stress, inflammation and apoptosis, effects on the renin-angiotensin-aldosterone system and arginine vasopressin, as well as direct damage to the heart, blood vessels, and kidneys.

Compliance with ethical standards. The study was approved by the Local Ethics Committee of the Yekaterinburg Medical Research Center for Prophylaxis and Health Protection of Industrial Workers of Rospotrebnadzor (protocol No. 3 of January 17, 2024). The study was conducted in accordance with the European Convention for the Protection of Vertebrate Animals Used for Experimental and Other Scientific Purposes (ETS N 123) and with the Directive 2010/63/EC of the European Parliament and of the Council of 22 September 2010 on the Protection of Animals Used for Scientific Purposes.

Authors’ contribution:
Sutunkova M.P. – study concept and design, scientific editing;
Minigalieva I.A. – study concept and design, scientific editing;
Gertan N.A. – data collection and processing, statistical analysis, text writing;
Nikogosyan K.M. – data collection and processing, editing.
All co-authors – approval of the final version of the article and are responsible for the integrity of all its parts.

Conflict of interest. The authors declare no apparent and potential conflicts of interest in relation to the publication of this article.

Funding. The study had no sponsorship.

Received: May 25, 2025 / Revised: November 6, 2025 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Poisoning by pulmonotoxicants is an urgent problem of modern toxicology due to its frequency, severity of cases, and insufficient understanding of underlying mechanisms, which hinders effective treatment. The aim of this study is to evaluate the status of the rat antioxidant system during the modeling of acute pulmonotoxicants poisoning.

Material and Methods. Acute poisoning by pulmonotoxic substances, perfluoroisobutylene and nitrogen dioxide in toxodoses of 1.67 mg/l∙min and 5.6 mg/l∙min, respectively, was in Modeled on nonlinear male rats in an inhalation chamber with a volume of 0.2 m³ for 15 minutes. Blood and lungs samples were taken 3, 6, and 24 hours after exposure to assess the activity of superoxide dismutase, catalase, and glutathione peroxidase, while plasma levels of malondialdehyde were also measured.

Results. In response to perfluoroisobutylene exposure, superoxide dismutase, catalase, and glutathione peroxidase activities in blood after 3 h reached minimum values – 75.6 U/ml, 229.2 and 11.1 mM/(l∙min) correspondingly, with subsequent partial recovery of catalase and glutathione peroxidase activities, and compensatory increase of superoxide dismutase activity within 24 h. The lung tissue response is manifested in a decreased activity of the enzymes studied, within 24 h. Related to nitrogen dioxode exposure, the superoxide dismutase and catalase peak activities in blood were recorded after 6 h – 157.7 U/ml and 513.3 mM/(l∙min), respectively, glutathione peroxidase’s peak activity – after 3 h – 19.5 mM/(l∙min). The enzymes’ activity dynamics in lung is indicative of the superoxide dismutase level increase up to 54,5 U/ml within 24 h, while changes of catalase and glutathione peroxidase activities are characterized by minimum peak values after 6 h – 20.4 and 6.4 mM/(l∙min), respectively. There was a sustainable malondialdehyde accumulation in blood plasma during the experiment, which exceeded the corresponding value in intact group of animals.

Conclusion. These findings suggest the significant effects of free-radical oxidation processes on the pulmonotoxic agents’ toxicity mode.

Limitation. The experimental study was performed on white outbred male rats (n = 30, body weight 200-240 g), kept in a standard vivarium conditions, and randomly divided into groups with the exclusion of weakened and affected animals from the study.

Compliance with ethical standards. The study was approved by the Local Ethics Committee of the State Research and Testing Institute of Military Medicine of the Ministry of Defense of the Russian Federation, Protocol No. 18 of 16.12.2023; conducted according to the European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (ETS No. 123), European Union Directive 2010/63 EU of 22.09.2010 on the protection of animals used for scientific purposes.

Author’s contribution:
Ustinova T.M. – research concept and design, text writing, statistical data processing;
Konshakov Yu.O. – text writing;
Vengerovich N.G. – editing;
Stepanov G.S. – collecting of the material, data processing.
All co-authors are responsible for approving the final version of the article and ensuring the integrity of all parts of the article.

Conflict of interest. The authors declare the absence of obvious and potential conflicts of interest in connection with the publication of this article.

Funding. The study had no sponsorship.

Received: August 8,2025 / Revised: March 4, 2026 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Current challenges in toxicology include the development and modernization of biological prevention strategies to reduce the risks of long-term toxic effects of lead.

The aim of this study was to determine changes in certain biochemical and histomorphological parameters of the reproductive system of male rats following subchronic exposure to lead acetate and to establish efficacy of a bioprophylactic complex (hereinafter referred to as BPC) specially developed to reduce the severity of toxic effects.

Material and methods. The experiment was conducted on albino outbred male rats aged from 4 to 6 months. The administration was carried out orally, daily for 45 days. The dose of lead acetate was 819 mg/L. Some of the animals received a vitamin and mineral complex, the composition of which was selected based on the mechanisms of lead toxicity. The effectiveness of BPC and the toxic effects of lead acetate were evaluated 21 days after the end of the exposure.

Results. According to the obtained data, lead exposure resulted in a significant decrease in the lumen of the seminiferous tubules and an increase in the proportion of Sertoli cells with degenerative and dystrophic changes. A significantly higher number of abnormal spermatozoa in testicular smears was detected in rats treated with lead acetate compared with control. An increase in the activity of the enzyme 3β-hydroxysteroid dehydrogenase was observed in exposed rats compared to controls.

Although this study did not measure sex hormone levels in the blood of laboratory animals, we believe that the observed increase in HSD3b1 is more likely a consequence of compensatory responses to the destruction and/or dysfunction of cells responsible for androgen synthesis than a direct consequence of lead toxicity.

Limitations. We did not assess sex hormone levels or the activity of the HSD3b2 isoform of the 3bHSD enzyme.

Conclusion. Male rats exposed to lead acetate showed a slight increase in the activity of 3β-hydroxysteroid dehydrogenase, an enzyme that plays an important role in regulating sex hormone synthesis and delta-ALA metabolism. The observed histomorphometric changes included a decrease in the lumen of the seminiferous tubules, an increase in the number of abnormal Sertoli cells and degenerated spermatozoa. Our findings prove the protective potential of biological prevention strategies but highlight the importance of further profound studies of the mechanisms of lead toxicity on the male reproductive system and the effects of BPC.

Compliance with ethical standards. The study was approved by the local Bioethics Committee of the Yekaterinburg Medical Research Center for Prophylaxis and Health Protection of Industrial Workers of Rospotrebnadzor (protocol 1A of February 3, 2025) and conducted in compliance with the European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (ETS No. 123) and Directive 2010/63/EC of the European Parliament and of the Council of September 22, 2010 on the protection of animals used for scientific purposes.

Authors’ contribution:
Nikogosyan K.M. – data collection and processing, writing, editing of the article;
Sutunkova M.P. – study design and editing;
Minigalieva I.A. – study conception and editing;
Gertan N.A. – data collection and processing;
Petrunina E.M., Sakhautdinova R.R. – data collection.
All co-authors approved the final version of the article and are responsible for the integrity of all its parts.

Conflict of interest. The authors declare the absence of obvious and potential conflicts of interest in connection with the publication of this article.

Funding. The study had no sponsorship.

Received: March 11, 2026 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Acute baclofen poisoning occupies a significant place in the structure of acute poisoning of chemical etiology. The increase in the frequency of baclofen poisoning is associated with the expansion of its use in neurological practice. Clinical toxicology challenges include the difficulties in identifying and diagnosing of baclofen poisoning due to the frequent mimicry of neurological pathology, leading to delays in treatment. In order to improve approaches to the diagnosis and treatment of baclofen poisoning, an epidemiological analysis was conducted.

The purpose of the study was to carry out a retrospective analysis of acute baclofen poisoning in St. Petersburg from 2021 to 2024.

Material and methods. Electronic medical records and the results of chemical and toxicological studies of biomaterial from patients hospitalized at the Acute Poisoning Center of the I.I. Dzhanelidze St. Petersburg Research Institute of Emergency Medicine for the period from 2021 to 2024 were studied. The epidemiological analysis included a quantitative assessment of the incidence of acute baclofen poisoning among residents of St. Petersburg and was calculated for 100 thousand people.

Results. In the period from 2021 to 2024, there was an upward trend in the number of acute baclofen poisoning (y = 0.834x − 0.525; R² = 0.6839). In the dynamic series, the period of increase in baclofen poisoning prevailed over the period of decline. 23% of patients were hospitalized in the intensive care unit of the Acute Poisoning Center, 41.8% of them required artificial lung ventilation (ALV).

Limitations. The limitations of the study are related to the retrospective nature of the analysis and the possible underestimation of cases of mild poisoning that do not require hospitalization. Nevertheless, the identified trends confirm the need to include baclofen in drug safety monitoring programs and the development of specialized antidotes, baclofen antagonists, which are under experimental research.

Conclusion. As a result of the study, a significant epidemiological significance of acute baclofen poisoning for residents of St. Petersburg was revealed, which requires improvement of diagnostic and treatment methods for these poisonings, as well as tightening of control measures to prevent the spread of this drug among the population.

Compliance with ethical standards. The study was approved by the local Ethics Committee of the I.I. Dzhanelidze St. Petersburg Research Institute of Emergency Medicin (Protocol No. 4 dated May 22, 2025) conducted according to the European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (ETS No. 123), European Union Directive 2010/63 EU of 22.09.2010 on the protection of animals used for scientific purposes.

Аuthor’s contribution:
Narzikulov R.A. – concept and design of the study, collecting and processing the material, text writing;
Batotsyrenov B.V. – concept and design of the study, editing;
Ikhaev Kh.S. – collecting and processing the material;
Medvedev A.A. – statistical data processing, text writing;
Lodyagin G.A. – text writing;
Merenkova E.N. – text writing.
All co-authors – final approval of the article, responsibility for the integrity of all parts of the article.

Conflict of interest. The authors declare no apparent and potential conflicts of interest in relation to the publication of this article.

Funding. The study had no sponsorship.

Received: June 23, 2025 / Revised: October 8, 2025 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Snake bites, characterized by a highly neurotoxic venom, are a significant but underestimated public health problem. Such incidents pose a high risk due to the lack of registered specific antidotes in Russia and limited clinical experience in the treatment of such patients.

The objective of the study was to demonstrate an interdisciplinary approach to the management of a patient with severe poisoning due to a snake bite of the family Elapidae, complicated by the development of necrosis of the soft tissues of the hand, with a description of the stages of toxicological intensive therapy and reconstructive plastic interventions.

Clinical observation. Patient S., 28 years old, was admitted to the Department of Acute Poisoning Treatment at the N.V. Sklifosovsky Research Institute of Emergency Medicine 1.5 hours after the bite of a supposedly monocle cobra in the wrist area. At the prehospital stage, a tourniquet was applied independently, and the patient experienced nausea, vomiting, and speech disturbances. Upon admission to the intensive care unit, the patient exhibited swelling of the hand and lower third of the forearm, ptosis, respiratory and consciousness depression, leading to stupor, and cardiac conduction disorders. The patient was intubated and connected to an artificial lung ventilation device. Electrolyte disturbances, signs of a systemic inflammatory response and the myotoxic effect of the venom were detected. Antidote therapy was not performed. The complex treatment included intestinal lavage, two plasma exchange sessions with an interval of 24 hours, infusion, gastroprotective, antibacterial, nutritional and metabolic, symptomatic and vitamin therapy, prevention of thromboembolic and infectious complications. The patient’s clinical and laboratory parameters and vital functions were monitored. By day 6, the neurotoxic effect of the venom was stopped, and the patient was able to breathe independently. Due to the development of soft tissue necrosis in the bite area, necrectomy was performed within the healthy tissues, and the wound was drained. Subsequently, sanitary surgical interventions were performed. By the 14^th day, the wound was cleaned and secondary sutures were applied. The total hospital stay was 16 days.

Conclusion. The presented clinical case of severe poisoning by asp snake venom, complicated by the development of extensive soft tissue necrosis, illustrates the need for an interdisciplinary approach at all stages of therapy, as well as constant monitoring of vital functions and laboratory parameters. The key areas of therapy included artificial ventilation to correct respiratory failure, administration of hormonal and antihistamine medications, intestinal lavage and plasma exchange, and timely involvement of surgeons to correct local complications.

Limitations. The described therapeutic approach is focused on the treatment of severe asp venom poisoning with a pronounced neurotoxic effect, complicated by soft tissue necrosis, and may be partially modified by bites from other snakes.

Compliance with ethical standards. The patient gave informed voluntary written consent to participate in the study and to publish her personal medical information in an anonymized form.

Аuthor’s сontribution. All co-authors contributed equally to the research and preparation of the article for publication.

Conflict of interest. The authors declare no apparent and potential conflicts of interest in relation to the publication of this article.

Funding. The study had no sponsorship.

Received: October 21, 2025 / Revised: January 15, 2025 / Accepted: March 27, 2026 / Published: April 30, 2026

Introduction. Nitrogen dioxide is one of the most common anthropogenic air pollutants that initiates oxidative stress and an inflammatory response. In recent years, there has been increased interest in the use of acetylcysteine as a means of preventing and treating conditions accompanied by oxidative stress.

Material and methods. The aim of the study was to evaluate the protective effect of oral administration of acetylcysteine ​​on the in rats exposed to long-term inhalation nitrogen dioxide. The protective effect of oral administration of acetylcysteine on the immunological profile and cellular composition of bronchoalveolar lavage fluid in rats during prolonged inhalation exposure to nitrogen dioxide was evaluated. Exposures to nitrogen dioxide (30–40 mg/m³) were carried out for 60 days (three times a day for 30 minutes with a half-hour interval between them). Every day, half an hour before exposure to nitrogen dioxide, the experimental group was administered a solution of acetylcysteine (50 mg/kg) through an esophageal tube, and the control group was administered a 0.9% sodium chloride solution. The cellular composition of bronchoalveolar lavage fluid, the content of pro-inflammatory mediators (TNF-α, IL-8), neutrophil elastase (NE), matrix metalloproteinase-12 (MMP-12), secretory immunoglobulin A (sIgA) and surfactant protein D (SP-D) were determined.

Results. Under the influence of 60-day exposure to nitrogen dioxide, the cytoimmunological profile of the bronchoalveolar space changed. The influx of neutrophils increased. The content of pro-inflammatory cytokines (TNF-α, IL-8) and proteases with destructive activity (NE, MMP-12) increased. The content of local immune defense markers (SP-D, sIgA) decreased due to a violation of the structural integrity of the bronchoalveolar epithelium. Daily oral administration of acetylcysteine for 60 days of nitrogen dioxide exposure contributed to the preservation of the basic structural and functional status of the lungs, which prevented the development of the inflammatory process and aberrant remodeling of lung tissue.

Limitations. the parameters of bronchoalveolar lavage fluid of animals were analyzed after exposure to nitrogen dioxide (30–40 mg/m³) for 60 days (three times a day for 30 minutes with a half-hour interval between them): the data obtained may differ under different experimental conditions.

Conclusion. The results show that acetylcysteine can serve as an effective prophylactic agent, preventing the negative consequences associated with lung exposure to the oxidative pollutant nitrogen dioxide.

Compliance with ethical standards. The experimental study was approved by the Independent Ethics Committee at the Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation (Protocol No. 273, December 20, 2022), conducted according to the European Convention for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (ETS No. 123), European Union Directive 2010/63 EU of 22.09.2010 on the protection of animals used for scientific purposes.

Authors contribution:
Preobrazhenskaya T.N. – conducting the experiment, data analysis, study design, article writing;
Lebedeva E.S. – conducting the experiment, data analysis, article writing.
All co-authors made significant contributions to the conception, conduct of the study and preparation of the article, and read and approved the final version before publication.

Conflict of interest. The authors declare that there are no conflicts of interest related to the publication of this article.

Funding. The study had no sponsorship.

Received: May 12, 2025 / Revised: March 04, 2026 / Accepted: March 27, 2026 / Published: April 30, 2026