Biochemistry (Moscow)最新文献

{"title":"Effects of the C.886C>T Mutation in the Mouse Tyrosine Hydroxylase Gene on Behavior and Dopamine System of the Brain","authors":"Ismail Alsalloum,&nbsp;Ilya A. Rakhov,&nbsp;Polina D. Komleva,&nbsp;Valentina N. Kuranova,&nbsp;Anastasia E. Bastrikova,&nbsp;Alexander V. Kulikov,&nbsp;Darya V. Bazovkina","doi":"10.1134/S0006297926600171","DOIUrl":"10.1134/S0006297926600171","url":null,"abstract":"<p>Dopamine (DA) is a critical regulator of physiological functions and adaptive behavior. The enzyme tyrosine hydroxylase (TH) catalyzes hydroxylation of L-tyrosine to 3,4-dihydroxyphenylalanine (DOPA), which is the first and rate-limiting step in the DA biosynthesis. Mutations in the human <i>TH</i> gene have been linked to dystonia, catalepsy, and catatonia. In the present study, we examined how the functional mutation c.886C&gt;T in the <i>Th</i> gene affects the brain DA system and behavior in mice. The C allele – which confers high TH enzyme activity – was introgressed from the <i>Mus musculus castaneus</i> subspecies into the C57BL/6 inbred background, yielding three congenic genotypes: B6-886CC, B6-886CT, and B6-886TT. Males of each genotype were evaluated in a battery of behavioral tests; and TH activity, levels of DA and DA metabolites, norepinephrine, and mRNA levels of the key DA system genes were measured across the brain structures. The three genotypes did not differ in body weight, locomotor activity, motor coordination, or cognitive performance. However, the B6-886TT mice showed significantly reduced exploratory activity in the open field test relative to the B6-886CC and B6-886CT animals. The B6-886TT mice also exhibited lower TH activity and DA content in the midbrain, and reduced DOPAC levels in the hypothalamus, compared to the B6-886CC animals. The c.886C&gt;T mutation had no detectable effect on expression of the genes encoding key DA metabolic enzymes or DA receptors. In a separate experiment, we genotyped 80 DNA samples from the <i>Mus musculus</i> collected across natural populations in Russia. The C and T allele frequencies were 0.981 and 0.019, respectively, suggesting that the T allele may be subject to negative natural selection.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 7","pages":"1200 - 1215"},"PeriodicalIF":2.1,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148628721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetic Retinopathy: From Molecular Mechanisms to Modern Therapy","authors":"Natalia G. Shebardina,&nbsp;Kristina A. Kazakova,&nbsp;Timur A. Asaevich,&nbsp;Sofia A. Belolipskaia,&nbsp;Ivan V. Rodionov,&nbsp;Sanchay S. Tulush,&nbsp;Mikhail L. Shishkin,&nbsp;Andrey R. Komarov,&nbsp;Olga A. Krasienko,&nbsp;Elizaveta S. Gromova,&nbsp;Andrey A. Zamyatnin Jr.,&nbsp;Anastasia M. Moisenovich,&nbsp;Evgeni Yu. Zernii","doi":"10.1134/S000629792660105X","DOIUrl":"10.1134/S000629792660105X","url":null,"abstract":"<p>Diabetic retinopathy (DR) remains one of the leading causes of vision loss. Its development is driven by complex interconnected pathophysiological mechanisms triggered by chronic hyperglycemia. Traditional diagnostic approaches, which rely on detecting visible microangiopathies, often identify the disease only after significant and progressive retinal damage had already occurred. Consequently, current therapeutic strategies are largely focused on managing advanced, proliferative stages of DR. A major direction in modern ophthalmology is the shift toward identifying and intervening at stages that precede clinical DR manifestations. This review presents current data on the pathogenesis and molecular mechanisms of DR, discusses associated biochemical alterations revealed through multi-omics approaches, and examines methods for preclinical diagnostics, innovative therapeutic strategies, and novel targets for early pathogenetic intervention. Overall, the evidence suggests that that effective treatment options for DR might include multi-target therapeutic approaches extending beyond the blockade of angiogenesis and aimed at addressing metabolic, inflammatory, and oxidative disorders causing neurodegeneration and vascular dysfunction.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 8","pages":"1319 - 1340"},"PeriodicalIF":2.1,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148837828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective Effect of Subconjunctival Melatonin Injections in 6-Hydroxydopamine-Induced Neurotoxic Eye Damage","authors":"Tatyana A. Pavlenko,&nbsp;Natalya B. Chesnokova,&nbsp;Olga A. Lisovskaya,&nbsp;Olga V. Beznos,&nbsp;Andrey V. Grigoryev","doi":"10.1134/S0006297925603880","DOIUrl":"10.1134/S0006297925603880","url":null,"abstract":"<p>The search for new effective methods of neuroprotection is relevant for the treatment of a wide range of common eye diseases such as age-related macular degeneration, glaucoma, and diabetic retinopathy. Using a rabbit model of neurotoxic eye damage induced by intravitreal injection of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA), we studied the effect of subconjunctival injections of 0.1% melatonin solution on pathophysiological and biochemical processes in the eye. Administration of 6-OHDA caused destruction of the retinal pigment epithelium, narrowing of retinal vessels, hemorrhages, decrease in ocular blood flow, and intraocular pressure, as well as reduced activity of α₂-macroglobulin and concentrations of matrix metalloproteinase-9 and angiotensin-converting enzyme in the aqueous humor, vitreous body, and retina. Subconjunctival melatonin injections over 9 days resulted in the 2-fold on average reduction of the area of retinal damage, and normalization of the minute volume of ocular blood flow and intraocular pressure. On day 14, an increase in the α₂-macroglobulin activity in the aqueous humor (0.66 ± 0.19 vs. 0.49 ± 0.13 nmol/min per 1 mg protein) and vitreous body (0.50 ± 0.15 vs. 0.21 ± 0.07 nmol/min per 1 mg protein, <i>p</i> &lt; 0.05) was observed, along with a decrease in the matrix metalloproteinase-9 concentration (118.4 ± 34.6 vs. 524.3 ± 163.2 ng/mg, <i>p</i> &lt; 0.05) and angiotensin-converting enzyme concentration (371.0 ± 52.1 vs. 596.1 ± 171.5 ng/mg, <i>p</i> &lt; 0.05) in the retina. This indicates reduction in the intensity of inflammation and vascular wall permeability. Melatonin could be considered a promising neuroprotective component in the complex therapy of retinal diseases.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 8","pages":"1396 - 1405"},"PeriodicalIF":2.1,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148837829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation, Glia–Neuron Crosstalk, and Energy Metabolism in Alcohol Use Disorder","authors":"Valentin Yu. Skryabin,&nbsp;Svetlana I. Sokolova,&nbsp;Anton V. Masyakin","doi":"10.1134/S0006297925604149","DOIUrl":"10.1134/S0006297925604149","url":null,"abstract":"<p>Chronic alcohol and other psychoactive substance use is accompanied not only by disturbances in classical neurotransmitter systems but also by persistent activation of innate and adaptive immunity, leading to neuroinflammation. This review summarizes experimental and clinical data on how microglia and astrocytes act as central mediators at the intersection of immune, metabolic, and neuronal processes in alcohol-related disorders. We discuss Toll-like receptor 4 (TLR4)-dependent pathways, activation of the NLRP3 inflammasome, impaired glutamate clearance, metabolic “reprogramming” of glia, and mitochondrial dysfunction. These changes lead to energy deficiency, oxidative stress, and persistent remodeling of reward, stress, and cognitive control networks. Particular attention is given to the impact of neuroinflammation on dopaminergic, glutamatergic, GABAergic, and serotonergic neurotransmission, including the shift of tryptophan metabolism toward the kynurenine pathway. We also consider the role of the gut–liver–brain axis, dysbiosis, endotoxemia, systemic inflammation, and impaired production of short-chain fatty acids in maintaining neuroimmune–metabolic stress. Contribution of hepatic and adipose tissue to the formation of a chronic inflammatory milieu and its effect on blood–brain barrier (BBB) permeability is discussed. Based on the combined data, the authors propose an integrative model of dependence as a state arising at the intersection of disrupted neural signaling, disordered energy metabolism, and altered inter-organ communication. Promising therapeutic targets are outlined, including normalization of glial function, modulation of the gut microbiota, reduction of systemic inflammation, and targeting energy metabolism. The need to develop biomarker panels to identify subgroups of patients with the pronounced neuroinflammatory burden is emphasized.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"847 - 866"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between Neuronal Metabolism and Signaling in Model Systems with Impaired α-Ketoglutarate Dehydrogenase Complex Activity","authors":"Márton Kokas,&nbsp;Attila Ambrus,&nbsp;László Tretter,&nbsp;Tímea Komlódi","doi":"10.1134/S0006297926600663","DOIUrl":"10.1134/S0006297926600663","url":null,"abstract":"<p>The α-ketoglutarate dehydrogenase complex (KGDHC) serves as a master regulator of cell’s molecular machinery. Beyond its classical role as a rate-limiting enzyme in the tricarboxylic acid (TCA) cycle, KGDHC has emerged as a critical redox sensor that can act as both a source and a target of reactive oxygen species (ROS), thereby regulating cellular redox homeostasis. This review summarizes evidence from genetically modified animal models and cell culture studies demonstrating that compromised KGDHC activity affects neuronal metabolism, redox homeostasis, and cellular signaling. KGDHC dysfunction causes mitochondrial failure, resulting in reduced ATP synthesis and activation of AMP-activated protein kinase (AMPK). Although inhibition of KGDHC reduces mitochondrial ROS formation, it also disrupts physiological ROS-dependent signaling mechanisms. In KGDHC-deficient mice, impaired ROS signaling and energy deficit decrease brain adaptability, increase susceptibility to neurotoxins, and disrupt crucial pathways by downregulating PGC-1α and Nrf2. These alterations result in suppression of antioxidant defences and lead to neuronal death in the hippocampus and memory impairment. Moreover, KGDHC dysfunction induces mitochondrial fragmentation and is strongly linked to excitotoxicity, further accelerating neuronal dysfunction. As observed in heterozygous models, even partial KGDHC deficiency can exacerbate persisting cellular and mitochondrial defects, leading to the development of more severe pathological conditions.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"893 - 909"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrogen Peroxide Dismutation by Immunoglobulins G from Patients with Schizophrenia","authors":"Daria V. Kazantseva,&nbsp;Liudmila P. Smirnova,&nbsp;Elena G. Kornetova,&nbsp;Svetlana A. Ivanova","doi":"10.1134/S0006297926600456","DOIUrl":"10.1134/S0006297926600456","url":null,"abstract":"<p>The mechanisms underlying the recently discovered catalase activity of immunoglobulin G (IgG) in patients with schizophrenia remain unclear. Using a series of rigorous criteria, it has been demonstrated that this activity is an intrinsic property of antibodies themselves. The present study shows that classical catalase inhibitors also suppress the catalase activity of IgG. Specifically, inhibitor analysis revealed a dose-dependent reduction in the IgG catalase activity following addition of sodium azide (IC₅₀ = 140 μM) and 3-aminotriazole (IC₅₀ = 16.06 μM), suggesting that the catalytic mechanism of IgG shares similarities with that of classical catalase and may be due to the ability of antibodies to bind metalloporphyrin complexes, including heme. IgG catalase activity in patients with schizophrenia during therapeutic remission was significantly reduced, being fourfold lower than in healthy controls (<i>p</i> = 0.0004) and twofold lower than in patients during disease exacerbation (<i>p</i> = 0.002). A moderate positive correlation was observed between the total Positive and Negative Syndrome Scale (PANSS) score and IgG catalase activity (R = 0.32, <i>p</i> = 0.01). Therefore, IgG catalase activity in patients with schizophrenia depends on the disease clinical state and may contribute to the regulation of reactive oxygen species (ROS) metabolism and the severity of oxidative stress in affected individuals.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"1023 - 1033"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1134/S0006297926600456.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Genetically Induced Metabolic Syndrome on the Outcomes of Photothrombotic Stroke in Leptin-Deficient and Leptin Receptor-Deficient Mice","authors":"Alexey D. Bocharnikov,&nbsp;Polina A. Abramicheva,&nbsp;Elmira I. Yakupova,&nbsp;Olga A. Averina,&nbsp;Olga O. Grigoryeva,&nbsp;Anastasia V. Priymak,&nbsp;Svetlana A. Garmash,&nbsp;Oleg A. Permyakov,&nbsp;Irina B. Pevzner,&nbsp;Anna A. Brezgunova,&nbsp;Nadezda V. Andrianova,&nbsp;Petr V. Sergiev,&nbsp;Egor Y. Plotnikov","doi":"10.1134/S0006297926600134","DOIUrl":"10.1134/S0006297926600134","url":null,"abstract":"<p>Diabetes and obesity are associated with poorer outcomes after ischemic stroke; however, it remains unclear whether this results from increased neuronal susceptibility to injury or from vascular dysfunction induced by metabolic syndrome. To minimize the contribution of vascular factors, we used a model of photoinduced thrombosis (PT) in cortical vessels, which generates lesions of reproducible size and is less dependent on collateral blood flow. PT was induced in wild-type (WT) mice, as well as in <i>ob</i>/<i>ob</i> (leptin-deficient) and <i>db</i>/<i>db</i> (leptin receptor-deficient) mice. Magnetic resonance imaging (MRI) revealed that PT produced comparable infarct volumes in all mouse groups. Several genes associated with inflammation and activation of microglia and macroglia in the peri-infarct area <i>(Cst7</i>, <i>Ccl3</i>, <i>Tlr2</i>, <i>Gfap</i>) exhibited similar expression patterns across all three mouse strains, while transcriptional response to cerebral ischemia of <i>Tnfa</i>, <i>Cxcl9</i>, <i>Il6</i>, <i>Cox2</i>, <i>Mmp3</i>, and <i>Bdnf</i> genes depended on the genotype. Overall, despite individual differences in the expression profiles of certain genes, disruption of leptin signaling (whether due to leptin deficiency or leptin receptor deficiency) caused no genotype-specific exacerbation of stroke-induced injury. Assessment of post-stroke neurological deficits revealed substantial differences in absolute scores between WT and <i>ob</i>/<i>ob</i> or <i>db</i>/<i>db</i> mice, attributable to baseline disparities in body weight and motor activity. In <i>db</i>/<i>db</i> mice, normalization of post-stroke neurological status scores to pre-injury values revealed a more pronounced relative functional decline compared to <i>ob</i>/<i>ob</i> mice, suggesting impairments in early compensatory mechanisms and an important role of leptin signaling in neuroplasticity rather than in the extent of acute neuronal damage. Thus, under conditions that minimize vascular complications, neither leptin deficiency nor leptin receptor deficiency exacerbated acute ischemic brain damage or neuroinflammation.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"939 - 955"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of AP-1 Proteins in Glucocorticoid Regulation of Tyrosine Hydroxylase Expression during Early Ontogeny","authors":"Tatyana S. Kalinina,&nbsp;Ekaterina V. Sukhareva,&nbsp;Veta V. Bulygina,&nbsp;Dmitriy A. Lanshakov,&nbsp;Nikolay N. Dygalo","doi":"10.1134/S0006297926600067","DOIUrl":"10.1134/S0006297926600067","url":null,"abstract":"<p>Elevated glucocorticoid levels during the sensitive period of early ontogenesis cause long-term changes in the functioning of neurotransmitter systems and the functions they regulate. One such system is the noradrenergic system, whose activity depends on the effects of stress or hormonal therapy during perinatal ontogenesis, altering stress response and psycho-emotional reactions in adult animals. Tyrosine hydroxylase (TH), a key enzyme in norepinephrine synthesis, is induced by glucocorticoids in the brain of fetal rats but remains unaffected by hormone administration on the 8th day of life. To evaluate the involvement of AP-1 transcriptional complex proteins in the age-dependent regulation of TH, we examined the relationship between the expression levels of the genes and proteins of the Jun and Fos families during and outside of hormonal induction of the enzyme gene. Hormonal induction of the TH gene and protein expression was found to occur during the periods of elevated Jun family gene expression (<i>JunB</i>, <i>c-Jun</i>, <i>JunD</i>) relative to Fos family genes (<i>c-Fos</i>, <i>FosB</i>) in the brainstem of 20-day-old fetuses and 3-day-old rat pups, and was absent when this ratio decreased on the day 8 of life. Chromatin immunoprecipitation followed by qPCR (ChIP-qPCR) demonstrated that, following dexamethasone administration on postnatal day 3, the number of the JunB protein-bound AP-1 sites on the <i>Th</i> gene promoter was significantly higher compared to the day 8. Consequently, the period of hormonal induction is accompanied by the relative predominance of the Jun/Jun homodimeric complexes on the <i>Th</i> gene promoter, which activate transcription of the regulated genes. This is in contrast to the day 8 of life, when the balance of Jun/Fos complexes shifts toward formation of heterodimers that do not alter transcription. The established dynamics of the ratio of AP-1 complex proteins may underlie the age-dependent manifestation of glucocorticoid induction of TH expression <i>in vivo</i> in the perinatal brain.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"910 - 922"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Enrichment May Mitigate Dexamethasone-Induced Changes in the Glycemic Curve","authors":"Ludmila P. Filaretova,&nbsp;Olga Yu. Morozova,&nbsp;Polina V. Punina,&nbsp;Olga P. Komkova,&nbsp;Tatiana T. Podvigina,&nbsp;Natalia I. Yarushkina","doi":"10.1134/S0006297926601000","DOIUrl":"10.1134/S0006297926601000","url":null,"abstract":"<p>Previously, we demonstrated that administration of dexamethasone (Dex) at a dose of 1 mg/kg, 24 h before an ulcerogenic stimulus exerts a pro-ulcerogenic effect, accompanied by disturbances in carbohydrate metabolism. In the present study, we examined the influence of housing conditions – standard conditions (SC), social isolation (SI), and environmental enrichment (EE) conditions – on the Dex-induced changes in carbohydrate metabolism, as well as on hematological parameters. Experiments were conducted with male rats during the winter period. Starting from the age of 30 days, the animals were housed for 6 weeks under SC, SI, or EE conditions. Dex (1 mg/kg, intraperitoneal) or its vehicle (control) was administered 24 h prior to the glucose tolerance test (GTT), after which food was removed. Following the GTT, indomethacin (IM) was administered at an ulcerogenic dose; 4 h later, the rats were decapitated, and blood samples were collected to assess corticosterone levels and hematological parameters, including calculation of the neutrophil-to-lymphocyte ratio (NLR). Alongside the IM administration experiment, a control experiment including vehicle administration was performed according to the same protocol, in which the vehicle of IM was administered instead of IM itself. Administration of glucose during the GTT led to the increase in the blood glucose levels, reaching maximum (peak) at 30 min in all control, previously fasted animals (SC, SI, EE groups). Beginning at 60 min, the glucose levels gradually declined in all control groups, returning to the baseline only in the control rats from the EE group. In the rats maintained under SC conditions, pretreatment with Dex resulted in the reduction in the peak of the glycemic curve, accompanied by the corresponding decrease in the area under the curve (AUC) and reduced rate of decline in the blood glucose levels compared with the respective control group. In the rats housed under EE condition, resistance to the effects of Dex was observed, as evidenced by the absence of changes in the glycemic curve peak, AUC, or rate of decline in the blood glucose levels relative to the corresponding control group. The control rats from the SI group exhibited lower values of the glycemic curve peak, AUC, and rate of decline in the blood glucose levels than the rats from the SC and EE groups. Administration of Dex did not produce any further changes in these parameters. Dex administration induced a marked increase in the NLR in all groups (SC, SI, and EE), both in the rats treated with IM and in the animals receiving its vehicle. Taken together, these findings indicate that a single administration of Dex (1 mg/kg; 24 h after injection) to the rats from the SC group could alter glycemic response and increase NLR. Housing under EE conditions prevents the Dex-induced changes in the glycemic curve.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"1034 - 1049"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose-Dependent Effects of Soy Lecithin Intake on Synaptic Ultrastructure in Brain Neurons and Behavioral Patterns of C57BL/6 Laboratory Mice","authors":"Lyubov A. Suldina,&nbsp;Ksenia N. Morozova,&nbsp;Konstantin S. Pavlov,&nbsp;Elena V. Kiseleva,&nbsp;Lidiya V. Boldyreva","doi":"10.1134/S0006297926600109","DOIUrl":"10.1134/S0006297926600109","url":null,"abstract":"<p>Phospholipid preparations, including lecithin, are widely used as hepatoprotective and neuroprotective agents, while soy lecithin is intensively used in food industry, with its total dose in the modern human diet potentially reaching high levels. Soy lecithin contains up to 70% of biologically active phospholipids: phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, and phosphatidic acid. These compounds perform a spectrum of key cellular functions, including neuromediation processes, and ensure formation of the cellular membrane structures and vesicles. Previously, in the mouse model of chronic intestinal inflammation, behavioral changes were observed together with the significant increase in the relative content of several phospholipid classes in the intestinal epithelial cells. The animals fed with soy lecithin, which contains a mixture of these phospholipids, showed similar behavioral changes in the absence of inflammation: impaired social recognition and behavior, reduced signs of compulsivity and anxiety, and increased aggression in males. In this study, we found that reducing the dose of soy lecithin in short-term administration restores normal social recognition and behavior in the healthy C57BL/6 animals, while reduction in anxiety is maintained. Comparative electron microscopy analysis of the neurons and synapses in the amygdala, hypothalamus, and frontal motor cortex of the C57BL/6 animals treated with soy lecithin was conducted. Dose-dependent and region-specific changes were observed. High-dose lecithin administration, both long-term and short-term, reduced synapse density in the neuropil, and irregular synaptic vesicles were detected in the amygdala and hypothalamus. Threefold reduction in the lecithin dosage resulted in the increase in the number of vesicles per synapse in the hypothalamus and motor cortex. The obtained results demonstrate dose-dependent effect of soy lecithin on the synaptic ultrastructure in the hypothalamus, amygdala, and motor cortex of the frontal lobe, as well as on the behavioral patterns of the healthy C57BL/6 laboratory mice.</p>","PeriodicalId":483,"journal":{"name":"Biochemistry (Moscow)","volume":"91 “Interaction","pages":"923 - 938"},"PeriodicalIF":2.1,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}