Publications by authors named "Alexey A Tinkov"

Cadmium (Cd) exposure is well-known to be hazardous to renal function. Although animal experiments suggest that selenium (Se) supplementation has beneficial effects on Cd-induced organ damage, epidemiological evidence on the mitigation of Se on Cd-induced renal damage is still insufficient. We used data from the National Health and Nutrition Examination Survey (NHANES) cycles from 2011 to 2018, and performed survey-weighted linear regression, logistic regression, and restricted cubic spline analyses to evaluate the associations of urine Cd (UCd), blood Cd (BCd), daily Se intake (DSe), and blood Se (BSe) with estimated glomerular filtration rate (eGFR), urine albumin creatinine ratio (UACR), and CKD risk, including the effects of DSe and BSe on the associations of UCd and BCd with renal health.

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Objectives: Midlife is a critical period for the onset of obesity and cognitive decline, which are often linked to disorders of iron and omega-3 long-chain polyunsaturated fatty acids (LCPUFAs). The aim was to investigate the effects of treadmill exercise on brain iron and LCPUFA metabolism.

Methods: Middle-aged male rats were fed either a control diet or a 50% high-fat diet (HFD), with or without iron enrichment (2 g ferric iron/kg diet), for 8 weeks to induce dysmetabolic iron overload syndrome (DIOS).

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Exposure to cadmium (Cd) and elevated weight-adjusted-waist index (WWI) are known risk factors for metabolic dysfunction-associated steatotic liver disease (MASLD). However, their roles in hepatic fibrosis (HF), the critical stage advancing to irreversible liver damage, remain unclear. The interactive effects of selenium (Se), an antioxidant, with Cd and WWI on oxidative stress regulation remain to be fully elucidated.

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This study sought to investigate the utility of the lobster cockroach (Nauphoeta cinerea) to understand the effect of aluminum (Al) exposure on neural tissues. We randomly divided lobster cockroach nymphs into three groups: control, 125 mg/g AlCl₁, and 250 mg/g AlCl₁. The cockroaches were maintained on an Al-containing dietary regimen for 3, 7 and 14 days and subsequently assessed for neurolocomotor indices.

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The objective of this review is to examine the direct evidence implicating epigenetic mechanisms in manganese (Mn)-induced neurotoxicity, with particular emphasis on the modulation of non-coding RNA (ncRNA) expression and histone modifications. Existing data demonstrate that Mn exposure modulates expression of various types of ncRNAs, especially micro RNAs (miRNAs or miRs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). Through regulation of target gene expression, these differentially expressed ncRNAs likely mediate Mn-induced neuronal oxidative stress, ferroptosis, apoptosis, autophagy, inflammation, as well as α-synuclein expression.

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The objective of the present study was to evaluate serum trace element and mineral levels in female patients with knee osteoarthritis (kOA) and concomitant knee and hip osteoarthritis (khOA). The study enrolled 61 healthy women without OA or any other pathology of joints (OA-free group), 180 subjects with bilateral kOA, and 99 patients with khOA. Age, anthropometric parameters, and the prevalence of concomitant diseases were registered.

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons. Drugs modulating the endocannabinoid system (ECS) emerge as promising tools for reducing symptomatology and/or progression of this disease. Here, the protective potential of ECS regulation against 6-hydroxydopamine (6-OHDA)-induced neuronal damage was evaluated in the nematode, Caenorhabditis elegans.

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The objective of this state-of-the-art review is to summarize contemporary data on the potential toxic effects of aluminum nanoparticles (AlNPs) and discuss the underlying molecular mechanisms. studies using laboratory rodents demonstrate that lungs, liver, brain, and the immune system are the primary targets for AlNPs toxicity. Specifically, inhalation exposure to AlNPs induces lung damage by promoting inflammatory infiltration, airway remodeling, septal thickening, and bronchial hyperresponsiveness.

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The objective of the present study was to review the potential protective effects of Se against T-2 toxin-induced adverse effects in cartilage and other tissues as well as to discuss the potential molecular mechanisms by which Se counteracts T-2 toxicity. Laboratory studies demonstrate that Se attenuates T-2 toxin-induced chondrocyte death by inhibition of the mitochondrial pathway of apoptosis. Protective effects of Se against T-2 toxin-induced oxidative stress in chondrocytes are mediated by improvement of antioxidant selenoprotein expression, which is altered upon mycotoxin exposure.

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The objective of the present study was to assess the patterns of trace element and mineral accumulation in 21 medicinal plants collected in the Altai Mountains foothills. The levels of trace elements and minerals in Hippophae rhamnoides, Aronia melanocarpa, Sorbus aucuparia, Viburnum opulus, Rosa canina, Crataegus sanguinea (fruits), Chamaenerion angustifolium, Echinacea purpurea, Fagopyrum esculentum, Trifolium pratense, Origanum vulgare, Achillea millefolium, Mentha piperita (herbs), Plantago major, Salvia officinalis, Urtica dioica (leaves), Panax ginseng, Rhaponticum carthamoides, Eleuterococcus senticosus, and Taraxacum officinale (roots), and Matricaria recutita flowers were assessed using inductively-coupled plasma mass-spectrometry. Comparative analysis revealed that R.

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The existing data demonstrate that aluminum (Al) and manganese (Mn) possess neurotoxic effects upon overexposure due to induction of neuronal oxidative stress and apoptosis, synaptic dysfunction and neurotransmitter metabolism, neuroinflammation, and cytoskeletal pathology. However, systematic evidence regarding contribution of these metals to development of neurological diseases are lacking. Therefore, in this review we provide a summary of the existing data on contribution of Al and Mn exposure to brain diseases and its symptoms.

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Manganese (Mn) is an essential trace element crucial for various physiological processes, but excessive exposure can lead to significant health concerns, particularly neurotoxicity. This review synthesizes current knowledge on Mn-induced oxidative stress and its role in cellular dysfunction and disease. We discuss how Mn promotes toxicity through multiple mechanisms, primarily through reactive oxygen species (ROS) generation, which leads to oxidative stress and disruption of cellular processes.

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Exposure to metal nanoparticles (NPs) is known to induce inflammatory responses in various tissues, thus limiting their therapeutic potential. NOD-like receptor protein 3 (NLRP3) inflammasome activation is an essential component of innate immunity playing a significant role in inflammation and development of inflammatory diseases. Therefore, the objective of the present review was to summarize data on the role of NLRP3 inflammasome in proinflammatory effects induced by metal NPs, and to discuss the underlying molecular mechanisms, including its dependence on the physical and chemical properties of metal NPs.

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The objective of the present study was to evaluate serum and fecal trace element and mineral levels in Red Steppe dairy cows with different daily milk yields during the transition from feedlot to pasture. Serum and fecal trace element and mineral levels were assessed using the inductively coupled plasma mass spectrometry. The obtained data demonstrate that serum Ca, Mg, K, and Na levels increased significantly in the pasture period, and this increase is more profound in cows with higher milk yield.

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The objective of the present study was to assess serum and cancerous tissue biometal levels in colorectal cancer (CRC) patients, and its relation to disease severity. A total of 90 CRC patients and 97 controls were involved in the present study. The level of biometals in blood serum and colon tissues (only in CRC cases) was evaluated by inductively-coupled plasma mass-spectrometry.

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Copper (Cu) is essential for brain development and function, yet its overload induces neuronal damage and contributes to neurodegeneration and other neurological disorders. Multiple studies demonstrated that Cu neurotoxicity is associated with mitochondrial dysfunction, routinely assessed by reduction of mitochondrial membrane potential. Nonetheless, the role of alterations of mitochondrial dynamics in brain mitochondrial dysfunction induced by Cu exposure is still debatable.

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Article Synopsis
  • Acrylonitrile (AN) is an organic compound that can cause neurotoxicity, but the mechanism behind this is not fully understood; HIF-1α plays a crucial role in cellular response to low oxygen levels and may help with survival.
  • In lab studies, AN reduced the levels of HIF-1α and other proteins associated with cell survival and function, leading to mitochondrial damage and increased cell death.
  • Treatment that activates HIF-1α (like cobalt chloride) showed protective effects against neurotoxicity, suggesting that enhancing this pathway could be a potential strategy for mitigating the harmful effects of AN exposure.
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  • Kashin-Beck disease (KBD) is a condition marked by abnormal cartilage cell death, linked to exposure to T-2 toxin, and is influenced by connective tissue growth factor (CTGF).
  • Researchers studied CTGF levels and apoptosis in cartilage samples from KBD patients and found that T-2 toxin exposure increases both CTGF and apoptosis markers in chondrocytes.
  • Curcumin was identified as a potential treatment that can inhibit CTGF and reduce chondrocyte apoptosis, suggesting it could help prevent cartilage damage in KBD.
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Manganese (Mn) is an essential trace element involved in various physiological processes, but excessive exposure may lead to toxicity. The vascular endothelium, a monolayer of endothelial cells within blood vessels, is a primary target of Mn toxicity. This review provides a comprehensive overview of the impact of Mn on vascular endothelium, focusing on both peripheral and brain endothelial cells.

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  • The study investigates how a probiotic supplement affects the gut microbiota and mineral metabolism in dairy cows, building on existing contradictory data about the gut microbiome's role in mineral regulation.
  • Fifteen cows were given a specific probiotic daily for a month, and their gut microbiota and serum mineral levels were analyzed using advanced sequencing and mass spectrometry techniques.
  • Results showed that the probiotic improved gut microbiota diversity, increased levels of essential minerals like calcium and zinc, and altered other serum parameters, suggesting probiotics may enhance mineral nutrition in cattle, although their impact on milk production remains to be studied.
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Zinc oxide nanoparticles (ZnONPs) are widely used in industry and biomedicine. A growing body of evidence demonstrates that ZnONPs exposure may possess toxic effects to a variety of tissues, including brain. Therefore, the objective of the present review was to summarize existing evidence on neurotoxic effects of ZnONPs and discuss the underlying molecular mechanisms.

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Article Synopsis
  • Aluminum (Al) exposure is linked to neurotoxic effects that may contribute to the development of Alzheimer's disease (AD) through epigenetic modifications.
  • Studies show that Al disrupts DNA methylation, alters histone modifications, and affects non-coding RNA expression in the brain, impacting key genes involved in neuroprotection and inflammation.
  • Changes in DNA and histone modifications due to Al exposure are correlated with cognitive decline in affected individuals, but more research is needed to fully understand these epigenetic mechanisms.
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The objective of the present review was to provide a timely update on the molecular mechanisms underlying the beneficial role of Se in Alzheimer's disease pathogenesis, and discuss the potential role of gut microbiota modulation in this neuroprotective effect. The existing data demonstrate that selenoproteins P, M, S, R, as well as glutathione peroxidases and thioredoxin reductases are involved in regulation of Aβ formation and aggregation, tau phosphorylation and neurofibrillary tangles formation, as well as mitigate the neurotoxic effects of Aβ and phospho-tau. Correspondingly, supplementation with various forms of Se in cellular and animal models of AD was shown to reduce Aβ formation, tau phosphorylation, reverse the decline in brain antioxidant levels, inhibit neuronal oxidative stress and proinflammatory cytokine production, improve synaptic plasticity and neurogenesis, altogether resulting in improved cognitive functions.

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Unlabelled: The objective of the present study was to retrospectively evaluate hair mercury (Hg) content in reproductive-age women living in Central Russia (Moscow and Moscow region), and to calculate the potential costs of the potential Hg-induced IQ loss in a hypothetical national birth cohort.

Materials And Methods: A total of 36,263 occupationally non-exposed women aged between 20 and 40 years living in Moscow (n = 30,626) or Moscow region (n = 5637) in the period between 2005 and 2021 participated in this study. Hair Hg content was evaluated with inductively coupled plasma-mass spectrometry (ICP-MS).

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