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Introduction: Iron and molybdenum are essential trace elements for cell metabolism. They are involved in maintaining proper functions of enzymes, cell proliferation, and metabolism of DNA.

Introduction: Nickel and iron are very commonly occurring metals. Nickel is used in industry, but nowadays it is also used in medical biomaterials. Iron is an element necessary for cell metabolism and is used in diet supplements and biomaterials, whence it may be released along with nickel.

Inosine pranobex (Isoprinosine) stimulates cell-mediated immune responses to viral infections in humans and might have also therapeutic use in animals. The aim of this study was to compare three in vitro cytotoxicity assays on mouse embryo fibroblasts and liver cancer cells and determine their ability to detect early cytotoxic effects for inosine pranobex.

Inosine pranobex (Methisoprinol, ISO, Isoprinosine) is an immuno-modulatory antiviral drug that has been licensed since 1971 in several countries worldwide. In humans, the drug is approved for the treatment of viral infections, and it might also have therapeutic use in animals. The aims of the presented work were to investigate the genotoxicity of inosine pranobex on BALB/3T3 clone A1 and HepG2 cell lines and to elucidate its mutagenicity using the Ames test.

Background: The mechanism of acute brain injury initiates a cascade of consequences which can directly cause lung damage, and this can contribute to poor neurological outcomes. The aim of this study was to evaluate concentration of different apoptotic molecules in the bronchoalveolar lavage fluid (BALF) in patients after severe brain injury and to correlate them with selected clinical variables and mortality., Methods: Patients with brain injury receiving BALF operation were included in the study. BALF samples were collected within the first 6-8 hours after traumatic brain injury (A) and at days 3 (B) and 7 (C) after admission to the intensive care unit (ICU). Changes in the BALF nuclear-encoded protein (Bax), apoptotic regulatory protein (Bcl-2), pro-apoptotic protein (p53) and its upregulated modulator (PUMA), apoptotic protease factor 1 (APAF-1), Bcl-2 associated agonist of cell death (BAD) and caspase-activated DNase (CAD) were analysed. These values were correlated with the selected oxygenation parameters, Rotterdam computed tomography (CT) score, the Glasgow Coma Score and 28-day mortality., Results: We found a significant increase in the concentration of selected apoptotic factors at admission (A), at day 3 (B) and day 7 (C) after severe brain damage contrasted with baseline level A ( p < 0.001, separately). That concentration of selected apoptotic factors was significantly correlated with the severity of the injury and mortality., Conclusions: Activation of different apoptotic pathways seems to be an important process occurring in the lungs of patients in the early phases after severe brain trauma. Levels of apoptotic factors in the BALF correlates with the severity of brain injury., Competing Interests: The authors declare no conflict of interest. Chiara Robba is serving as one of the Guest editors of this journal. We declare that Chiara Robba had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to Gernot Riedel., (© 2023 The Author(s). Published by IMR Press.)

The application of nano-Ag grains as antiviral and antibacterial materials is widely known since ancient times. The problem is the toxicity of the bulk or big-size grain materials. It is known that nano-sized silver grains affect human and animal cells in some medical treatments. The aim of this study is to investigate the influence of nano-Ag grains embedded in a carbonaceous matrix on cytotoxicity, genotoxicity in fibroblasts, and mutagenicity. The nanocomposite film is composed of silver nanograins embedded in a carbonaceous matrix and it was obtained via the PVD method by deposition from two separated sources of fullerenes and silver acetate powders. This method allows for the preparation of material in the form of a film or powder, in which Ag nanograins are stabilized by a carbon network. The structure and morphology of this material were studied using SEM/EDX, XRD, and Raman spectroscopy. The toxicology studies were performed for various types of the material differing in the size of Ag nanograins. Furthermore, it was found that these properties, such as cell viability, genotoxicity, and mutagenicity, depend on Ag grain size.

Objective: The interaction between the brain and lungs has been the subject of many clinical reports, while the exact impact of brain injury on the physiology of the respiratory system is still subject to numerous experimental studies. The purpose of this study was to investigate the activation of selected caspases levels in bronchoalveolar lavage fluid (mini BALF) of patients after isolated brain injury and their correlation with the severity of the injury., Methods: The analysis was performed on patients who were admitted to the intensive care unit (ICU) for severe isolated brain injury from March 2018 to April 2020. All patients were intubated and mechanically ventilated. Mini BALF was collected within the first 6-8 h after trauma and on days 3 and 7 after admission. The concentrations of selected caspases were determined and correlated with the severity of brain injury evaluated by the Rotterdam CT Score, Glasgow Coma Score, and 28-day mortality., Results: Our results showed significantly elevated levels of selected caspases on days 3 and 7 after brain injury, and revealed apoptosis activation during the first 7 days after brain trauma. We found a significant different correlation between the elevation of selected caspases 3, 6, 8, and 9, and the Glasgow Coma Score, Rotterdam CT scale, and 28-day mortality., Conclusions: The increased levels of selected caspases in the mini BALF in our patients indicate an intensified activation of apoptosis in the lungs, which is related to brain injury itself via various apoptotic pathways and correlates with the severity of brain injury., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Siwicka-Gieroba, Terpilowska, Robba, Barud, Kubik-Komar and Dabrowski.)

A traumatic brain injury (TBI) initiates an inflammatory response with molecular cascades triggered by the presence of necrotic debris, including damaged myelin, hemorrhages and injured neuronal cells. Molecular cascades prominent in TBI-induced inflammation include the release of an excess of proinflammatory cytokines and angiogenic factors, the degradation of tight junctions (TJs), cytoskeletal rearrangements and leukocyte and protein extravasation promoted by increased expression of adhesion molecules. The brain-gut axis consists of a complex network involving neuroendocrine and immunological signaling pathways and bi-directional neural mechanisms. Importantly, modifying the gut microbiome alters this axis, and in turn may influence brain injury and neuroinflammatory processes. In recent years it has been demonstrated that the activity and composition of the gastrointestinal (GI) microbiome population influences the brain through all of above-mentioned pathways affecting homeostasis of the central nervous system (CNS). The GI microbiome is involved in the modulation of cellular and molecular processes which are fundamental to the progression of TBI-induced pathologies, including neuroinflammation, abnormal blood brain barrier (BBB) permeability, immune system responses, microglial activation, and mitochondrial dysfunction. It has been postulated that interaction between the brain and gut microbiome occurs mainly via the enteric nervous system and the vagus nerve through neuroactive compounds including serotonin or dopamine and activation by bacterial metabolites including endotoxin, neurotransmitters, neurotrophic factors, and cytokines. In recent years the multifactorial impact of selected immunomodulatory drugs on immune processes occurring in the CNS and involving the brain-gut axis has been under intensive investigation., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The aim of this study was to examine the effect of chromium(III), iron(III), molybdenum(III) and nickel(II) and their combinations on pro- and antioxidant activity in mouse embryo fibroblasts and liver cancer cells. The present study shows that chromium(III), iron(III), nickel(II) and molybdenum(III) induce oxidative stress. In the case of chromium(III), nickel(II) and molybdenum(III) the intracellular ROS were dominant. However, in the case of iron(III) MDA was dominant - the end product of lipid peroxidation. Antioxidant activity of superoxide dismutase and catalase increased in low concentration of chromium(III); however, they decreased in higher concentrations. The same enzymes decreased after iron(III), nickel(II) and molybdenum(III) treatment in dose dependent manner. The activity of glutathione peroxidise decreased in dose dependent manner in all used microelements. Additions of Cr(III) at 200 μM plus Fe(III) at 1000 μM showed synergistic effect in ROS production and in lowering antioxidant activity. The same type of interaction in pairs Cr(III) at 1000 μM plus Fe(III) or Ni(II) or Mo(III) at concentration of 200 μM was observed. The protective effects of Cr(III) in antioxidant activity and in lowering intracellular ROS production in pairs of Cr(III) at 200 μM and Ni(II) or Mo(III) at concentration of 1000 μM were observed., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The aim of this study was to examine the effect of chromium(iii), iron(iii), molybdenum(iii) and nickel(ii) and their combinations on the cell cycle and mitochondrial transmembrane potential (MTP) in BALB/3T3 and HepG2 cells. A statistically significant dose related decrease of the percentage of cells in the G0/G1 and S phases was observed. However, a statistically significant dose related increase of the percentage of cells in the G2/M phase after exposure to chromium(iii), nickel(ii) or molybdenum(iii) at 200-1000 μM concentrations in both cell lines was observed. Moreover, an increase of the percentage of cells in the subG1 phase was observed. In both cell lines a statistically significant dose related decrease of the percentage of cells in the G2/M phase after exposure to iron(iii) at 200-1000 μM concentrations was observed. However, a statistically significant dose related increase of the percentage of cells in the G0/G1 phase after exposure to iron(iii) at 200-1000 μM concentrations was observed. A concentration dependent statistically significant decrease in the level of the MTP was observed in both cell lines after exposure to chromium(iii), iron(iii), nickel(ii) and molybdenum(iii). The results obtained from both cell lines show that HepG2 cells are more sensitive when compared to BALB/3T3 cells. Additions of Cr(iii) at 200 μM plus Fe(iii) at 1000 μM showed a synergistic effect on the cell cycle and MTP. In the case of Cr(iii) at 200 μM plus Mo(iii) at 1000 μM, an antagonistic effect was observed in both analyses. In the case of Cr(iii) at 1000 μM plus Mo(iii), Ni(ii) and Fe(iii) at 200 μM, no changes in the percentage of cells in all phases were observed in both cell lines in both analyses.

The aim of this study was to examine the effect of chromium(III) and iron(III) and molybdenum(III) and nickel(II) and their combinations on cyto-, genotoxicity and mutagenicity in BALB/3T3 and HepG2 cells. The results obtained from cytotoxicity assays indicate that there are differences between BALB/3T3 and HepG2 cell lines in their sensitivity to chromium chloride, iron chloride, molybdenum trioxide and nickel chloride. The statistically significant increase of DNA damage of all used microelements in both cell lines was observed. The micronucleus assay performed with the use of all concentrations shows statistically significant induction of chromosomal aberrations in all tested microelements in both cell lines. Moreover, treated cells display characteristic apoptosis in comparison to control cells. In all tested microelements, the increase of number of reverse mutations was observed with and without metabolic activation. Additions of Cr(III) at 200 μM plus Fe(III) at 1000 μM showed synergistic effect in decrease of cell viability and increase of comets, micronuclei and number of revertants in both cell lines. In case of Cr(III) at 200 μM plus Mo(III) at 1000 μM, a protective effect of chromium against molybdenum at 1000 μM toxicity in both cell lines (assessed by MTT, LDH and NRU, comet, micronucleus and Ames assays) was observed. The protective effect of Cr(III) in decrease of cell viability was observed in pair of Cr(III) at 200 μM and Ni(II) at 1000 μM in BALB/3T3 and HepG2 cell lines assessed by MTT, LDH and NRU, comet, micronucleus and Ames assays., (Copyright © 2018 Elsevier Ltd. All rights reserved.)