Search

In this study, the effect of ozonation process on the poly(ADP-ribose) polymerase 1 gene expression (PARP-1) and related the NADPH metabolism in strawberry fruit during storage was determined. Our results showed that ozonation with gas at both 10 and 100 ppm concentrations increased the expression of PARP-1 in the fruit during storage. Furthermore, the ozonation process initially increased the level of NAD

Abstract—Tris(2,3-dibromopropyl)isocyanurate (TBC or TDBP-TAZTO) is a new brominated flame retardant (BFR) used as a replacement of classic BFR, such as tetrabromobisphenol A. TBC is supposed to be safer than classic BFRs, but reports show that it may induce a similar toxic effect. Therefore, the aim of the present study was to determine the impact of TBC on the inflammation and activation of the apoptosis process in mouse cortical astrocytes in vitro. Our results have shown that TBC increases caspase-1 and caspase-3 activity in mouse astrocytes in vitro, which suggests inflammation-induced apoptosis. Further analyses have revealed that TBC indeed increases the level of inflammation markers, e.g. Cat, IL-1β and IL-1βR1 proteins, but decreases the level of proliferation marker protein Ki67. However, our study has demonstrated that TBC does not change the morphology of astrocytes and does not increase the number of apoptotic bodies - a well-established marker of late apoptosis. Moreover, the concentration of 50 µM TBC also increases caspase-3 activity with no formation of apoptotic bodies. However, since 10 and 50 µM TBC have never been detected in living organisms, we can assume that the compound is safe at the low concentrations that are detected.

The aim of the study was to determine totoxicity of bisphenol A (BPA) and its derivatives (bisphenol S (BPS), bisphenol F (BPF), and tetrabromobisphenol A (TBBPA)) due to its high accumulation in environment. The performed analysis revealed the toxicity of the BPA, BPF, and BPS against Kurthia gibsoni, Microbacterium sp., and Brevundimonas diminuta as the most sensitive, reaching microbial toxic concentrations in the range of 0.018–0.031 mg ∙ L−1. Moreover, the genotoxicity assay shows the ability of all tested compounds to increase in the β-galactosidase level at the concentration range 7.81–500 µM (in Escherichia coli, PQ37). In turn, the matbolic activation of tested bishpenols has caused the enhacement of the genotoxicity and cytotoxicity effect. Interestingely, the highest phytotoxicity effect was pointed for BPA and TBBPA at the concentrations of 10 mg ∙ L−1 and 50 mg ∙ L−1, which cause the inhibition of root growth by 58% and 45%, respectively (especially for S. alba and S. saccharatum). Furthermore, the cytotoxicity analyses show the ability of BPA, BPS, and TBBPA to significantly decrease the metabolic activity of human keratynoctes in vitro after 24 h of treatment at the micromolar concentrations. Simialry, the impact of the certain bisphenols on proliferation-, apoptosis-, and inflammation-related mRNA expression was shown in tested cell line. Summarizing, the presented results have proved that BPA and its derrivatives are able to show high negative effect on certain living orgnisms such as bacteria, plants, and human cells, which is strict related to pro-apoptotic and genotoxic mechanism of action.

Encapsulation procedures are used to decrease the contact of toxic nanoparticles with cells; however, this field is still not well explored. Therefore, the aim of this paper was to evaluate the effect of encapsulation of silver nanoparticles in L-α-phosphatidylcholine/cholesterol-based liposomes on a human keratinocyte cell line (HaCaT). The homogenous (PdI = 0.171) spherical (~161 nm diameter) complexes were prepared by thin film hydration with the extrusion method. The UV–Vis scan and Dynamic Light Scattering measurement did not show any “free” silver nanoparticles in solutions, which was confirmed by Transmission Electron Microscope analysis. Moreover, the liposomes were tested on HaCaT cells, showing that the encapsulation process reduced the toxicity by 30%-10% at the 100 nM and 1 pM concentrations, respectively, in comparison to “free” nanoparticles, measured by resazurin reduction and lactate dehydrogenase release assays. Moreover, the caspase-3 activity was lower after 48-h treatment with LipoAgNPs than with AgNPs. The level of reactive oxygen species (ROS) after 1, 6, 48, and 72 h of treatment of HaCaT cells was significantly lower in comparison to cells treated with “bare” silver nanoparticles analyzed with the H2DCF-DA probe. The metabolic activity was strictly correlated with toxicity, indicating a lower negative impact of encapsulated nanoparticles than the “bare” ones.

Tris (2,3-dibromopropyl) isocyanurate (TDBP-TAZTO or TBC) is a heterocyclic hexabromated flame retardant. It is widely used during the production of many synthetic compounds. High concentrations of TDBP-TAZTO were found in river water, surface sediments, soil, earthworms, and carp tissues. Moreover, it has been shown that this compound can cross the blood–brain barrier and accumulate in the gut and brain of carp. The aryl hydrocarbon receptor (AhR) has been characterized as a multifunctional intracellular sensor and receptor. AhR is an activator of cytochrome P450 1A1 and 1A2, which metabolize various toxic compounds. The aim of the study was to explain how/whether TDBP-TAZTO increases the expression and/or activity of the CYP1A1 enzyme and the AhR and TUBB3 expression during SH-SY5Y cell differentiation. SH-SY5Y cells were differentiated for 7 and 14 days using retinoic acid. Cell viability, ethoxyresorufin-O-deethylase (EROD) activity, and mRNA expression of CYP1A1, AhR, and TUBB3 were assessed. Our experiment showed that, during the differentiation process, the ability of TDBP-TAZTO to induce EROD activity in SH-SY5Y cells subsequently decreased, which may have been an effect of cell differentiation into neurons. Moreover, the results suggest that TDBP-TAZTO can affect the differentiation process. Since no CYP2B6 mRNA expression was detected, the CAR receptor may not be involved in the TDBP-TAZTO mechanism of action. However, more research is needed in this field to elucidate this mechanism precisely.

BACKGROUND The present study aimed to determine whether the ozonation process affects the flavonoid biosynthesis in highbush blueberry (Vaccinum corymbosum L.) fruit. Flavanone 3β-hydroxylase (F3H) was used as a marker of the flavonoid biosynthesis pathway. The activity of F3H, the expression of gene encoding F3H and the antioxidant status in blueberries treated with ozone at a concentration of 15 ppm for 30 min, every 12 h of storage, and maintained at 4 °C for 4 weeks were investigated. RESULTS The results showed that ozonation process increases the expression of the F3H gene after 1 week of storage, which translates into a higher catalytic capacity of protein, as well as a higher content of flavonoids and total antioxidant potential of ozonated blueberries compared to non-ozonated fruits. CONCLUSION The present study provides experimental evidence indicating that ozone treatment in proposed process conditions positively affects flavonoid metabolism in highbush blueberry fruit leading to the maintainance of the high quality of the fruit during storage. © 2021 Society of Chemical Industry.

The potential usefulness of silver nanoparticles (AgNPs) in anticancer therapy has been postulated for many years. However, little is known to date about the exact impact of such NPs on intracellular detoxication pathways. Therefore, the aim of this study was to determine the impact of AgNPs on the AhR-PPARγ-CYP1A1 pathway in neuroblastoma (SH-SY5Y) cells. The obtained results showed a decrease in the metabolic activity of the SH-SY5Y cells at the 50 and 100 μg/mL concentrations with an increase in caspase-3 activity. An increase in the intercellular ROS production was observed at the 1 and 10 μg/mL concentrations. The co-treatment of the AgNP-treated cells with the AhR and PPARγ inhibitors abolished the effect of the tested AgNPs in the SH-SY5Y cells. In turn, the CYP1A1 activity assay showed a decrease in this parameter in the AgNP-treated cells. Moreover, the gene expression analysis demonstrated that AgNPs were able to increase the AhR and CYP1A1 mRNA expression and decrease the PPARγ gene expression after the 6-h treatment. In turn, an increase in the AhR and PPARγ protein expression was observed after 24 h. Summarizing, the study shows for the first time that AgNPs with a 5-nm diameter size are able to exert a cytotoxic effect on SH-SH5Y cells in a ROS-dependent manner affect the AhR-PPARγ-CYP1A1 pathway inter alia by inhibiting the activity of CYP1A1. This is important due to given present research approaches using such NPs as enhancer agents in the modern PPARγ inhibitor-based anticancer therapy.

The purpose of this study was to investigate the biological properties of an extract obtained from the waste of blueberry fruit. The study covered the optimization of extraction of antioxidants from blueberry pomace and the determination of antioxidant properties of the extract using HaCaT as the model organism. Research showed that the yield of antioxidants extraction from blueberry waste was dependent on the applied extraction conditions. Based on the mathematical models, the optimal conditions of extraction process in which the maximum quantity of antioxidant compounds is achieved from the waste mass unit, i.e., the relation of the waste mass to the volume of ethanol equal to 1:17.36, and process time equal to 1000 s. The obtained extract was characterized by high antioxidant activity, which was shaped by high content of polyphenols, mainly anthocyanins. Moreover, the extract showed a high ability to protect HaCaT cells from the occurrence of oxidative stress induced by H2O2. Cells treated with the extract and H2O2 generated a lower amount of ROS than cells treated with H2O2 only. The obtained results will be base of further studies on applying the extract in production of diet supplements and functional foods with increased antioxidant activity. Moreover, the main research material is blueberry pomace which is a troublesome waste material for juice producers. Consequently, according to a sustainable development idea, the study results will provide an opportunity to increase interest in the problem of rational use of the waste material to a certain extent.

4-Thiazolidinones and related derivatives are regarded as privileged structures in medicinal chemistry and a source of new drug-like compounds. To date it is known that thiazolidinones are able to induce CYP1A1 activity in 3T3-L1 cells. Therefore, to extend the knowledge of the mechanism of thiazolidinones in the cell, four chemically synthesized heterocycles were tested on 3T3-L1 cells. The 3T3-L1 cells were exposed to Les-2194, Les-3640, Les-5935, and Les-6166. Our study showed that 1 μM βNF, Les-2194, and Les-6166 decreased the expression of Ahr mRNA. In turn, βNF, Les-2194, and Les-3640 increased the Cyp1a1 mRNA expression at the same time interval. On the other hand, Les-5935 was found to decrease the Cyp1a1 mRNA expression. Interestingly, the expression of Cyp1a2 mRNA was activated only by βNF and Les-2194. The expression of Cyp1b1 mRNA in the 3T3 cell line increased after the βNF and Les-2194 treatment but declined after the exposure to Les-5935 and Les-6166. Moreover, the Les-2194 and Les-5935 compounds were shown to increase the activity of EROD, MROD, and PROD. Les-3640 increased the activity of EROD and decreased the activity of PROD. In turn, the treatment with Les-6166 resulted in an increase in the activity of EROD and a decrease in the activity of MROD and PROD in the 3T3-L1 cells.

Interest in the use of metallic nanoparticles (NPs) in medicine is constantly increasing. The key challenge to the introduction of NPs into anticancer treatment is to limit the contact of their surface with healthy cells and to enable specific targeting of certain tissues, for example, cancerous cells. These aspects have raised a question whether the recent methods of drug delivery allow restricting the contact of NPs with healthy and/or nontarget cells. NPs can be restricted by encapsulation, which involves entrapping them into organic layers. This review is the first to present the different approaches for the encapsulation of metallic NPs, using liposomes, dendrimers, and proteins. The types and methods of entrapping are shown in an accessible way, enriched with graphics, and the pros and cons of these methods are disputable. Furthermore, the potential uses of NP complexes in medicine are described.

The major aim of this study was to investigate the effect of ozonation process on the level of oxidative stress markers in blueberry fruit during cold storage (4 °C). Blueberry (Vaccinum corymbosum L.) fruit was ozonated with an ozone concentration of 15 ppm for 30 min, every 12 h for 28 days of storage at 4 °C. The results indicated that ozone treatment activated a defense mechanism against oxidative stress in blueberry fruit. Ozonated fruit was characterized by higher activity of antioxidant enzymes i.e. superoxide dismutase, glutathione peroxidase, and phenylalanine ammonia-lyase than non-ozonated fruit, over the first 21 days of storage. In turn, the level of superoxide anion radical and hydrogen peroxide in ozonated fruit was significantly lower compared with the untreated material. However, after 21 days of storage, ozone treatment contributed to the oxidative modification of protein which could be a reason of decreasing enzymes activity, involved in cell protection against oxidative stress.

Epidemiological studies have shown the presence of triclosan (TCS) in the brain due to its widespread use as an antibacterial ingredient. One of the confirmed mechanisms of its action is the interaction with the aryl hydrocarbon receptor (AhR). In nerve cells, sirtuins (Sirt1 and Sirt3) act as cellular sensors detecting energy availability and modulate metabolic processes. Moreover, it has been found that Sirt1 inhibits the activation of estrogen receptors, regulates the androgen receptor, and may interact with the AhR receptor. It is also known that Sirt3 stimulates the production of estradiol (E

Elastin-derived peptides (EDPs) contain replications of the Val-Gly-Val-Ala-Pro-Gly (VGVAPG) hexapeptide. It has been described that the VGVAPG peptide induces reactive oxygen species (ROS) production in murine monocytes and astrocytes, human fibroblasts, and the human neuroblastoma (SH-SY5Y) cell line. To date, there is growing evidence that calcium channel blockers (CCBs) reduce oxidative stress and development of inflammation in the nervous system. Therefore, the aim of the present study was to evaluate the impact of such CCBs as Nifedipine, Verapamil, and MK-801 on the expression of peroxisome proliferator-activated receptor (Pparγ), i.e. ROS-related and inflammation-related proteins, in mouse astrocytes exposed in vitro to the VGVAPG peptide. The experiments showed that Nifedipine or MK-801 used in co-treatment with the VGVAPG peptide potentiated the effect of this peptide on the Pparγ level after the 24-h and 48-h treatment. Moreover, all studied compounds decreased the VGVAPG-induced caspase-1 activity in both time intervals. The data also showed that the VGVAPG peptide decreased the interleukin 1 beta (IL-1β) level in both studied time intervals. Upon a short-time exposure, the use of CCBs intensified the decrease in IL-1β stimulated by the VGVAPG peptide, opposite to the longer treatment. Moreover, the VGVAPG peptide decreased the IL-1βR1 level in both studied time intervals. After 24 h, Nifedipine and Verapamil potentiated the effect of the VGVAPG peptide. The VGVAPG peptide decreased the catalase (Cat) protein expression only after 24 h, whereas CCBs did not affect the expression of Cat induced by the VGVAPG peptide. The VGVAPG peptide increased the expression of the superoxide dismutase 1 (Sod1) protein. After 24 h of exposure, Nifedipine and Verapamil potentiated the increase in the Sod1 protein expression. Finally, our data showed that VGVAPG did not change the level of estradiol (E

Tissues are subjected to dynamic communication between cells and the extracellular matrix (ECM), resulting in ECM remodeling. One of the ECM components is elastin, which releases elastin-derived peptides (EDPs) during the aging process. Therefore, the aim of the present study was to evaluate the impact of the VGVAPG hexapeptide and elastin-like peptide VVGPGA (control) on certain metabolism parameters in human breast adenocarcinoma (MCF-7) and human lung carcinoma (A549) cell lines. The results did not show a significant effect of the peptides on metabolic activity and caspase-3 activity. However, more specific analysis revealed that VGVAPG and VVGPGA were able to increase KI67 protein expression in both tested cell lines after 24-h treatment. Moreover, the same correlation was observed at the KI67 gene level. VGVAPG also increased the P53, ATM and SHH gene expression in the A549 cells up to 19.08%, 20.74%, and 28.77%, respectively. Interestingly, the VGVAPG peptide exerted an effect on the expression of antioxidant enzymes SOD2 and CAT in the A549 and MCF-7 cells, especially after the 24-h treatment. Lastly, both peptides influenced the CAV1 and CLTC1 expression. Our results show that the tested EDPs have an effect on both A549 and MCF-7 cells at the cellular level. This may be correlated with the multidrug-resistance (MDR) phenotype in these cancer cells, which is an emerging problem in the current anticancer treatment. However, more research is needed in this field.

Celem prezentowanych badań było określenie wpływu procesu ozonowania na poziom związków polifenolowych oraz aktywność wybranych enzymów zaangażowanych w metabolizm polifenoli w owocach borówki wysokiej (Vaccinum corymbosum L.) podczas przechowywania. Materiał badawczy stanowiły owoce borówki wysokiej odmiany Bluecrop, które były ozonowane gazem o stężeniu 15 ppm, przez 30 min, co 12 godzin przechowywania w temperaturze 4°C przez 28 dni. Owoce były poddawane analizie zawartości związków polifenolowych, aktywności antyoksydacyjnej oraz aktywności enzymów uczestniczących w ich biosyntezie oraz rozkładzie. Wyniki pokazały, że proces ozonowania aktywuje szlak biosyntezy polifenoli w owocach borówki wysokiej. W owocach ozonowanych stwierdzono wyższą aktywność hydroksylazy 3ß-flawononu oraz syntazy flawonolu niż w owocach nieozonowanych, co korespondowało z wyższą zawartością większości analizowanych polifenoli i aktywnością antyoksydacyjną. Ponadto, po 2 tygodniu przechowywania stwierdzono niższą aktywność oksydazy polifenolowej w owocach ozonowanych. Powyższa odpowiedź metaboliczna owoców przyczyniła się do większej odporności owoców na stres abiotyczny, jak również do utrzymania wysokiej jakości owoców, w tym wartości biologicznej podczas przechowywania. Powyższe wyniki badań zostały zaprezentowane na Ogólnopolskiej Konferencji Naukowej pt. „Człowiek - Żywność -Środowisko” dnia 15 października 2021 r. w Rzeszowie.

Development of cancer drug-resistance is still an ongoing problem in the modern anticancer treatment. Therefore, there is a need to search for a new active substance, which may become a potential anticancer agent. 4-Thiazolidinones are well-described substances with cytotoxicity against cancer cells in vitro. Therefore, the aim of this study was to evaluate the effect of two 4-thiazolidinone-based derivatives (Les-2769 and Les-3266) on the PPARγ-dependent cytotoxicity in normal human skin fibroblasts (BJ) and squamous cell carcinoma (SCC-15) in vitro. The data obtained showed a cytotoxic effect of Les-2769 and Les-3266 used in micromolar concentrations on SCC-15 and BJ cells, manifesting by a decrease in the metabolic activity, an increase in the release of lactate dehydrogenase, and caspase-3 activity. The co-treatment of the cells with Les-3266 and an antagonist (GW9662) or an agonist (rosiglitazone) of the PPARγ receptor induced changes in the above-mentioned parameters in the BJ and SCC-15 cells, compared to the Les-3266 alone exposure; this was not found in the Les-2769-treated cells. The further analysis of the compounds indicated changes in the expression of the PPARγ, KI67, and NF-κB genes. Moreover, the tested compounds caused an increase in the level of PPARγ mRNA expression in a similar way to rosiglitazone in SCC-15, which may indicate the affinity of the compounds for PPARγ. Molecular docking is consistent with experimental in vitro data about the potential agonistic activity of Les-2769 and Les-3266 towards PPARγ receptors. Summarizing, the anticancer effect of both compounds was observed in the SCC-15 cells in vitro; moreover, the mechanism of action of Les-3266 in cells is mediated probably by interaction with the PPARγ receptor pathway, which needs in-depth study.

Drug-resistance of bacteria is an ongoing problem in hospital treatment. The main mechanism of bacterial virulency in human infections is based on their adhesion ability and biofilm formation. Many approaches have been invented to overcome this problem, i.e. treatment with antibacterial biomolecules, which have some limitations e.g. enzymatic degradation and short shelf stability. Silver nanoparticles (AgNPs) may be alternative to these strategies due to their unique and high antibacterial properties. Herein, we report on yeast Saccharomyces cerevisiae extracellular-based synthesis of AgNPs. Transmission electron microscopy (TEM) revealed the morphology and structure of the metallic nanoparticles, which showed a uniform distribution and good colloid stability, measured by hydrodynamic light scattering (DLS). The energy dispersive X-ray spectroscopy (EDS) of NPs confirms the presence of silver and showed that sulfur-rich compounds act as a capping agent being adsorbed on the surface of AgNPs. Antimicrobial tests showed that AgNPs inhibit the bacteria growth, while have no impact on fungi growth. Moreover, tested NPs was characterized by high inhibitory potential of bacteria biofilm formation but also eradication of established biofilms. The cytotoxic effect of the NPs on four mammalian normal and cancer cell lines was tested through the metabolic activity, cell viability and wound-healing assays. Last, but not least, ability to deep penetration of the silver colloid to the root canal was imaged by scanning electron microscopy (SEM) to show its potential as the material for root-end filling.

Elastin is one of the main structural matrix proteins of the arteries, lung, cartilage, elastic ligaments, brain vessels, and skin. These elastin fibers display incredible resilience and structural stability with long half-life. However, during some physiological and pathophysiological conditions, elastin is prone to proteolytic degradation and, due to the extremely low turnover rate, its degradation is practically an irreversible and irreparable phenomenon. As a result of elastin degradation, new peptides called elastin-derived peptides (EDPs) are formed. A growing body of evidence suggests that these peptides play an important role in the development of age-related vascular disease. They are also detected in the cerebrospinal fluid of healthy people, and their amount increases in patients after ischemic stroke. Recently, elastin-like polypeptides have been reported to induce overproduction of beta-amyloid in a model of Alzheimer's disease. Nevertheless, the role and mechanism of action of EDPs in the nervous system is largely unknown and limited to only a few studies. The article summarizes the current state of knowledge on the role of EDPs in the nervous system.

The surface of silver nanoparticles (AgNPs) is characterized by high reactivity resulting in prooxidative and cytotoxic properties. These effects are observed both in normal and in cancer cells, which overexpress the Epidermal Growth Factor Receptor (EGFR). In our previous paper, we have demonstrated that, with the use of liposomes labeled with the Epidermal Growth Factor (EGF), it is possible to direct the toxic effect of AgNPs in EGFR-overexpressing cells. Unfortunately, the mechanism of uptake and toxicity induction by such liposomes is still unknown. Therefore, the aim of this study was to determine the impact of EGF-LipoAgNPs on certain genes related to endocytosis and toxicity induction by such liposomes in human lung (A549) and tongue (SCC-15) cancer cells. The siRNA knock-out gene method was used in this study to determine the engagement of EGFR in this process. The confocal microscopy study revealed that the number of liposomes in the cytoplasm of the A549

The oral cancer is presumably caused by genetic factors and exposure to substances derived from cosmetics and disinfectants. Triclosan (TCS) is widely spread in many consumer products and oral care products. Since TCS can affect DNA methylation, which is one of the key mechanisms of gene expression that may lead to cancerogenesis, it is necessary to study this mechanism in oral cell carcinoma. The aim of the present study was to evaluate the impact of TCS on metabolic parameters, oxidative stress, gene expression, and DNA methylation and hydroxymethylation in the SCC-15 cell line. The experiments have shown TCS toxicity to SCC-15 cells only in the highest concentrations of 50 and 100 µM. TCS in a wide range of concentrations increases ROS production and caspase-3 activity. Our experiments have shown that TCS in the nontoxic concentrations of 10 µM exerts an impact on SOD2 mRNA expression and SOD activity in the SCC-15 cell line. Finally, our experiments have demonstrated that 6-h treatment with TCS decreases the mRNA expression of DNMT3A and DNMT3B. After 72-h exposure to TCS, an increased level of 5-methylcytosine and 5-hydroxymethylcytosine was observed in the SCC-15 cell line, but it was abolished by the NAC treatment. However, it is very likely that these results can be an effect of TET enzyme activity, especially in the case of the decrease in 5mC and the increase in 5hmC after the 48-h exposure to TCS, which was accompanied with a decrease in the mRNA expression of DNMT3A and DNMT3B.

Silver nanoparticles (AgNPs) are the most toxic nanostructures for both cancer and healthy cells. Thus, their usefulness in the anticancer therapy is limited. Interestingly, the epidermal growth factor receptor (EGFR) is overexpressed in many cancer cells, e.g. in lung and tongue cancers. Therefore, the aim of this study was to develop a way to direct the cytotoxic effect of AgNPs against cancer cells, saving healthy ones by entrapping these NPs inside liposomes labeled with the epidermal growth factor (EGF-LipoAgNPs) and directing these structures into EGFR-overexpressing cancer cells. The obtained results showed spherical structures with a 107.9 nm size and - 16.60 mV zeta-potential. The UV-Vis scan and TEM images did not show free AgNPs in the solution. The obtained complexes were able to decrease the metabolic activity in the A549 and SCC-15 cells more effectively than native AgNPs. Furthermore, the ROS production, lactate dehydrogenase release, and caspase-9 and -3 activity were significantly increased after the treatment with EGF-LipoAgNPs for 24 and 48 h. The expression of genes encoding catalase, superoxide dismutase, and p53 protein increased significantly, while the KI67 gene expression decreased, especially in the A549 and SCC-15 cells. Moreover, the KI67 protein expression was lower than in the cells treated with native AgNPs, while catalase activity was decreased significantly after the treatment with the obtained complexes. In turn, SOD activity increased more efficiently in the EGFR-overexpressing cancer cells. In all tested parameters, EGF-LipoAgNPs exerted a lower toxic effect on the BJ cells than native AgNPs. Summarizing, the created liposomal system reduces the toxicity of AgNPs against normal human fibroblasts and enhances the toxic and proapoptotic effect of these NPs, which may be caused by improvement of their uptake by EGFR-overexpressing cancer cells.

Triclosan (TCS) is a well-known compound that can be found in disinfectants, personal care products. There is one publication concerning the involvement of PPARγ in the mechanism of action of TCS. It is known that activation of PPARγ regulates the expression of the NF-κB mediated inflammation by acting on nitric oxide synthase (NOS) genes. However, there are no studies demonstrating a relationship between the effects of TCS on the PPARγ signaling pathway, changes in NF-κB expression, and NOS isoform synthesis. Therefore, the aim of this study was to evaluate the effect of TCS on the expression of PPARγ, NF-κB, nNOS, iNOS, and eNOS in mouse neocortical neurons. In addition, the effects of co-administration of synthetic alpha-naphthoflavone (αNF) or beta-naphthoflavone (βNF) flavonoids and triclosan were investigated. Our results show that TCS alters PPARγ, NF-κB, iNOS, and eNOS expression in mouse neurons in vitro. After 48 h of exposure, TCS increased PPARγ expression and decreased NF-κB expression. Moreover, under the influence of TCS, the expression of iNOS was increased and at the same time the expression of nNOS was decreased, which was probably caused by high levels of ROS. The experiments have shown that both αNF and βNF are able to modulate the effects of TCS in primary cultures of mouse cortical neurons.

Reactive oxygen species (ROS) are central elements of a number of physiological processes such as differentiation and intracellular signaling, as well as pathological processes, e.g., inflammation or apoptosis. ROS are involved in the growth and proliferation of stem cells, cell communication, cell aging, all types of inflammation, cancer development and proliferation, or type 2 diabetes. Elastin-derived peptides (EDPs) are detected in all these conditions and, according to the current state of knowledge, the role of the extracellular matrix (ECM) protein is crucial. It is believed that EDPs are a result of the aforementioned pathological conditions and are generated during degradation of ECM. However, as shown in the literature, the production of EDPs can be induced not only by inter alia chemical, enzymatic, and physical factors but also directly by ROS. No comprehensive study of the impact of ROS on EDPs and EDPs on ROS production has been conducted to date; therefore, the aim of this paper is to summarize the current state of knowledge of the relationship between ROS and ECM with special involvement of EDPs in the processes mentioned above. Depending on the type of cells, tissue, or organism, the relationships between ROS and ECM/EDPs may differ completely.

Nowadays, diabetes mellitus type 2 (T2DM) is a serious problem in western European societies and in the United States. Thiazolidinediones (TZDs) are a broad group of compounds used to decrease insulin resistance in TDM2. To date, it has been believed that TZDs act mainly through activation of peroxisome proliferator-activated receptor gamma (PPARγ). The PPARγ receptor is important in differentiation of preadipocytes into mature adipocytes. Therefore, given the potential of structurally related thiopyrano[2,3-d]thiazoles Les-2194 and Les-3377 and 4-thiazolidinone derivative Les-3640 to interact with the PPARγ receptor, the aim of the present study was to evaluate the impact of the 4-thiazolidinone-based derivatives mentioned above on the process of 3T3-L1 cell line differentiation into adipocytes. In the first part of our study, we prove that Les-2194, Les-3377, and Les-3640 are cytotoxic to 3T3-L1 cells. In the next stage, we determine that Les-2194, Les-3377, and Les-3640 stimulate lipid accumulation (using the ORO staining method) and induce specific gene expression (Dlk1, Fabp4, Vegfa, Pai-1, Resistin, Adiponectin, and Pparγ). Our data show that rosiglitazone, pioglitazone, Les-2194, and Les-3640 at a concentration of 2 μM do not affect 3T3-L1 cell viability and do not activate the apoptotic process. Only Les-3377 decreased the number and metabolism of the cells. Although all the studied compounds influenced the expression of Dlk1, Fabp4, Vegfa, Pai-1, Resistin, Adiponectin, and Pparγ genes, none of them caused gene expression similar to that induced by rosiglitazone or pioglitazone. The ORO staining showed that rosiglitazone and pioglitazone induced lipid accumulation in the 3T3-L1 cell line, which is a marker of mature adipocytes. Only rosiglitazone increased Pparγ protein expression after 14 days of differentiation.

Background Synthesis of nanoparticles (NPs) and their incorporation in materials are amongst the most studied topics in chemistry, physics and material science. Gold NPs have applications in medicine due to their antibacterial and anticancer activities, in biomedical imaging and diagnostic test. Despite chemical synthesis of NPs are well characterized and controlled, they rely on the utilization of harsh chemical conditions and organic solvent and generate toxic residues. Therefore, greener and more sustainable alternative methods for NPs synthesis have been developed recently. These methods use microorganisms, mainly yeast or yeast cell extract. NPs synthesis with culture supernatants are most of the time the preferred method since it facilitates the purification scheme for the recovery of the NPs. Extraction of NPs, formed within the cells or cell-wall, is laborious, time-consuming and are not cost effective. The bioactivities of NPs, namely antimicrobial and anticancer, are known to be related to NPs shape, size and size distribution. Results Herein, we reported on the green synthesis of gold nanoparticles (AuNPs) mediated by pyomelanin purified from the yeast Yarrowia lipolytica. A three levels four factorial Box–Behnken Design (BBD) was used to evaluate the influence of temperature, pH, gold salt and pyomelanin concentration on the nanoparticle size distribution. Based on the BBD, a quadratic model was established and was applied to predict the experimental parameters that yield to AuNPs with specific size. The synthesized nanoparticles with median size value of 104 nm were of nanocrystalline structure, mostly polygonal or spherical. They exhibited a high colloidal stability with zeta potential of − 28.96 mV and a moderate polydispersity index of 0.267. The absence of cytotoxicity of the AuNPs was investigated on two mammalian cell lines, namely mouse fibroblasts (NIH3T3) and human osteosarcoma cells (U2OS). Cell viability was only reduced at AuNPs concentration higher than 160 µg/mL. Moreover, they did not affect on the cell morphology. Conclusion Our results indicate that different process parameters affect significantly nanoparticles size however with the mathematical model it is possible to define the size of AuNPs. Moreover, this melanin-based gold nanoparticles showed neither cytotoxicity effect nor altered cell morphology.

PPARγ regulate the expression of genes involved in peripheral insulin sensitivity, adipogenesis, and glucose homeostasis. Moreover, PPARγ agonists, such as pioglitazone and rosiglitazone, are used in the treatment of various diseases, e.g. diabetes (type II), atherosclerosis, inflammatory skin disease, and some types of cancers. PPARγ agonists have also been found to reduce oxidative-stress (OS) and OS-induced apoptosis. Therefore, the aim of the present study was to evaluate the impact of 4-thiazolidinone-based derivatives Les-2194, Les-3377, and Les-3640 on the expression of antioxidant enzymes in human squamous cell carcinoma (SCC-15), lung carcinoma (A549), colon adenocarcinoma (CACO-2), and skin fibroblast (BJ) cell lines. After 24 h of exposure, Les-2194 caused an increase in ROS production in the SCC-15 and CACO-2 cell lines; however, no changes in caspase-3 activity and metabolic activity were observed. Nevertheless, the Ki67 level was significantly decreased. Les-3377 was able to increase ROS production in all tested cell lines, but no impact on metabolic activity and caspase-3 activity were noticed. In turn, Les-3640 was able to induce ROS overproduction in BJ, SCC-15, and CACO-2 and did not affect metabolic activity. However, an increase in caspase-3 activity was observed at the 10 µM concentration in all tested cell lines. All tested compounds were able to influence CAT and SOD1 expression and decreased (Les-2194 in the BJ cells) or increased (Les-3640 in the SCC-15 and CACO-2 cells) PPARγ expression.