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As a noninvasive treatment, sonodynamic therapy (SDT) has been widely used in the treatment of tumors because of its ability to penetrate deep tissue with few side effects. As the key factor of SDT, it is meaningful to design and synthesize efficient sonosensitizers. Compared with organic sonosensitizers, inorganic sonosensitizers can be easily excited by ultrasound. In addition, inorganic sonosensitizers with stable properties, good dispersion, and long blood circulation time, have great development potential in SDT. This review summarizes possible mechanisms of SDT (sonoexcitation and ultrasonic cavitation) in detail. Based on these mechanisms, the design and synthesis of inorganic nanosonosensitizers can be divided into three categories: traditional inorganic semiconductor sonosensitizers, enhanced inorganic semiconductor sonosensitizers, and cavitation-enhanced sonosensitizers. Subsequently, the current efficient construction methods of sonosensitizers are summarized including accelerated semiconductor charge separation and enhanced production of reactive oxygen species through ultrasonic cavitation. Furthermore, the advantages and disadvantages of different inorganic sonosensitizers and detailed strategies are systematically discussed on how to enhance SDT. Hopefully, this review could provide new insights into the design and synthesis of efficient inorganic nano-sonosensitizers for SDT., (© 2023 Wiley-VCH GmbH.)

The present study describes the development and evaluation of a novel biocompatible dendrimer-based nano drug delivery system which is readily soluble in water prepared by condensing Phloroglucinol and Succinic Acid (PGSA) and could efficiently encapsulate a well known hydrophobic photodynamic therapy (PDT) agent, protoporphyrin Ⅸ (PpⅨ). The (dark and photo) cytotoxicity of the PGSA-PpⅨ (dendrimer-drug) formulation towards Dalton Lymphoma Ascites (DLA) cancer cell lines upon visible light treatment is reported and evaluated the cytotoxic Reactive Oxygen Species (ROS) generation efficiency of the Protoporphyrin Ⅸ in free and dendrimer encapsulated forms. The in vitro toxicity demonstrated by PpⅨ loaded PGSA dendrimer nanoformulation, on DLA cells reveals that this novel PGSA nanocarrier reduces the toxic nature of PpⅨ when compared to free PpⅨ without light treatment which satisfy the aim of our study. On the other hand, treatment of DLA cells with PGSA dendrimer formulation in combination with light resulted in significant enhancement in therapeutic efficacy of the PDT agent, PpⅨ.

Skin cancer is currently diagnosed as one in every three cancers. Melanoma, the most aggressive form of skin cancer, is responsible for 79% of skin cancer deaths and the incidence is rising faster than in any other solid tumor type. Previously, we have demonstrated that dimethylacrylshikonin (DMAS), isolated from the roots of Onosma paniculata (Boraginaceae), exhibited the lowest IC50 values against different tumor types out of several isolated shikonin derivatives. DMAS was especially cytotoxic towards melanoma cells and led to apoptosis and cell cycle arrest. In this study, we performed a comprehensive gene expression study to investigate the mechanism of action in more detail. Gene expression signature was compared to vehicle-treated WM164 control cells after 24 h of DMAS treatment; where 1192 distinct mRNAs could be identified as expressed in all replicates and 89 were at least 2-fold differentially expressed. DMAS favored catabolic processes and led in particular to p62 increase which is involved in cell growth, survival, and autophagy. More in-depth experiments revealed that DMAS led to autophagy, ROS generation, and loss of mitochondrial membrane potential in different melanoma cells. It has been reported that the induction of an autophagic cell death represents a highly effective approach in melanoma therapy.

Non-photoresponsive catalysis, Piezocatalysis, Thermocatalysis, Pyrocatalysis, Tribocatalysis, ROS generation, Dye degradation, Water splitting Keywords: Non-photoresponsive catalysis; Piezocatalysis; Thermocatalysis; Pyrocatalysis; Tribocatalysis; ROS generation; Dye degradation; Water splitting EN Non-photoresponsive catalysis Piezocatalysis Thermocatalysis Pyrocatalysis Tribocatalysis ROS generation Dye degradation Water splitting 1 1 1 05/04/23 20230502 NES 230502 B In recent years b , numerous photocatalysts and electrocatalysts have been developed to address energy and environmental issues, however, some properties such as low efficiency and easy charge recombination limit their applications. Here, recent advances in exploiting diverse catalytic techniques that can be used in dark environments, including piezocatalysis, thermocatalysis, pyrocatalysis, tribocatalysis and hybrid catalysis (piezocatalysis with pyrocatalysis and tribocatalysis with pyrocatalysis) are summarized. [Extracted from the article]

Schematic representation of photoreduction and antimicrobial activity of Ag/CaTiO 3. [Display omitted] • Synthesis of CaTiO 3 by a simple sol–gel method followed by the decoration of different weight percentages of Ag on the surface of the CaTiO 3 wetness impregnation method. • Characterization of the prepared catalyst (XRD, FTIR, SEM, UV–VIS DRS) showed a better result towards morphological, optical, and also towards its activity in wastewater remediation. • Silver nanoparticle also shows good antimicrobial activity against gram-negative bacteria Salmonella typhi and Shigella flexneri because it easily makes holes in the bacterial membrane. • However, the catalyst is environmentally benign and they can be reutilized and maintain the environmental sustainability. CaTiO 3 was synthesized by a simple sol–gel method followed by the decoration of different weight percentages of Ag on the surface of the CaTiO 3 wetness impregnation method (AgCTO). Characterization of the prepared catalyst (XRD, FTIR, SEM, HRTEM, UV–VIS DRS, PL) showed a better result for morphological, optical, and also towards its activity in wastewater remediation. X-ray diffraction study delineates CaTiO 3 perovskite possesses an orthorhombically distorted structure and after the distribution of Ag on the surface of CaTiO 3 maintains crystallinity. The loading of Ag reduces the difference in band gap from 2.8 to 2.10 eV and extends the photocatalyst towards the visible range. This is mostly caused by the localized surface plasmon resonance effect (LSPR). The Schottky junction formed at the CaTiO 3 and Ag contact effectively facilitates electron transport. This results in a reduction in the photocatalytic activity's recombination of photoinduced electrons and holes. Presence of Silver also showed good antimicrobial activity against gram-negative bacteria Salmonella typhi and Shigella flexneri because it easily makes holes in the bacterial membrane. However, the catalyst is environmentally benign and can be reutilized for environmental sustainability. [ABSTRACT FROM AUTHOR]

[Display omitted] • Synthesis a new class of nanozyme using cerium ferrite (CeFe 2 O 4) nanoparticles decorated onto polyethyleneimine (bPEI) coated flower-like molybdenum disulfide (MoS 2) nanoflower. • A rational approach for improving deficiencies and refining the photothermal conversion efficiency to MoS2 nanoflowers by introducing CeFe 2 O 4. • The unique CeFe 2 O 4 NPs with MoS 2 nanoflowers as powerful nanozymes for dual-performance cancer therapies (PTT and ROS generation). Two-dimensional (2D) nanomaterial hybrid with metal nanoferrite nanoparticles will enhance their catalytic activity and photothermal therapy (PTT) through their synergistic coupling effects. This strategy also increases the photothermal conversion efficiency (PCE), blood circulation time, biostability, and cellular uptake efficiency of 2D materials. Herein, we first time report a new class of cerium ferrite (CeFe 2 O 4) nanoparticles (NPs) decorated onto branched polyethyleneimine (bPEI) coated flower-like molybdenum disulfide nanoflowers (MoS 2 NFs). The CeFe 2 O 4 NPs on the MoS 2 NF surface could be designed rationally to improve deficiencies and refine the PCE of MoS 2 NFs and tumor ablation effectiveness in the treated MDA-MB-231 breast cells. Importantly, MoS 2 -bPEI-CeFe 2 O 4 NFs consist of MoS 2 in the inner core and CeFe 2 O 4 in the outer shell, designed to generate heat efficiently and enhanced intracellular reactive oxygen species (ROS) generation in the tumor environment. Furthermore, using sheep blood cells, bare MoS 2 and MoS 2 -bPEI-CeFe 2 O 4 NFs showed hemolytic activity levels of 6 and 2.7 %, respectively. Moreover, MoS 2 -bPEI-CeFe 2 O 4 NFs exhibit 53.6 % of PCE, which effectively induced up to 80 % cytotoxicity and higher levels of ROS generation in the MDA-MB-231 cells when exposed to the 808 nm NIR laser (1.5 W/cm2, 5 min). These findings demonstrate the unique CeFe 2 O 4 NPs with MoS 2 NF as a powerful nanozyme for dual-performance cancer therapies (PTT and ROS generation) and reveal a novel PCE refinement strategy for MoS 2 NFs. It was successfully established as a new cancer therapeutic platform. [ABSTRACT FROM AUTHOR]

Pancreastatin (PST), an anti-insulin peptide derived from chromogranin A. Its levels increase in cases of obesity, which contributes to adipose tissue inflammation and insulin resistance. This study aims to investigate the immunometabolic effect of PST inhibitor (PSTi8) against PST by using in vitro and in vivo finding. 3T3-L1 cells were differentiated with or without PSTi8, and Oil Red O staining was performed. J774A.1 cells were used for macrophage polarization study. The diet-induced obesity and T2DM model was developed in C57BL/6 mice through high-fat diet for 8 weeks. Alzet osmotic pumps were filled with PSTi8 (release rate: 2 mg/kg/day) and implanted in mice for eight weeks. Further, insulin and glucose tolerance tests were performed. Liver and eWAT sections were stained with hematoxylin and eosin. FACS was used to measure mitochondrial ROS and membrane potential, while Oroboros O2k was used to measure oxygen consumption rate. Immunocytochemistry and qRT-PCR were done for protein and gene expression, respectively. PSTi8 inhibited the expression of lipolytic genes and proteins in 3T3-L1 adipocytes. PSTi8 improved the inulin sensitivity, lipid profile, MMP, and OCR levels in the 3T3-L1 adipocyte and eWAT. It also increased the M1 to M2 macrophage polarization in J77A.1 cells and eWAT. Further, PSTi8 attenuated inflammatory CD4+ T, CD8+ T cells and increased the anti-inflammatory T-reg and eosinophil populations in the eWAT. It also reduced the expression of pro-inflammatory genes like Mcp1, Tnfα, and Il-6. Collectively, PSTi8 exerted its beneficial effect on adipose tissue inflammation and restored energy expenditure against diet-induced obesity. [Display omitted] • PST enhanced and PSTi8 attenuated the lipid accumulation in the 3T3-L1 adipocyte. • Higher level of PST contributes to development of dyshomeostasis in the DIO mice. • Inhibition of PST through PSTi8 improved the insulin sensitivity and decreased IR. • PSTi8 increased enhanced the macrophages polarization from M1 to M2 macrophages. • PSTi8 enhanced the mitochondrial fitness and improved the energy expenditure. [ABSTRACT FROM AUTHOR]

Green synthesis of nanoparticles has drawn huge attention in the last decade due to their eco-friendly, biocompatible nature. Phyto-assisted synthesis of metallic nanoparticles is widespread in the field of nanomedicine, especially for antimicrobial and anticancer activity. Here in the present research work, investigators have used the stem extract of the Himalayan plant Hippophae rhamnoides L, for the synthesis of copper nanoparticles (CuNPs). The synthesized of CuNPs were analyzed by using sophisticated instruments, i.e., Fourier transform infrared spectroscopy (FTIR), UV-Vis spectroscopy, X-ray diffraction (XRD), high-performance liquid chromatography (HPLC), and scanning electron microscope (SEM). The size of the synthesized CuNPs was varying from 38 nm to 94 nm which were mainly spherical in shape. Further, the potential of the synthesized CuNPs was evaluated as an anticancer agent on the Hela cell lines, by performing an MTT assay. In the MTT assay, a concentration-dependent activity of CuNPs demonstrated the lower cell viability at 100 μg/mL and IC 50 value at 48 μg/mL of HeLa cancer cell lines. In addition to this, apoptosis activity was evaluated by reactive oxygen species (ROS), DAPI (4',6-diamidino-2-phenylindole) staining, Annexin V, and Propidium iodide (PI) staining, wherein the maximum ROS production was at a dose of 100 µg per mL of CuNPs with a higher intensity of green fluorescence. In both DAPI and PI staining, maximum nuclear condensation was observed with 100 μg/mL of CuNPs against HeLa cell lines., 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 © 2023 Dadhwal, Dhingra, Dwivedi, Alarifi, Kalasariya, Yadav and Patel.)

Here, we report a new synthetic protocol based on microwave-assisted synthesis (MAS) for the preparation of higher yields of zinc and copper in MOFs based on different bis(pyrazolyl)-tagged ligands ([M(BPZ)] n where M = Zn(II), Cu(II), H 2 BPZ = 4,4'-bipyrazole, [M(BPZ-NH 2 )] n where M = Zn(II), Cu(II); H 2 BPZ-NH 2 = 3-amino-4,4'-bipyrazole, and [M x (Me 4 BPZPh)] where M = Zn(II), x = 1; Cu(II), x = 2; H 2 Me 4 BPZPh = bis-4'-(3',5'-dimethyl)-pyrazolylbenzene) and, for the first time, a detailed study of their antibacterial activity, tested against Gram-negative ( E. coli ) and Gram-positive ( S. aureus ) bacteria, as representative agents of infections. The results show that all MOFs exert a broad-spectrum activity and strong efficiency in bacterial growth inhibition, with a mechanism of action based on the surface contact of MOF particles with bacterial cells through the so-called "chelation effect" and reactive oxygen species (ROS) generation, without a significant release of Zn(II) and Cu(II) ions. In addition, morphological changes were elucidated by using a scanning electron microscope (SEM) and bacterial cell damage was further confirmed by a confocal laser scanning microscopy (CLSM) test.

Background and Purpose: Previous studies highlighted that chemoprevention curcumin analog-1.1 (CCA-1.1) demonstrated an antitumor effect on breast, leukemia, and colorectal cancer cells. By utilizing immortalized MDA-MB-231 and HCC1954 cells, we evaluated the anticancer properties of CCA-1.1 and its mediated activity to promote cellular death., Experimental Approach: Cytotoxicity and anti-proliferation were assayed using trypan blue exclusion. The cell cycle profile after CCA-1.1 treatment was established through flow cytometry. May-Grünwald-Giemsa and Hoechst staining were performed to determine the cell cycle arrest upon CCA-1.1 treatment. The involvement of CCA-1.1 in mitotic kinases (aurora A, p-aurora A, p-PLK1, and p-cyclin B1) expression was investigated by immunoblotting. CCA-1.1-treated cells were stained with the X-gal solution to examine the effect on senescence. ROS level and mitochondrial respiration were assessed by DCFDA assay and mitochondrial oxygen consumption rate, respectively., Findings/results: CCA-1.1 exerted cytotoxic activity and inhibited cell proliferation with an irreversible effect, and the flow cytometry analysis demonstrated that CCA-1.1 significantly halted during the G2/M phase, and further assessment revealed that CCA-1.1 caused metaphase arrest. Immunoblot assays confirmed CCA-1.1 suppressed aurora A kinase in MDA-MB-231 cells. The ROS level was elevated after treatment with CCA-1.1, which might promote cellular senescence and suppress basal mitochondrial respiration in MDA-MB-231 cells., Conclusion and Implications: Our data suggested the in vitro proof-of-concept that supports the involvement in cell cycle regulation and ROS generation as contributors to the effectiveness of CCA-1.1 in suppressing breast cancer cell growth., Competing Interests: All authors declared no conflict of interest in this study, (Copyright: © 2023 Research in Pharmaceutical Sciences.)

Glucotoxicity and lipotoxicity are major hallmarks of metabolic disorder. High consumption of fat or carbohydrate rich food is a major risk of metabolic disorder. However, the evolution of high fat or high carbohydrate diet-induced metabolic disorder is not clear. In the study, we tried to find distinguished and common ways involved in the pathogenesis of insulin resistance induced by high fat (HF) and high sucrose (HS) diet. We found that HS diet induced mild glucose intolerance (2 month), followed by a “temporary non-symptom phase” (3 month), and then induced significant metabolic abnormality (4 month). HF diet induced an early “responsive enhancement phase” (2 month), and then gradually caused severe metabolic dysfunction (3–4 month). After a mild induction of mitochondrial ROS generation (2 month), HS diet resulted in a “temporary non-symptom phase” (3 month), and then induced a more significant mitochondrial ROS production (4 month). The impairment of mitochondrial function induced by HS diet was progressive (2–4 month). HF diet induced gradual mitochondrial ROS generation and hyperpolarization. HF diet induced an early “responsive enhancement” of mitochondrial function (2 month), and then gradually resulted in severe decrease of mitochondrial function (3–4 month). Despite the patterns of HS and HF diet-induced insulin resistance were differential, final mitochondrial ROS generation combined with mitochondrial dysfunction may be the common pathway. These findings demonstrate a novel understanding of the mechanism of insulin resistance and highlight the pivotal role of mitochondrial ROS generation and mitochondrial dysfunction in the pathogenesis of metabolic disorder. [ABSTRACT FROM AUTHOR]

Plasticizers are suspected to be toxic and/or to modulate or disrupt the endocrine system of humans and to cross the placental barrier, being embryonic and fetal development a particularly vulnerable period. This work investigates the comparative toxicity and ability to interfere with the synthesis of steroids and to generate reactive oxygen species (ROS) of a selected number of plasticizers, including bisphenol A (BPA), nonyl- (NP) and octylphenol (OP), benzyl butyl phthalate (BBP), dibutyl phthalate (DBP), di(2-ethylhexyl)phthalate (DEHP) and dimethyl phthalate (DMP), in the human placenta JEG-3 cells. Moreover, the bioavailability of chemicals in culture medium has been investigated. After 24 h exposure, OP and NP showed the highest cytotoxicity (EC 50 : 36–40 μM) followed by BPA (138–219 μM), whereas no significant toxicity was observed for phthalates. Notwithstanding, BBP and DBP significantly decreased P450 aromatase activity (experimental IC 50 : 14–15 μM), while NP and OP (20 μM) increased the activity. Overall, this study evidences the differential toxicity and ability to modulate placental aromatase activity of some of the compounds nowadays used as plasticizers, and highlights the need of an accurate determination of the bioavailability of chemicals to improve the sensitivity of in-vitro tests. [ABSTRACT FROM AUTHOR]

Here, the intensity and ratio of superoxide anion (O ), hydrogen peroxide (HO) and hydroxyl anion (OH) formation along the in vitro shootlets of four pear ( Pyrus communis L.) rootstocks (i.e., Pyrodwarf, OH × F40, OH × F69 and OH × F333) were scrutinized under E. amylovora inoculation, over 144 hpi. Furthermore, following identifying the most tolerant and susceptible pear rootstocks (i.e., OH × F69 and OH × F40, respectively), the dynamic expression profiles of three ROS-scavenging enzymatic genes including superoxide dismutase ( SOD), Catalase ( CAT) and ascorbate peroxidase ( APX) were elucidated in response to E. amylovora, over 96 hpi. The highest disease tolerance was observed in OH × F69, and OH × F333, Pyrodwarf and OH × F40 occupied the next descending positions, respectively. Furthermore, the O generation rates were almost similar in all the pears studied, though the accumulation of HO and OH and intensities thereof were considerably distinctive and significantly followed up the levels of disease resistance. Comparing to the controls (0 hpi), in both susceptible and tolerant pear rootstocks, transcription activity of SOD, CAT, and APX genes were overall stimulated with relatively high abundance over 24, 48, 72 and 96 hpi, though some fluctuations were also recorded. Our ROS results, altogether, indicated that E. amylovora is capable enough to stimulate ROS formation in pear, though its progress is extremely dependent upon the susceptibility ratio of the plant. Lastly, the particular expression patterns and different response time of three genes designated that pear rootstocks differentially activates genes encoding antioxidant enzymes to mitigate the possible damage of ROS during E. amylovora invasion. [ABSTRACT FROM AUTHOR]

Cancer-specific anticancer drugs are still an elusive goal. Using light as the temporal control to generate cytotoxic species from photo-activated prodrug in the presence or absence of molecular oxygen has shown potential application targeted chemotherapy as in photodynamic therapy (PDT). In the present work we explored the chemistry of several photo-active ( μ -oxo)diiron(III) complexes of the following formulation [{Fe( μ -O) ( L -his)(B)} 2 ](ClO 4 ) 2 ( 1a - 1c ), [Fe 2 ( μ -O)(H 2 O) 2 B 4 ](ClO 4 ) 4 ( 2b , 2c ) and [Fe 2 ( μ -O)( μ -O 2 CMe)B 4 ](ClO 4 ) 3 ( 3b , 3c ), L -his = l -histidine, B is 2,2′-bipyridine, 1,10-phenanthroline (phen) and dipyrido[3,2-d:2′,3′-f]quinoxaline (dpq) complexes for tumor-specific anticancer activity. Facile redox chemistry and photochemical aspects of the complexes prompted us to investigate the cytotoxic as well as the photo-activated cytotoxic properties of the complexes to the cancer cells. In the present investigation we explored the cancer-specific condition of excess concentration of H 2 O 2 for our approach to targeted chemotherapy. Cytotoxic effect of the complexes to the cancer cells was found to be significantly higher than in normal cells indicating tumor-specific anticancer activity of the complexes. Cytotoxic effect was even more pronounced when the cancer cells treated with the complexes were exposed to the visible light (400–700 nm). There was >12 fold increase in cytotoxicity of the photoactivated complexes in cancer cells (MCF-7) in comparison to the normal cells (MCF-10a). We have defined a factor viz . cancer cell specificity factor ( f ) describing the targeted photochemotherapeutic effect of the complexes at their specific concentration. The factor ( f ) > 1 indicated the cancer cell specificity of the complexes, while f > 2.5 for the complexes under the visible light exposure suggested photodynamic effect. DCFDA assay indicated the presence of excess of ROS in the treated HeLa cells. ROS concentration was found to increase even more on visible light exposure. Increased ROS in the cancer cells disturb the cellular redox mechanism inducing oxidative stress to lethality. Decarboxylation of photo-activated diiron(III) complexes generate OH radical responsible for cell death. Overall, the high efficacy and selectivity of the ( μ -oxo)diiron(III) complexes potentially make them suitable for in vivo applications and extensive testing toward transfer into the clinical arena. [ABSTRACT FROM AUTHOR]

Cervical cancer is the fourth major cause of cancer-related deaths in women worldwide and is the most common cancer in developing countries. Therefore, a search for novel treatment modalities is warranted. The present study is designed to investigate the effect of pan histone deacetylase inhibitor, ‘panobinostat’, on cervical cancer cells alone and in combination with topoisomerase inhibitors. We assessed the effect of panobinostat on two cervical cancer cell lines, HeLa and SiHa, for cell viability, apoptosis, oxidative stress and mitochondrial function using various assays. The results indicate that panobinostat reduces the viability of cervical cancer cells in a dose- and time-dependent manner; it arrests HeLa cells in G0/G1 and SiHa cells in G2/M phase of the cell cycle. Panobinostat induced apoptosis through an increase in the ROS production and the disruption of mitochondrial membrane potential. Concomitantly the expression of anti-apoptotic gene Bcl-xL was reduced, while levels of CDK inhibitor p21 and caspase-9 were increased. Panobinostat increased the acetylation of histone H3 indicating HDAC inhibition. In addition, panobinostat also showed synergistic effect with topoisomerase inhibitors mediated by increased activation of caspase-3/7 activity compared to that in cells treated with panobinostat alone. These results suggest a combination therapy using inhibitors of histone deacetylase and topoisomerase together could hold the promise for an effective targeted therapeutic strategy. [ABSTRACT FROM AUTHOR]

Lanthanide-based nanoparticles (LNs) hold great promise in medicine. A variety of nanocrystals, including LNs, elicits potent inflammatory response through activation of NLRP3 inflammasome. We have previously identified an LNs-specific surface coating peptide RE-1, with the sequence of ‘ACTARSPWICG’, which reduced nanocrystal-cell interaction and abrogated LNs-induced autophagy and toxicity in both HeLa cells and liver hepatocytes. Here we show that RE-1 coating effectively inhibited LNs-induced inflammasome activation, mostly mediated by NLRP3, in mouse bone marrow derived macrophage (BMDM) cells, human THP-1 cells and mouse peritoneal macrophages and also reduced LNs-elicited inflammatory response in vivo. RE-1 coating had no effect on cellular internalization of LNs in BMDM cells, in contrast to the situation in HeLa cells where cell uptake of LNs was significantly inhibited by RE-1. To elucidate the molecular mechanism underlying the inflammasome-inhibiting effect of RE-1, we assessed several parameters known to influence nanocrystal-induced NLRP3 inflammasome activation. RE-1 coating did not reduce potassium efflux, which occurred after LNs treatment in BMDM cells and was necessary but insufficient for LNs-induced inflammasome activation. RE-1 did decrease lysosomal damage induced by LNs, but the inhibitor of cathepsin B did not affect LNs-elicited caspase 1 activation and IL-1β release, suggesting that lysosomal damage was not critically important for LNs-induced inflammasome activation. On the other hand, LNs-induced elevation of intracellular reactive oxygen species (ROS), critically important for inflammasome activation, was largely abolished by RE-1 coating, with the reduction on NADPH oxidase-generated ROS playing a more prominent role for RE-1's inflammasome-inhibiting effect than the reduction on mitochondria-generated ROS. ROS generation further triggered Ca 2+ influx, an event that was mediated by Transient Receptor Potential M2 (TRPM2) and was necessary for inflammasome activation, and this event was completely inhibited by RE-1 coating. We conclude from these studies that inhibition of ROS production, and the subsequent abrogation of TRPM2-mediated Ca 2+ influx, is the primary mechanism underlying RE-1's inhibitory effect on LNs-induced inflammasome activation. The ability of regulating the inflammatory response of nanocrystals through peptide surface coating may be of great value for in vivo applications of LNs and other engineered nanomaterials. [ABSTRACT FROM AUTHOR]

In this work, synthesis of alkylamino and aralkylamino derivatives of sesquiterpene quinone avarone and its model compound tert -butylquinone was described. For all obtained derivatives biological activity was studied. Cytotoxic activity of the synthesized derivatives towards multidrug resistant MDR human non-small cell lung carcinoma NCI-H460/R cells, their sensitive counterpart NCI-H460 and human normal keratinocytes (HaCaT) as well as detection of cell death superoxide anion generation were investigated. Antimicrobial activity towards Gram positive and Gram negative bacteria and fungal cultures was determined. The results showed that strong cytotoxic activity toward cancer cells was improved with simple avarone mimetics. Some derivatives were selective towards MDR cancer cells. The most active derivatives induced apoptosis in both cancer cell lines, but not in normal cells. Superoxide production was induced by 2,6-disubstituted compounds in MDR cancer cells and not by less active 2,5-disubstituted compounds and was accompanied by the collapse of the mitochondrial transmembrane potential. Two tert -butylquinone derivatives were particularly selective towards MDR cancer cells. Some tert -butylquinone derivatives exhibited a strong antimicrobial activity. [ABSTRACT FROM AUTHOR]

Cervical cancer has been the fourth most common cancer killing many women across the world. Carnosic acid (CA), as a phenolic diterpene, has been suggested to against cancer, exerting protective effects associated with inflammatory cytokines. It is aimed to demonstrate the therapeutic role of carnosic acid against cervical cancer and indicate its underlying molecular mechanisms. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2- H -tetrazolium bromide (MTT) was performed to assess the possible anti-proliferative effects of carnosic acid. And also, colony formation was used to further estimate carnosic acid’s ability in suppressing cervical cancer cells proliferation. Flow cytometry assays were performed here to indicate the alterations of cervical cancer cells cycle and the development of apoptosis. Western blot assays and RT-PCR were also applied to clarify the apoptosis-associated signaling pathways affected by reactive oxygen species (ROS) generation. And immunofluorescence was used to detect ROS-positive cells. In vivo experiments, CaSki xenograft model samples of nude mice were involved to further elucidate the effects of carnosic acid. In our results, we found that carnosic acid exerted anti-tumor ability in vitro supported by up-regulation of apoptosis and ROS production in cervical cancer cells. Also, acceleration of ROS led to the phospharylation of (c-Jun N-terminal kinase (JNK) and its-related signals, as well as activation of Endoplasmic Reticulum (ER) stress, promoting the progression of apoptosis via stimulating Caspase3 expression. The development and growth of xenograft tumors in nude mice were found to be inhibited by the administration of carnosic acid for five weeks. And the suppressed role of carnosic acid in proliferation of cervical cancer cells and apoptosis of nude mice with tumor tissues were observed in our study. Taken together, our data indicated that carnosic acid resulted in apoptosis both in vitro and vivo experiments via promoting ROS and activating JNK signaling pathways in human cervical cancer cells, which supplied a potential therapy for the application of carnosic acid in clinical treatment. [ABSTRACT FROM AUTHOR]

ABSTRACT In this study, the chronic toxic effects of tributyltin (TBT), an antifouling paints commonly present in surface and ground water, on morphological indices, reactive oxygen species (ROS) generation, and ATPase activity and heat shock protein (Hsp) 70 protein in tissues (liver, gill, and white muscle) of common carp were investigated. Fish were exposed at sublethal concentrations of TBT (75 ng/L, 0.75 μg/L, and 7.5 μg/L) for 60 days. When compared with the control, there was significant lower condition factor in fish exposed at the higher concentration of TBT. ROS levels in three tissues increased significantly at higher TBT concentrations (0.75 and 7.5 μg/L). The hepatic antioxidant enzymes (total antioxidative capacity and superoxide dismutase) activities were induced at higher concentrations (0.75 μg/L) of TBT. When compared with the hepatic antioxidant enzymes activities in fish exposed to 0.75 μg/L of TBT, there was a decreasing trend in those exposed to TBT with a concentration of 7.5 μg/L. However, all the antioxidant enzymes activities were significantly inhibited in gill and muscle of fish exposed to higher TBT concentrations (0.75 and 7.5 μg/L). Moreover, there was significant lower Na-K-ATPase in three tissues after long-term exposure to higher concentration of TBT, but a significant higher Hsp70 protein levels was observed. In short, environmental concentrations of TBT could not induce obvious impacts on fish, but long-term exposure to higher concentrations of TBT could affect seriously the health status of fish. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 937-944, 2016. [ABSTRACT FROM AUTHOR]

Mitochondrial complex I (NADH:ubiquinone oxidoreductase) is a key enzyme in cellular energy metabolism and provides approximately 40% of the proton-motive force that is utilized during mitochondrial ATP production. The dysregulation of complex I function – either genetically, pharmacologically, or metabolically induced – has severe pathophysiological consequences that often involve an imbalance in the production of reactive oxygen species (ROS). Slow transition of the active (A) enzyme to the deactive, dormant (D) form takes place during ischemia in metabolically active organs such as the heart and brain. The reactivation of complex I occurs upon reoxygenation of ischemic tissue, a process that is usually accompanied by an increase in cellular ROS production. Complex I in the D-form serves as a protective mechanism preventing the oxidative burst upon reperfusion. Conversely, however, the D-form is more vulnerable to oxidative/nitrosative damage. Understanding the so-called active/deactive (A/D) transition may contribute to the development of new therapeutic interventions for conditions like stroke, cardiac infarction, and other ischemia-associated pathologies. In this review, we summarize current knowledge on the mechanism of A/D transition of mitochondrial complex I considering recently available structural data and site-specific labeling experiments. In addition, this review discusses in detail the impact of the A/D transition on ROS production by complex I and the S-nitrosation of a critical cysteine residue of subunit ND3 as a strategy to prevent oxidative damage and tissue damage during ischemia–reperfusion injury. This article is part of a Special Issue entitled Respiratory complex I, edited by Volker Zickermann and Ulrich Brandt. [ABSTRACT FROM AUTHOR]

In plant cells, as in most eukaryotic organisms, peroxisomes are probably the major sites of intracellular H2O2 production, as a result of their essentially oxidative type of metabolism. In recent years, it has become increasingly clear that peroxisomes carry out essential functions in eukaryotic cells. The generation of the important messenger molecule hydrogen peroxide (H2O2) by animal and plant peroxisomes and the presence of catalase in these organelles has been known for many years, but the generation of superoxide radicals (O2-) and the occurrence of the metalloenzyme superoxide dismutase was reported for the first time in peroxisomes from plant origin. Further research showed the presence in plant peroxisomes of a complex battery of antioxidant systems apart from catalase. The evidence available of reactive oxygen species (ROS) production in peroxisomes is presented, and the different antioxidant systems characterized in these organelles and their possible functions are described. Peroxisomes appear to have a ROS-mediated role in abiotic stress situations induced by the heavy metal cadmium (Cd) and the xenobiotic 2,4-D, and also in the oxidative reactions of leaf senescence. The toxicity of Cd and 2,4-D has an effect on the ROS metabolism and speed of movement (dynamics) of peroxisomes. The regulation of ROS production in peroxisomes can take place by posttranslational modifications of those proteins involved in their production and/or scavenging. In recent years, different studies have been carried out on the proteome of ROS metabolism in peroxisomes. Diverse evidence obtained indicates that peroxisomes are an important cellular source of different signaling molecules, including ROS, involved in distinct processes of high physiological importance, and might play an important role in the maintenance of cellular redox homeostasis. [ABSTRACT FROM AUTHOR]

We have synthesized two new complexes of platinum ( 1 ) and ruthenium ( 2 ) with α-amino acid, l -alanine, and 2,3-dihydroxybenzaldehyde derived Schiff base ( L ). The ligand and both complexes were characterized by using elemental analysis and several other spectroscopic techniques viz; IR, 1 H, 13 C NMR, EPR, and ESI-MS. Furthermore, the protein-binding ability of synthesized complexes was monitored by UV–visible, fluorescence and circular dichroism techniques with a model protein, human serum albumin (HSA). Both the PtL 2 and RuL 2 complexes displayed significant binding towards HSA. Also, in vitro cytotoxicity assay for both complexes was carried out on human hepatocellular carcinoma cancer (HepG2) cell line. The results showed concentration-dependent inhibition of cell viability. Moreover, the generation of reactive oxygen species was also evaluated, and results exhibited substantial role in cytotoxicity. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) generation and radical scavenging are dual properties of hydrophilic C 60 derivatives (hC 60 s). hC 60 s eliminate radicals in dark, while they produce reactive oxygen species (ROS) in the presence of irradiation and oxygen. Compared to the pristine C 60 suspension, the aqueous solution of hC 60 s is easier to handle in vivo . hC 60 s are diverse and could be placed into two general categories: covalently modified C 60 derivatives and pristine C 60 solubilized non-covalently by macromolecules. In order to present in detail, the above categories are broken down into 8 parts: C 60 (OH) n , C 60 with carboxylic acid, C 60 with quaternary ammonium salts, C 60 with peptide, C 60 containing sugar, C 60 modified covalently or non-covalently solubilized by cyclodextrins (CDs), pristine C 60 delivered by liposomes, functionalized C 60 -polymer and pristine C 60 solubilized by polymer. Each hC 60 shows the propensity to be ROS producer or radical scavenger. This preference is dependent on hC 60 s structures. For example, major application of C 60 (OH) n is radical scavenger, while pristine C 60 /γ-CD complex usually serves as ROS producer. In addition, the electron acceptability and innate hydrophobic surface confer hC 60 s with O 2 uptake inhibition, HIV inhibition and membrane permeability. In this review, we summarize the preparation methods and biological applications of hC 60 s according to the structures. [ABSTRACT FROM AUTHOR]

Background: Cancer is a major health problem and exploiting natural products have been one of the most successful methods to combat this disease. Verbesina encelioides is a notorious weed with various pharmacological properties. The aim of the present investigation was to screen the anticancer potential of V. encelioides extract against human lung cancer (A-549), breast cancer (MCF-7), and liver cancer (HepG2) cell lines. Methods: A-549, MCF-7, and HepG2 cells were exposed to various concentrations of (10-1000 µg/ml) of V. encelioides for 24 h. Further, cytotoxic concentrations (250, 500, and 1000 µg/ml) of V. encelioides induced oxidative stress (GSH and LPO), reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest, and DNA damage in HepG2 cells were studied. Results: The exposure of cells to 10-1000 µg/ml of extract for 24 h, revealed the concentrations 250-1000 µg/ml was cytotoxic against MCF-7 and HepG2 cells, but not against A-549 cells. Moreover, the extract showed higher decrease in the cell viability against HepG2 cells than MCF-7 cells. Therefore, HepG2 cells were selected for further studies viz. oxidative stress (GSH and LPO), reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP), cell cycle arrest, and DNA damage. The results revealed differential anticancer activity of V. encelioides against A-549, MCF-7 and HepG2 cells. A significant induction of oxidative stress, ROS generation, and MMP levels was observed in HepG2 cells. The cell cycle analysis and comet assay showed that V. encelioides significantly induced G2/M arrests and DNA damage. Conclusion: These results indicate that V encelioides possess substantial cytotoxic potential and may warrant further investigation to develop potential anticancer agent. [ABSTRACT FROM AUTHOR]

Elderberry (EDB) Sambucus nigra L. is one of the oldest medicinal plants which is useful for therapeutic and nutritional purposes due to a large amount of biologically active constituents, including compounds with a high antioxidant capacity. The present study focused on the antioxidant potential of the colon-available EDB fruit extract, derived from the artificial gastrointestinal tract, with regard to human colonic mucosa cells cultured in vitro . Despite the significant loss of EDB bioactive compounds due to the digestion process, the colon-digested extract was able to reduce the excessive intracellular ROS production (22%) and oxidative DNA damage (46%) in the colon cells at a dose of 1 mg of freeze-dried EDB powder/ml. Moreover, the colon-digested EDB extract inhibited oxidant-induced mutagenicity (26%) in the Salmonella typhimurium TA102 strain, as determined by the Ames test. In conclusion, the current in vitro study confirmed that the fruits of S. nigra are capable of protecting colonic cells against the detrimental effects of oxidative stress. [ABSTRACT FROM AUTHOR]

Background: Doxorubicin (DOX) is a small molecular cytotoxic agent that can be transferred efficiently to cancer cells by nanocarriers. This anthracycline antibiotic serves as an effective anti-neoplastic drug against both hematological and solid malignancies. Here, we set out to assess the capacity of a novel doxorubicin - transferrin conjugate (DOX-TRF) to provoke apoptosis in human normal and leukemia cells through free radicals produced via a redox cycle of doxorubicin (DOX) when released from its conjugate. Methods: After DOX-TRF exposure, we determined the time-course of apoptotic and necrotic events, the generation of reactive oxygen species (ROS), changes in mitochondrial membrane potential, as well as alterations in cytochrome c levels and intracellular calcium concentrations in human leukemia-derived cell lines (CCRF-CEM, K562 and its doxorubicin-resistant derivative K562/DOX) and normal peripheral blood-derived mononuclear cells (PBMC). Results: We found that DOX-TRF can induce apoptosis in all leukemia-derived cell lines tested, which was associated with morphological changes and decreases in mitochondrial membrane potential. In comparison to free DOX treated cells, we observed a time-dependency between a higher level of ROS generation and a higher drop in mitochondrial membrane potential, particularly in the doxorubicin-resistant cell line. In addition, we found that the apoptotic cell death induced by DOX-TRF was directly associated with a release of cytochrome c from the mitochondria and an increase in intracellular calcium level in all human leukemia-derived cell lines tested. Conclusions: Our data indicate that DOX-TRF is considerably more cytotoxic to human leukemia cells than free DOX. In addition, we show that DOX-TRF can effectively produce free radicals, which are directly involved in apoptosis induction. [ABSTRACT FROM AUTHOR]

The main objective of the current study was to investigate the effect of Curcacycline A and B against heat stress induced apoptosis. Cumulus-oocyte complexes (COCs) were allocated in several groups were cultured at 39 °C and 42 °C in TCM-199 supplemented either with hormones alone, or with two cyclic peptides isolated from the latex of Jatropha curcas , namely Curcacycline A and B. In general, the results revealed a concrete reduction in the maturation rate of sheep oocytes cultured in TCM-199 medium at 42 °C. At the same temperature, higher percentages of sheep oocytes cultured with Curcacycline A or A + B were matured compared with TCM-199 medium alone. Both the expression of apoptotic related-genes (Bax, Bcl-2, Caspase 3, P53 and C-myc) and the generation of reactive oxygen species (ROS) increased significantly in oocytes cultured in TCM-199 medium at 42 °C. The addition of Curcacycline A and B supplements to the culture media at 42 °C suppressed the effect of heat stress on the expression of apoptotic genes and on the generation of ROS. In conclusion, results indicated that the two cyclic peptides inhibited the negative effect of heat stress on meiotic maturation, expression of apoptotic genes and ROS generation in oocytes. [ABSTRACT FROM AUTHOR]

Binuclear copper(I)-benzimidazole complex enters cells and accumulates in nuclei, shows antiproliferative activity against human cancer cell lines, and causes DNA lesion and ROS-dependent mitochondrial dysfunction inducing apoptosis. [Display omitted] • Two Cu(I)-benzimidazole complexes with effective anti-proliferative against human cancer cell lines were synthesized. • Copper complex can enter the human cancer cell and accumulate in the nuclei. • Copper complex induced DNA lesion and ROS-dependent mitochondrial dysfunction. Two binuclear Cu(I) complexes [Cu 2 (L1)(PPh 3) 2 I 2 ] (1) and [Cu 2 (L2)(PPh 3) 2 Br 2 ] (2) derived from the ligands 1,4-bis((5-bromo-2-(pyridin-2-yl)-1H-benzoimidazol-1-yl)methyl)benzene (L1) and 1,4-bis((2-(pyrazin-2-yl)-1H-benzoimidazol-1-yl)methyl)benzene (L2) were prepared and characterized in this study. Both complexes were found to bind to CT-DNA in a groove-binding mode via spectroscopic studies and molecular docking, and cleave pBR322 DNA efficiently in the presence of H 2 O 2. In vitro antitumor activity test revealed that both complexes exhibited effective anti-proliferative activities against four human cancer cell lines (HCT116, HeLa, SMMC7721, and TFK-1), and that SMMC7721 cells were the most sensitive to complex 1 , which is consistent with the finding that the cell uptake of complex 1 is superior to that of complex 2. In SMMC7721 cells, complex 1 mainly accumulated in the nuclei, arrested the cell cycle at the G2/M phase, and caused severe DNA fragmentation. Concomitantly, the generation of reactive oxygen species (ROS) elicited by complex 1 is probably involved in arising mitochondrial dysfunction and apoptosis. [ABSTRACT FROM AUTHOR]

Mitochondrial reactive oxygen species (ROS)generation plays an essential role in the process of adipocyte differentiation and is involved in the development of obesity and associated metabolic diseases. Various dietary flavonoids possess the substantial anti-adipogenic activity. However, it is unclear whether these flavonoids inhibit adipocyte differentiation by reducing ROS generation. In this study, the effects of six common dietary flavonoids on adipocyte differentiation were assessed in 3T3-L1 cells. The flavonoids with the same backbone of 5,7-dihydroxylflavone, including flavones apigenin, chrysin, luteolin and flavonols kaempferol, myricetin, quercetin, dose-dependently inhibited 3T3-L1 adipocyte differentiation, suggesting an associated hierarchy of inhibitory capability: luteolin > quercetin > myricetin > apigenin/kaempferol > chrysin. Meanwhile, six flavonoids were found to inhibit adipogenic gene expression and the early stage of adipocyte differentiation. Among the tested flavonoids, luteolin significantly reduced both intracellular and mitochondrial ROS generation during adipocyte differentiation. Further, luteolin treatment depressed the elevation of H2O2 concentration in the early stage of 3T3-L1 differentiation and reversed the facilitated effects of exogenous H2O2 on 3T3-L1 adipocyte differentiation and ROS generation. Altogether, the activity comparison of six dietary flavonoids identifies that luteolin inhibits 3T3-L1 adipocyte differentiation through reducing ROS generation, elucidating a new mechanism underlying the anti-adipogenic actions of flavonoids. [ABSTRACT FROM AUTHOR]

[Display omitted] • Optimal synthesis of silica nanocomposites (SNs) doped with Cu (2−x) S nanoparticles. • Chemodynamic activity of the SNs affected by heating and reductive effect of biothiols. • Ability of SNs to stand against reductive effect of biothiols affected by exterior layer. • Synergistic interference of chemodynamic and photothermal activities of Cu (2−x) S@SNs. • Impact of chemodynamic activity of Cu (2−x) S@SNs on cancer cell dearth generation. The present work introduces the factors controlling the encapsulation of oleate-oleylamine-stabilized Cu (2−x) S nanoparticles (NPs) into silica nanocomposites (SNs) through the water-in-oil microemulsion method. The tendency of the Cu (2−x) S NPs to form negatively charged aggregates is highlighted as the factor restricting their loading into the SNs. The different preliminary treating of Cu (2−x) S NPs reveals that the recharging is rather than the de-aggregation facilitates their loading into the SNs. The treating of Cu (2−x) S NPs by [Ru(dipy) 3 ]2+ complexes both facilitates their loading into the SNs and gain in their luminescence. The interfacial post-treating of the SNs by pluronic F-127 (F-127) is represented as the factor affecting both aggregation behavior and therapeutic function of the SNs. The electron spin resonance (ESR) spectroscopy results reveal the factors (heating, treating by F-127, addition of glutathione) that suppress and enhance the generation of reactive oxygen species (ROS) by the SNs. The luminescence of the SNs reveals the specificity in the intracellular trafficking of their treated and untreated counterparts. The cytotoxicity enhancement under the low power NIR-irradiation of the cancer cells incubated by the SNs is explained by the heating-induced increase in the level of ROS generation. The greater cytotoxicity of the treated by F-127 vs the untreated SNs both in "dark" and NIR-irradiated conditions is correlated with the difference in their ability to stand against the suppressive effect of glutathione. [ABSTRACT FROM AUTHOR]

Biofilms are microbial colonies that remain enclosed in an organic polymeric matrix substance on biotic and abiotic surfaces, allowing them to colonize medical equipments and involved in most device associated life intimidating infections. Due to their antimicrobial resistance there is an urgent need to discover novel biofilm preventive and therapeutic agents. ZnO NPs were synthesized using cyanobacteria Gleocapsa gelatinosa cell extract through green and cost-effective approach. Physiochemical characterization was done to determine their morphologies and size distribution. Antibiofilm and eradication activity of ZnO NPs was determined. Cell viability and internalization ability of ZnO NPs into biofilm was analyzed by flow cytometry. Confocal microscopy was done to visualize the disrupted biofilm morphology treated with ZnO NPs. It was observed that ZnONPs were spherical in shape with 31–35 nm size and were moderately dispersed. ZnO NPs exhibited high antibiofilm activity against B. cereus and E. coli with minimum biofilm inhibitory concentration (MBIC) of ZnO NPs at 46.8 µg ml−1 and 93.7 µg ml−1. Flow cytometry analysis confirmed the reduced bacterial cell viability due to increased permeability, altered bacterial growth and enhanced production of intracellular ROS. Disruption of membrane integrity exhibited with reduced exopolysaccharides secretion and leakage of nucleic acids through UV–Vis spectroscopy. Results of confocal microscopy highlighted strong interaction of ZnO NPs with intracellular components leading to biofim destruction. This study emphasizes the potential mechanisms underlying the selective bactericidal properties of ZnO NPs and highlighted the strong interaction of ZnO NPs with intracellular components leading to biofim destruction. Therefore, ZnO NPs could be considered as a promising antibiofilm agent and thus could expand the possibility to use as therapeutic agent. [Display omitted] • ZnO NPs were synthesized from cyanobacteria Gleocapsa gelatinosa extract. • Physicochemical characterization evidenced spherical particle with 31–35 nm in size. • ZnO NPs showed potent biofilm inhibition against multi-drug resistant bacteria pathogens. • ZnO NPs reduced the bacterial cell viability and eradicate the biofilms. • ZnO NPs targets cell membrane induced ROS generation as bactericidal mechanism. [ABSTRACT FROM AUTHOR]

Conventional chemotherapy usually fails to achieve its intended effect because of the poor water solubility, poor tumor selectivity, and low tumor accumulation of chemotherapy drugs. The systemic toxicity of chemotherapy agents is also a problem that cannot be ignored. It is expected that smart nano-drug delivery systems that are able to respond to tumor microenvironments will provide better therapeutic outcomes with decreased side effects of chemotherapeutics. Nano-drug delivery systems capable of breaking the redox balance can also increase the sensitivity of tumor cells to chemotherapeutics. In this study, using polymer-containing disulfide bonds, ester bonds, and d-α-tocopherol polyethylene glycol succinate (TPGS), which can amplify reactive oxygen species (ROS) in tumor cells, we have successfully prepared a smart glutathione (GSH) and esterase dual-responsive nano-drug delivery system (DTX@PAMBE-SS-TPGS NPs) with the ability to deplete GSH as well as amplify ROS and effectively release an encapsulated chemotherapy drug (DTX) in tumor cells. The potential of DTX@PAMBE-SS-TPGS NPs for enhanced antitumor effects was thoroughly evaluated using in vitro as well as in vivo experiments. Our research offers a promising strategy for maximizing the efficacy of tumor therapy.

Catalysis plays a crucial role in all the major applications and challenges in the environment, including energy generation and environmental remediation. Although photocatalysts and electrocatalysts are useful in addressing energy and environmental issues, they have some major drawbacks, such as low efficiency and easy charge recombination which limits their applications. Hence, it is imperative to design and explore new catalytic techniques that include non-photoresponsive catalysts. In this review, the detailed possibilities, characteristics and prospects of non-photoresponsive catalysts, such as piezocatalysts, thermocatalysts, pyrocatalysts, and tribocatalysts along with hybrid catalysts are described. The overall mechanism of each catalytic technique and its applications in different fields such as energy generation, environmental remediation, and carbon dioxide reduction are discussed., (© 2023 Wiley-VCH GmbH.)

Extensive uses of calcium titanate nanoparticles (CaTiO 3 -NPs) and erbium oxide nanoparticles (Er 2 O 3 -NPs) increase their release into the environment and human exposure, particularly through skin contact. However, there are almost no studies available on the effect of these nanoparticles on skin integrity. Therefore, this study was undertaken to estimate CaTiO 3 -NP- or Er 2 O 3 -NP-induced cytotoxicity and genotoxicity in normal human skin fibroblast (HSF) cells. Cell viability was measured using sulforhodamine B (SRB) assay, while the level of DNA damage was detected using the alkaline comet assay. The intracellular levels of reactive oxygen species (ROS) as well as the expression level of p53, Bax, and Bcl2 genes were detected. Although the viability of HSF cells was non-markedly changed after 24 h, prolonged treatment with CaTiO3-NPs or Er2O3-NPs for 72 h induced concentration-dependent death of HSF cells. Treatment of normal HSF cells with IC50/72 h of CaTiO3-NPs or Er2O3-NPs did not cause marked changes in the intracellular level of ROS, DNA damage parameters, and expression levels of apoptosis genes compared to their values in the untreated HSF cells. We thus concluded that CaTiO3-NPs or Er2O3-NPs cause time- and concentration-dependent cytotoxicity toward normal HSF cells. However, safe and non-genotoxic effects were demonstrated by the apparent non-significant changes in intracellular ROS level, DNA integrity, and apoptotic genes' expression after exposure of normal HSF cells to nanoparticles. Thus, it is recommended that further studies be conducted to further understand the toxic and biological effects of CaTiO 3 -NPs and Er2O3-NPs., (© 2022. The Author(s).)

Biological activities of a series of palladium(II) complexes (M1-M9) bearing N ∩ N, N ∩ S, and N ∩ O chelating ligands are reported. The palladium complexes were tested for their cytotoxic properties against human cervical cancer (HeLa) cells and antibacterial activity against Gm +ve and Gm -ve bacteria. Among the palladium complexes studied (M1-M9), the complex M5, M8, and M9 were found to be more effective in inhibiting the proliferation of HeLa cells. Hence, these complexes were further investigated for their potential role in cellular damage and apoptosis. DCFDA staining, Rhodamine 123 staining and DNA cleavage assay revealed that complex M5, M8 and M9 induced apoptotic cell death in HeLa cells through ROS generation, DNA damage and mitochondrial depolarization. Computational and titration studies also indicated strong electrostatic interaction with DNA groove. Most of the complexes exhibited good antibacterial activity against both Gm +ve and Gm -ve bacteria. The antibacterial activity of the compounds could not be correlated with their anticancer activity indicating a differential mechanism at their effective concentrations. The detailed study on the antibacterial mechanism of the most potent complex M7 revealed that it exerted its antibacterial activity by inhibiting the function of FtsZ and perturbing the localization of the Z-ring at the mid cell., (© 2023 Wiley-VHCA AG, Zurich, Switzerland.)

Radiotherapy (RT) incorporated multidisciplinary treatment is producing excellent clinical results, but its efficacy in treating late-stage gastric cancer is constrained by radioresistance and RT-related toxicity. Especially, since reactive oxygen species are the pivotal effectual molecules of ionizing radiation, improving ROS production by nanoparticles and other pharmacological modulation to amplify oxidation of polyunsaturated fatty acids and subsequent ferroptotic cell death is shown to enhance cancer cell radioresponse. Herein, we constructed a nanosystem by loading Pyrogallol (PG), a polyphenol compound and ROS generator, into mesoporous organosilica nanoparticles named as MON@ p G. The nanoparticles exhibit proper size distribution with amplified ROS production and substantial glutathione depletion under X-ray radiation in gastric cancer cell line. Meanwhile, MON@PG enhanced radiosensitivity of gastric cancer in xenograft tumor model by ROS-mediated accumulation of DNA damage and apoptosis. Furthermore, this augmented oxidative process induced mitochondrial dysfunction and ferroptosis. In summary, MON@PG nanoparticles show the capacity to improve RT potency in gastric cancer by disrupting redox balance and augmenting ferroptosis., 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 © 2023 Wang, Niu, Luo, Zhu, Xiang, He, Chen, Li and Hu.)