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Plastic is a fossil-based synthetic polymer that has become an essential material in our daily life. Plastic pollution resulting from the accumulation of plastic objects has become problematic for our environment. Bioplastic can be a biodegradable environmentally friendly alternative for the synthetic plastic. In this paper, bioplastics based on polyvinyl alcohol (PVA)/gellan gum (GG) blend have been produced in three different compositions and their chemical structure, mechanical, morphological and thermal properties have been studied. Glycerol has been used as a plasticizer. To add extra features to the PVA/GG bioplastic, Psidium guajava (guava) leaves, GL, and chickpea, CP, extracts have been added to the PVA/GG (30/70) blend. Water and aqueous ethanol have been used in the extraction of GL and CP, respectively. The addition of the plant’s extracts enhanced the tensile properties of the PVA/GG bioplastic. Weathering acceleration tests have been carried out to examine the degradation of the prepared bioplastics. Cytotoxicity studies revealed that the prepared bioplastic is safe to be used in food packaging applications. Water and oxygen permeability for the new PVA/GG bioplastic have also been studied. The addition of the plant extracts (GL and CP extracts) increased the oxygen and water permeability to different extents. Bioplastic life cycle assessment (LCA) and CO 2 emissions in comparison to fossil-based plastic have been investigated. From all the results, PVA/GG based bioplastic proved to be a degradable, safe and effective alternative for fossil-based plastics in food packaging applications.

Nanotherapy has emerged as a promising strategy for the targeted and efficient treatment of melanoma, the most aggressive and lethal form of skin cancer, with minimized systemic toxicity. However, the therapeutic efficacy of cobalt oxide nanoparticles (Co 3 O 4 NPs) in melanoma treatment remains unexplored. This study aimed to assess the therapeutic potential of Co 3 O 4 NPs in melanoma treatment by evaluating their impact on cell viability, genomic DNA and mitochondrial integrity, reactive oxygen species (ROS) generation and apoptosis induction in melanoma A-375 cells. Our findings demonstrated a concentration-dependent reduction in cell viability upon treatment with five Co 3 O 4 NP concentrations (0.2, 2, 20, 200, and 2000 µg/ml), with an IC50 value of 303.80 µg/ml. Treatment with this IC50 concentration significantly increased ROS generation, induced dramatic DNA damage, and disrupted mitochondrial membrane potential integrity. Flow cytometric analysis revealed apoptosis and necrosis induction following Co 3 O 4 NP exposure at the IC50 concentration value. Results of qRT-PCR analysis demonstrated remarkable dysregulation of apoptotic and mitochondrial genes, including a significant downregulation of apoptotic p53 and mitochondrial ND3 genes and marked upregulation of the anti-apoptotic gene Bcl2. These findings highlight the novel potential of Co 3 O 4 NPs as potent inducers of melanoma A-375 cell death in a concentration-dependent manner through excessive ROS production, genomic instability, mitochondrial dysfunction and dysregulation of apoptotic and mitochondrial gene expression, ultimately promoting apoptosis in A-375 cells. This study thus underscores the potential of Co 3 O 4 NPs as a promising nanotherapeutic candidate for melanoma treatment, warranting further exploration to elucidate their full biological and clinical applicability.

The aggressive nature of pancreatic cancer, coupled with the limitations of current treatment options, underscores the urgent need for more effective and targeted therapies. Nanoparticle-based approaches offer promising alternatives, with calcium hydroxide nanoparticles (Ca(OH) 2 NPs) emerging as a potential candidate due to their biocompatibility, high alkalinity, and ability to modify the tumor microenvironment. However, their therapeutic potential against pancreatic cancer remains largely unexplored. This study thus estimated the effects of Ca(OH) 2 NPs on the viability of normal oral epithelial cells (OECs) and pancreatic cancer PANC-1 cells, moreover, the impact of Ca(OH) 2 NPs on genomic DNA and mitochondrial membrane integrity, reactive oxygen species (ROS) generation, and apoptosis induction in PANC-1 cells was assessed. Sulforhodamine B cytotoxicity assay demonstrated a strong, targeted concentration-dependent cytotoxic effect of Ca(OH) 2 NPs on PANC-1 cells following exposure to five different concentrations (0.01, 1, 10, 100, and 1000 µg/ml) for 72 h, with an IC50 value of 152.40 µg/ml. In contrast, minimal cytotoxicity was observed in normal OECs, which had an IC50 value of 481.66 µg /ml. The calculated selectivity index of 3.16 further confirmed the preferential cytotoxicity of Ca(OH) 2 NPs towards PANC-1 cells. Moreover, exposure of PANC-1 cells to the IC50 concentration of Ca(OH) 2 NPs (152.40 µg/ml) led to excessive ROS generation, marked genomic instability, and loss of mitochondrial membrane integrity. These effects were accompanied by dysregulation of key apoptotic genes, including upregulation of p53 and mitochondrial ND3, along with downregulation of the anti-apoptotic Bcl-2 gene, ultimately inducing mitochondrial apoptosis in PANC-1 cells. Ca(OH) 2 NPs exhibit potent, selective cytotoxicity against PANC-1 cells while exerting minimal toxicity on normal OECs. Their mechanism of action appears to involve excessive ROS generation, leading to severe genomic DNA and mitochondrial damage, ultimately triggering apoptosis in pancreatic cancer cells. These findings highlight the potential of Ca(OH) 2 NPs as a novel therapeutic agent for pancreatic cancer. However, further in vitro and in vivo studies are warranted to fully explore their clinical applicability and underlying molecular mechanisms in pancreatic cancer treatment.

Triple-negative breast cancer (TNBC) is among the most aggressive breast cancer subtypes, characterized by the absence of estrogen receptor, progesterone receptor, and HER2 expression. The lack of these molecular targets, combined with the limitations of current treatment, particularly chemotherapy, which suffers from poor tumor selectivity, systemic toxicity, rapid development of resistance, and high recurrence rates, underscores the urgent need for innovative therapeutic strategies. Nanoparticle-based therapies have emerged as promising alternatives to overcome these challenges. Bioactive glass nanoparticles (BGNps), in particular, are recognized for their biocompatibility and multifunctional biological activity, yet their anticancer potential against TNBC remains fully unexplored. This study therefore aimed to investigate the therapeutic efficacy and molecular mechanisms of BGNps in highly aggressive triple-negative MDA-MB-231 breast cancer cells. Cells were treated with two-fold increasing concentrations of BGNps (7.8–1000 µg/ml), and cytotoxicity was assessed using the MTT assay. Genomic DNA integrity was evaluated using the alkaline comet assay, while oxidative stress and mitochondrial function were measured with 2′,7′-dichlorodihydrofluorescein diacetate (2′,7′-DCFH-DA) and Rhodamine-123 staining, respectively. Apoptotic induction was further examined using DAPI nuclear staining and chromatin diffusion assays, and transcriptional regulation of apoptosis- and mitochondria-related genes was analyzed by qRT-PCR. The results of MTT assay demonstrated that BGNps exerted potent, concentration-dependent cytotoxicity in MDA-MB-231 cells, with an IC50 value of 184.3 µg/ml. Treatment with BGNps at the IC50 concentration induced excessive reactive oxygen species (ROS) generation, severe mitochondrial membrane depolarization, extensive genomic DNA damage, and pronounced apoptotic cell death in MDA-MB-231 cancer cells. These effects were associated with marked upregulation of p53 and concurrent downregulation of anti-apoptotic Bcl-2 and mitochondrial ND3 genes, amplifying oxidative stress and mitochondrial dysfunction. In conclusion, BGNps display strong potential as a novel nanotherapeutic for TNBC, offering an effective alternative to conventional chemotherapy. Their multi-step mechanism; encompassing ROS induction, mitochondrial disruption, and apoptosis activation, highlights their promise in overcoming the intrinsic resistance and therapeutic limitations of this highly aggressive breast cancer subtype.

Calcium hydroxide nanoparticles (Ca(OH) 2 NPs) possess potent antimicrobial activities and unique physical and chemical properties, making them valuable across various fields. However, limited information exists regarding their effects on genomic DNA integrity and their potential to induce apoptosis in normal and cancerous human cell lines. This study thus aimed to evaluate the impact of Ca(OH) 2 NPs on cell viability, genomic DNA integrity, and oxidative stress induction in human normal skin fibroblasts (HSF) and cancerous hepatic (HepG2) cells. Cell viability and genomic DNA stability were assessed using the Sulforhodamine B (SRB) assay and alkaline comet assay, respectively. Reactive oxygen species (ROS) levels were measured using 2,7-dichlorofluorescein diacetate, while the expression level of apoptosis-related genes (p53, Bax, and Bcl-2) were quantified using real-time PCR (qRT-PCR). The SRB cytotoxicity assay revealed that a 48-hour exposure to Ca(OH) 2 NPs caused concentration-dependent cell death and proliferation inhibition in both HSF and HepG2 cells, with IC50 values of 271.93 µg/mL for HSF and 291.8 µg/mL for HepG2 cells. Treatment with the IC50 concentration of Ca(OH) 2 NPs selectively induced significant DNA damage, excessive ROS generation, and marked dysregulation of apoptotic (p53 and Bax) and anti-apoptotic (Bcl-2) gene expression in HepG2 cells, triggering apoptosis. In contrast, exposure of HSF cells to the IC50 concentration of Ca(OH) 2 NPs caused no significant changes in genomic DNA integrity, ROS generation, or apoptotic gene expression. These findings indicate that Ca(OH) 2 NPs exhibit concentration-dependent cytotoxicity in both normal HSF and cancerous HepG2 cells. However, exposure to the IC50 concentration was non-genotoxic to normal HSF cells while selectively inducing genotoxicity and apoptosis in HepG2 cancer cells through DNA breaks and ROS-mediated mechanisms. Further studies are required to explore the biological and toxicological properties and therapeutic potential of Ca(OH) 2 NPs in hepatic cancer treatment.

The widespread human consumption of food and commercial products containing acrylamide and titanium dioxide (TiO 2 ) nanoparticles highlights the need to assess the risks of their concurrent exposure. However, almost no studies have explored the effect of acrylamide and TiO 2 nanoparticles co-exposure on genomic DNA integrity and inflammation induction in hepatic tissues. Consequently, this study aimed to estimate the impact of acrylamide and TiO 2 nanoparticles coadministration on the genomic DNA integrity, reactive oxygen species (ROS) generation and expression level of apoptotic and inflammatory genes in mice hepatic tissues. Mice were orally administered acrylamide (3 mg/kg) or/and TiO 2 nanoparticles (5 mg/kg) five times a week over two successive weeks. Genomic DNA integrity was assessed using alkaline Comet and Laddered DNA fragmentation assays, while ROS level was measured using 2, 7- Dichlorofluorescein diacetate dye. The expression level of inflammatory and apoptotic genes was quantified using quantitative real-time PCR (qRT-PCR). The results indicated that either acrylamide (3 mg/kg) or TiO 2 nanoparticles (5 mg/kg) alone significantly disrupted DNA integrity, increased ROS level, and upregulated inflammatory (INOS, COX-2) and apoptotic (p53) gene expression, while downregulating the anti-inflammatory HO-1 gene. However, the coadministration of acrylamide and TiO 2 nanoparticles resulted in even greater DNA damage, higher ROS production, and a further increase in inflammatory and apoptotic gene expression, along with a more pronounced decrease in HO-1 expression compared to the effects of either agent alone. In conclusion these findings suggest that chronic coadministration of acrylamide and TiO2 nanoparticles, even at low doses, amplifies the genomic DNA damage and inflammation induced by each agent individually, exacerbating hepatic cell stress. Therefore, avoiding simultaneous exposure to acrylamide and TiO2 nanoparticles is recommended to reduce the risk of severe toxic effects.

Cervical cancer remains a leading cause of cancer-related mortality, emphasizing the need for safer, more selective therapies. Yttrium oxide nanoparticles (Y 2 O 3 -NPs) have unique physicochemical properties, but their anticancer potential in cervical carcinoma remains underexplored. This study therefore estimated the cytotoxic effects of Y 2 O 3 -NPs in HeLa cervical cancer cells and normal HFB4 melanocytes, with mechanistic analyses focused on HeLa cells. Cells were exposed to Y₂O₃-NPs various concentrations and viability was assessed via MTT assay. Mechanistic endpoints; including total ROS generation, mitochondrial membrane potential, DNA damage, apoptotic morphology, and expression of apoptosis- and mitochondria-related genes, were analyzed using fluorescence assays, alkaline Comet assay, nuclear staining, and quantitative RT-PCR. Y 2 O 3 -NPs reduced HeLa cell viability in a concentration-dependent manner with markedly low IC50 value of 52.22 µg/mL (0.231 mM), whereas HFB4 cells were less affected and exhibited markedly greater IC50 value of 264.10 µg/mL (1.169 mM); high selectivity index of 5.06 demonstrating preferential cytotoxicity toward Hela cancer cells. Exposure to the IC50 concentration induced marked ROS overproduction, dramatic mitochondrial depolarization, severe DNA damage, and observable apoptotic nuclear changes in cancerous HeLa cells, accompanied by upregulation of apoptotic p53, anti-apoptotic Bcl-2 , and mitochondrial ND3 gene expression. Conclusion: These findings Y 2 O 3 -NPs exert strong and selective cytotoxic effects against HeLa cervical cancer cells while causing minimal toxicity to normal HFB4 melanocytes. This preferential cytotoxicity appears to be mediated by Y 2 O 3 -NPs–induced oxidative stress, genomic DNA damage, mitochondrial depolarization, and activation of mitochondrial-related apoptotic pathways. Although these results highlight the potential anticancer activity of Y 2 O 3 -NPs, further in vivo studies and detailed mechanistic investigations are needed to confirm their therapeutic efficacy and safety.

Intensive uses of Calcium hydroxide (Ca(OH) 2 NPs), calcium titanate (CaTiO 3 NPs) and yttrium oxide (Y 2 O 3 NPs) nanoparticles increase their environmental release and human exposure separately or together through contaminated air, water and food. However, too limited data are available on their genotoxicity. Therefore, this study explored the effect of Ca(OH) 2 NPs, CaTiO 3 NPs or/and Y 2 O 3 NPs administration on the genotoxicityand oxidative stress induction in mice hepatic tissue. Mice were orally administered Ca(OH) 2 NPs, CaTiO 3 NPs and Y 2 O 3 NPs separately or simultaneously together at a dose level of 50 mg/kg b.w. for two successive weeks (3 days per week). Marked induction of DNA damage noticed after oral administration of Ca(OH) 2 NPs or CaTiO 3 NPs alone together with high Ca(OH) 2 NPs induced reactive oxygen species (ROS) generation and a slight CaTiO 3 NPs induced ROS production were highly decreased after simultaneous coadministration of administration of Y 2 O 3 NPs with Ca(OH) 2 NPs and CaTiO 3 NPs up to the negative control level. Oral administration of Y 2 O 3 NPs alone also did not cause observable changes in the genomic DNA integrity and the ROS generation level compared to the negative control levels. Similarly, significant elevations in P53 gene expression and high reductions in Kras and HSP-70 genes expression were observed only after administration of Ca(OH) 2 NPs alone, while, remarkable increases in the Kras and HSP-70 genes expression and non-significant changes in p53 gene expression were noticed after administration of CaTiO 3 NPs and Y 2 O 3 NPs separately or simultaneously together with Ca(OH) 2 NPs. Conclusion: Ca(OH) 2 NPs exhibited the highest genotoxic effect through oxidative stress induction and disruption of apoptotic (p53 and Kras) and protective (HSP-70) genes expression. Slight DNA damage was noticed after CaTiO 3 NPs administration. However, administration of Y 2 O 3 NPs alone was non-genotoxic and coadministration of Y 2 O 3 NPs with Ca(OH) 2 NPs and CaTiO 3 NPs restored genomic DNA integrity and normal expression of apoptotic p53 and protective HSP-70 genes disrupted by Ca(OH) 2 NPs and CaTiO 3 NPs. Thus co-administration of Y 2 O 3 NPs with Ca(OH) 2 NPs and CaTiO 3 NPs is recommended to counter Ca(OH) 2 NPs and CaTiO 3 NPs induced genotoxicity and oxidative stress.

The Kidneys remove toxins from the blood and move waste products into the urine. However, the accumulation of toxins and fluids in the body leads to kidney failure. For example, the overuse of acrylamide and titanium dioxide nanoparticles (TiO 2 NPs) in many food and consumer products increases human exposure and risks; however, there are almost no studies available on the effect of TiO 2 NPs coadministration with acrylamide on the integrity of genomic and mitochondrial DNA. Accordingly, this study was conducted to estimate the integrity of genomic and mitochondrial DNA in the renal tissue of mice given acrylamide and TiO 2 NPs. To achieve this goal, mice were administrated orally TiO 2 NPs or/and acrylamide at the exposure dose levels (5 mg/kg b.w) and (3 mg/kg b.w), respectively, five times per week for two consecutive weeks. Concurrent oral administration of TiO 2 NPs with acrylamide caused remarkable elevations in the tail length, %DNA in tail and tail moment with higher fragmentation incidence of genomic DNA compared to those detected in the renal tissue of mice given TiO 2 NPs alone. Simultaneous coadministration of TiO 2 NPs with acrylamide also caused markedly high elevations in the reactive oxygen species (ROS) production and p53 expression level along with a loss of mitochondrial membrane potential and high decreases in the number of mitochondrial DNA copies and expression level of β catenin gene. Therefore, from these findings, we concluded that concurrent coadministration of acrylamide with TiO 2 NPs augmented TiO 2 NPs induced genomic DNA damage and mitochondrial dysfunction through increasing intracellular ROS generation, decreasing mitochondrial DNA Copy, loss of mitochondrial membrane potential and altered p53 and β catenin genes expression. Therefore, further studies are recommended to understand the biological and toxic effects resulting from TiO 2 NPs with acrylamide coadministration.

Crude oil pollution of water bodies is a worldwide problem that affects water ecosystems and is detrimental to human health and the diversity of living organisms. The objective of this study was to assess the ability of water hyacinth (Eichhornia crassipes (Mart.) Solms) combined with the presence of magnetic nanoparticles capped with natural products based on Myrrh to treat fresh water contaminated by crude petroleum oil. Magnetic nanoparticles based on magnetite capped with Myrrh extracts were prepared, characterized, and used to adsorb heavy components of the crude oil. The hydrophobic hexane and ether Myrrh extracts were isolated and used as capping for magnetite nanoparticles. The chemical structures, morphologies, particle sizes, and magnetic characteristics of the magnetic nanoparticles were investigated. The adsorption efficiencies of the magnetic nanoparticles show a greater efficiency to adsorb more than 95% of the heavy crude oil components. Offsets of Water hyacinth were raised in bowls containing Nile River fresh water under open greenhouse conditions, and subjected to varying crude oil contamination treatments of 0.5, 1, 2, 3, and 5 mL/L for one month. Plants were harvested and separated into shoots and roots, oven dried at 65 °C, and grounded into powder for further analysis of sulphur and total aromatic and saturated hydrocarbons, as well as individual aromatic constituents. The pigments of chlorophylls and carotenoids were measured spectrophotometrically in fresh plant leaves. The results indicated that the bioaccumulation of sulphur in plant tissues increased with the increased level of oil contamination. Water analysis showed significant reduction in polyaromatic hydrocarbons. The increase of crude oil contamination resulted in a decrease of chlorophylls and carotenoid content of the plant tissues. The results indicate that the water hyacinth can be used for remediation of water slightly polluted by crude petroleum oil. The presence of magnetite nanoparticles capped with Myrrh resources improved the remediation of water highly polluted by petroleum crude oil.