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Curcumin is the primary polyphenol in turmeric’s curcuminoid class. It has a wide range of therapeutic applications, such as anti-inflammatory, antioxidant, antidiabetic, hepatoprotective, antibacterial, and anticancer effects against various cancers, but has poor solubility and low bioavailability. Objective: To improve curcumin’s bioavailability, plasma concentration, and cellular permeability processes. The nanocurcumin approach over curcumin has been proven appropriate for encapsulating or loading curcumin (nanocurcumin) to increase its therapeutic potential. Conclusion: Though incorporating curcumin into nanocurcumin form may be a viable method for overcoming its intrinsic limitations, and there are reasonable concerns regarding its toxicological safety once it enters biological pathways. This review article mainly highlights the therapeutic benefits of nanocurcumin over curcumin.

Obesity is a global health challenge characterized by excessive fat accumulation and associated with life-threatening comorbidities such as type 2 diabetes, cardiovascular diseases, and certain cancers. Conventional treatments, including lifestyle modification and pharmacotherapy, often have limited long-term efficacy and potential side effects, highlighting the need for safer alternatives. Natural bioactive compounds, such as quercetin, a dietary flavonoid with antioxidant, anti-inflammatory, and metabolic regulatory properties, have emerged as promising anti-obesity agents. However, poor bioavailability limits its therapeutic application, prompting the development of nanoformulations. This study therefore estimated the anti-obesity potential of quercetin and nanoquercetin in a high-fat diet (HFD)-induced obesity model in male Wistar rats. Following acute toxicity testing, 36 rats were divided into six groups: non-obese control, obese HFD control, and non-obese or obese rats orally received quercetin or nanoquercetin at 10% of the safe dose daily for four weeks. Outcomes assessed included body weight, lipid profile, serum total protein, genomic DNA integrity, Adiponectin and Leptin gene expression, and histological changes in liver and pancreatic tissues. In non-obese rats, quercetin and nanoquercetin did not affect body weight and genomic DNA integrity but improved lipid profiles. Nanoquercetin additionally increased total protein levels. Both compounds upregulated Adiponectin expression in the liver, with nanoquercetin also enhancing pancreatic Adiponectin expression. Histology revealed preserved tissue architecture. In obese rats, administration of quercetin or nanoquercetin significantly reduced body weight, improved lipid and protein parameters, restored genomic DNA integrity, upregulated Adiponectin , downregulated Leptin , and markedly improved hepatic and pancreatic histological architecture. Nanoquercetin consistently produced more pronounced effects than quercetin.nIn. These findings demonstrate the therapeutic potential of quercetin, particularly its nanoform, as a multi-targeted anti-obesity agent. Its effects on metabolic regulation, genomic protection, and tissue preservation support further preclinical and clinical studies to explore its role as a safe and effective strategy for managing obesity.

Acrylamide is used in the industry and can be a by-product of high-temperature food processing which has toxic potential in various tissues, and titanium dioxide nanoparticles (TiO 2 NPs) are widely used in toothpaste, sweets, food perseveration, chewing gum and medicines. Consequently, humans are daily exposed to large amounts of acrylamide and TiO 2 NPs mainly through food intake. However, limited studies are available on the effect of simultaneously intake of acrylamide and TiO 2 NPs on the integrity of genomic DNA and the induction of apoptosis in brain tissues. Therefore, this study estimated the influence of acrylamide coadministration on TiO 2 NPs induced genomic instability and oxidative stress in the brain tissues of mice. To achieve this, mice were orally administrated acrylamide (3 mg/kg b.w) or/and TiO 2 NPs (5 mg/kg b.w) for two successive weeks (5 days per week). The comet assay results showed that concurrent oral administration of acrylamide and TiO 2 NPs strongly induced single- and double stranded DNA breaks, and that the level of reactive oxygen species (ROS) was also highly elevated within neural cells after simultaneous oral intake of acrylamide and TiO 2 NPs compared to those observed after administration of acrylamide or/TiO 2 NPs alone. Moreover, oral co-administration of acrylamide with TiO 2 NPs increased apoptotic DNA damage to neurons by upregulating the expression levels of P53, TNF-α, IL-6 and Presenillin-1 genes compared to groups administered TiO 2 NPs. Therefore, from these results, the present study concluded that coadministration of acrylamide renders TiO 2 NPs more genotoxic and motivates apoptotic DNA damage and oxidative stress induced by TiO 2 NPs in brain cells, and thus it is recommended to avoid concurrent oral acrylamide administration with TiO 2 NPs.

Pancreatic cancer is a hard-to-treat tumor with a poor prognosis. While traditional pancreatic cancer therapies can be effective, issues like cytotoxicity, low selectivity, and drug resistance still pose major challenges. Nanotechnology has shown promise in improving cancer diagnosis and treatment. Yttrium oxide nanoparticles (Y 2 O 3 -NPs), for example, have demonstrated potent selective cytotoxicity against triple negative breast cancer cells; but their effects on pancreatic cancer cells have not been explored. This study aimed to explore the impact of Y 2 O 3 -NPs on cell proliferation, DNA integrity, and oxidative stress in pancreatic cancer (PANC-1) and human skin fibroblast (HSF) cells. The cytotoxicity of Y 2 O 3 -NPs after 72 h were estimated using Sulforhodamine (SRB) cytotoxicity assay, while alkaline Comet assay was done to study genomic DNA integrity. Generation level of reactive oxygen species (ROS) and integrity of mitochondrial membrane potential were also analyzed. Apoptosis induction was investigated using Flow Cytometry and expression level of apoptotic (p53), anti-apoptotic (Bcl2) and mitochondrial (ND3) genes was measured using quantitative RTPCR. Our findings exhibited that Y 2 O 3 -NPs had strong selective cytotoxicity against PANC-1 cells with an IC50 value of 31.06 µg/ml, while having minimal effect on normal HSF cells (IC50 = 319.21 µg/ml). Treatment of PANC-1 cells with Y 2 O 3 -NPs at the IC50 concentration for 72 h significantly increased intracellular ROS levels and DNA damage, along with a notable reduction in mitochondrial membrane potential. Additionally, a significant rise in necrotic, early, and late apoptotic cells was observed, accompanied by downregulation of the anti-apoptotic Bcl2 gene and upregulation of the apoptotic p53 and mitochondrial ND3 genes. These findings highlight the selective toxicity of Y 2 O 3 -NPs towards cancerous PANC-1 cells, with minimal impact on normal cells. Y 2 O 3 -NPs appear to induce apoptosis in cancer cells by increasing ROS generation, damaging DNA, disrupting mitochondrial function, and triggering cell death. This study suggests that Y 2 O 3 -NPs may be a promising candidate for pancreatic cancer treatment. Further research is needed to fully explore their therapeutic potential.

Calcium hydroxide (Ca(OH) 2 NPs), calcium titanate (CaTiO 3 NPs) and yttrium oxide (Y 2 O 3 NPs) nanoparticles are prevalent in many industries, including food and medicine, but their small size raises concerns about potential cellular damage and genotoxic effects. However, there are very limited studies available on their genotoxic effects. Hence, this was done to investigate the effects of multiple administration of Ca(OH) 2 NPs, CaTiO 3 NPs or/and Y 2 O 3 NPs on genomic DNA stability, mitochondrial membrane potential integrity and inflammation induction in mouse brain tissues. Mice were orally administered Ca(OH) 2 NPs, CaTiO 3 NPs or/and Y 2 O 3 NPs at a dose level of 50 mg/kg b.w three times a week for 2 weeks. Genomic DNA integrity was studied using Comet assay and the level of reactive oxygen species (ROS) within brain cells was analyzed using 2,7 dichlorofluorescein diacetate dye. The expression level of Presenilin-1, tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6) genes and the integrity of the mitochondrial membrane potential were also detected. Oral administration of Ca(OH) 2 NPs caused the highest damage to genomic DNA and mitochondrial membrane potential, less genomic DNA and mitochondrial damage was induced by CaTiO 3 NPs administration while administration of Y 2 O 3 NPs did not cause any remarkable change in the integrity of genomic DNA and mitochondrial membrane potential. Highest ROS generation and upregulation of presenilin-1, TNF-α and IL-6 genes were also observed within the brain cells of mice administrated Ca(OH) 2 NPs but Y 2 O 3 NPs administration almost caused no changes in ROS generation and genes expression compared to the negative control. Administration of CaTiO 3 NPs alone slightly increased ROS generation and the expression level of TNF-α and IL-6 genes. Moreover, no remarkable changes in the integrity of genomic DNA and mitochondrial DNA potential, ROS level and the expression level of presenilin-1, TNF-α and IL-6 genes were noticed after simultaneous coadministration of Y 2 O 3 NPs with Ca(OH) 2 NPs and CaTiO 3 NPs. Coadministration of Y 2 O 3 NPs with Ca(OH) 2 NPs and CaTiO 3 NPs mitigated Ca(OH) 2 NPs and CaTiO 3 NPs induced ROS generation, genomic DNA damage and inflammation along with restoring the integrity of mitochondrial membrane potential through Y 2 O 3 NPs scavenging free radicals ability. Therefore, further studies are recommended to study the possibility of using Y 2 O 3 NPs to alleviate Ca(OH) 2 NPs and CaTiO 3 NPs induced genotoxic effects.

Titanium dioxide nanoparticles (TiO 2 -NPs) have found wide applications in medical and industrial fields. However, the toxic effect of various tissues is still under study. In this study, we evaluated the toxic effect of TiO 2 -NP on stomach, liver, and kidney tissues and the amelioration effect of clove oil nanoemulsion (CLV-NE) against DNA damage, oxidative stress, pathological changes, and the apoptotic effect of TiO 2 -NPs. Four groups of male mice were subjected to oral treatment for five consecutive days including, the control group, the group treated with TiO 2 -NPs (50 mg/kg), the group treated with (CLV-NE) (5% of the MTD), and the group treated with TiO 2 -NPs plus CLV-NE. The results revealed that the treatment with TiO 2 -NPs significantly caused DNA damage in the liver, stomach, and kidney tissues due to increased ROS as indicated by the reduction of the antioxidant activity of SOD and Gpx and increased MDA level. Further, abnormal histological signs and apoptotic effect confirmed by the significant elevation of p53 expression were reported after TiO 2 -NPs administration. The present data reported a significant improvement in the previous parameters after treatment with CLV-NE. These results showed the collaborative effect of the oils and the extra role of nanoemulsion in enhancing antioxidant effectiveness that enhances its disperse-ability and further promotes its controlled release. One could conclude that CLV-NE is safe and can be used as a powerful antioxidative agent to assess the toxic effects of the acute use of TiO 2 -NPs.

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.

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 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.