Therapeutic Perspectives of Metal Nanoformulations
Abstract
:1. Introduction
1.1. Significance of Metals in Human Body
1.2. Major Function of Metals in Human Body
1.2.1. Manganese (Mn)
1.2.2. Iron (Fe)
1.2.3. Cobalt (Co)
1.2.4. Nickel (Ni)
1.2.5. Copper (Cu)
1.2.6. Zinc (Zn)
1.2.7. Gold (Au)
1.3. Size, Shape, Material, and Surface of Nanoparticles
1.4. Major Nanodrug Delivery Systems
1.5. Scopes of Metal Nanoparticles in Remedies
1.6. Major Challenges of Using Nanoparticles in Medical Treatment
2. Therapeutic Applications of Metal NPs
2.1. Therapeutic Interventions of Gold Nanoparticles (Au-NPs)
- Nanotherapeutic Application of Gold
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effect | |||||
Au-nanopopcorn (28 nm) | LNCaP (prostate cancer cells) | 0.5 mL | Popcorn-shaped Au-NPs enhanced Raman intensity to recognize prostate cancer cells. | Prostate and breast cancer | [105] |
Au-NPs | Y79 (MTT analysis) | 1.75, 3.5, 7, 14, 28 and 56 μg/mL | Forty-eight hours after applying Au-NPs, 0.5 to 11 min hyperthermia is applied, which shows 50% cell viability after 4.5 min, but without NPs, 9 min is required to obtain same effect. | Hyperthermia in cancer | [115] |
Au-NS (30 and 60 nm) | MB49 bladder cancer cell line in mice | 0.1 nM | Synergistic immuno photo nanotherapy (SYMPHONY) produce better survival than other groups. In photo thermal monotherapy Au-NPs has much efficiency than nanoshells. | Bladder cancer | [117] |
Silica coated Au nanorods | Mammary carcinoma cells | - | Showed efficient in vivo and in vitro antitumor activity in targeting CD44+ receptor. | Breast cancer | [118] |
DOX@ Au-NPs (2 nm Au-NPs) | Breast Cancer Cell lines (MCF-7 and MDA-MB-231); Murine Mammary 4T1; CD-1 Mice | 5 mg/kg dose | Good renal clearance with fruitful targeting. Decreased normal tissue toxicity with improved antitumor efficacy. | Breast cancer | [119] |
PDC-PEG-Au-NPs (25–50 nm GNPs) | Murine lymphoma cells (A20) | Up to 50 µM dose | Half-life of drug increased, toxicity observed in targeted cells, and effective for a long time. | Anticancer | [120] |
BLM-DOX-PEG-Au-NPs (13 nm GNPs) | HeLa, cervical cancer cell line | 10–100 nM dose | Cancer cell environment-mediated drug release and improve EC50 | Cervical cancer | [121] |
Au-nanostars (Au-NS) (30 and 60 nm) | Glioblastoma model on mice | 0.1 nM | 7.2% ID/g uptake of Au-NPs in the brain tumor, which is identified by PET/CT scan. | Brain tumor | [127] |
Chitosan/Au-NPs | HepG-2 and Caco-2 cell lines | 0.1, 0.05, 0.025, 0.0015 mg/mL | Cancer cell proliferation is inhibited more than chitosan. | Cancer and bacterial infection | [128] |
NP-based nucleic acid conjugates Au@GO NP-NACs | Result identified by in vitro microfluidic models. Bcl-2 | 100 μg/mL of Au-NPs | Better live cancer cell identification by SERS and synergistic and specific killing of cancer cells. | Anticancer | [129] |
Cancer-targeting peptide-functionalized NP (3.52 nm) using Au-NPs (26.2 nm) and TA-peptide complex | MCF-7 and T47D (breast cancer cell lines), on tumor containing mice | - | Targeted cell death by apoptosis. Considerable hemocompatibility, higher release of cytochrome c, and higher antitumor activity is found. | Breast cancer | [130] |
Chitosan coated Au-nanospheres | RAW264.7 cells | IC50 value 127 μM | This study compares the cellular uptake of Au-NPs and found that Stars < rods < triangles (lowest to highest uptake order). The mechanism of cellular uptake was endocytosis. Au-NP nanorods showed greater cellular uptake and high cytotoxicity against RAW264.7 cells. | Anticancer | [131,132] |
Chitosan coated Au-NS | IC50 value 81.8 μM | ||||
Chitosan-coated Au-nanorods | IC50 value 22.7 μM | ||||
Au-NPs | Osteosarcoma mouse model | - | Au-NPs with CD133 and hyaluronic acid increased the photo thermal antitumor therapy. HA can gourd the photosensitive drugs from photo-degradation and inhibited the proliferation of osteosarcoma cells. | Bone cancer | [133] |
Au-NPs covered with multivalent hydrocarbon. (6.9 ± 2.9 nm) | Xenograft mouse model with the HeLa, SCC7, and SKBR3 cancer cell lines | 100 nM–10 mM | Tumor growth was considerably suppressed in C18@F127 injected in xenograft mice compared with the control group. | Breast cancer | [134] |
Anti-HER2 functionalized Au-on-silica nanoshells | RAW 264.7 cells | LD50: 1 mg/mL and 10 µg/mL for cationic carrier. | Targeted action; precisely eliminating cancer cells while protecting healthy tissues | Breast cancer | [135] |
Au-NPs produced from Enterococcus sp. | Colorectal tumor cells (HT-29) | 5–24 μg/mL | Inducing ROS and caspase-3 expression, weakening the potential of mitochondrial membrane. | Anticancer | [136] |
PTX-TNFα-PEG-Au-NPs (32.6 nm) | Ovarian cancer cell line (A2780); B16/F10 tumor induce C57BL/6 mice | 2.5 mg/kg dose | Specific delivery of NPs to tumor and improved efficacy | Ovarian cancer | [137] |
DOX-PEG-Au-NPs (41 nm Au-NPs) | Ovarian cancer cell line (A2780); CD-1 mice | 6 mg/kg dose | Significantly reduced normal tissue toxicity | Ovarian cancer | [138] |
CIS-GLC-PEG-Au-NP (20 nm GNPs) | Skin cancer cell line A-431; A-431 cell line bearing mice | 10 mg/kg dose; 25 Gy at 6 MV | Same type effect to free cisplatin; improved result when used in combination with radiation | Skin cancer | [139] |
Alginate conjugate with Au-NPs and CIS (44 nm NP) | Cervical cancer cell line (KB) | 20 µg/mL dose of Au-NP along with 5 µg/mL CIS; 4 Gy at 6 MV | ACA and radiotherapy found increased efficacy over cisplatin and radiation. Using photothermal therapy further enhanced the anticancer effect. | Cervical cancer | [140] |
5-FU/GSH-GNPs (9–17 nm Au-NPs) | Colorectal cancer cell lines (isolated frompatients) | 0.5–1.5 mg/mL dose | Better anticancer effect, and minimized the drug doses as a result. | Colorectal cancer | [141] |
Cs-Au-NPs-DOX (21 nm GNPs) | MCF-7, Breast cancer cell line | 0.05–0.3 mM dose; 0.5, 1, and 3 Gy at 6 MV | Improved test results, decreased survival fraction, upregulated apoptosis, and DNA damage. | Breast cancer | [142] |
Au-NP-PEG-RGD; CIS (10 nm Au-NPs with 435 nM CIS) | MDA-MB-231, Breast Cancer Cell line | 0.3 nM dose; 2 Gy at 6 MV | Increased efficacy of treatment compared to cicplatin or radiation alone. | Breast cancer | [143] |
Au-NP-PEG-RGD; DTX (17.2 nm GNPs) | Breast Cancer Cell line (MDA-MB-231) and Cervical Cancer Cell line (HeLa) | 0.2 nM Au-NPs with 50 nM DTX; 2 Gy at 6 MV | Greater retention of Au-NPs due to cell synchronicity induced by DTX. Synergistic therapeutic action observed when Au-NPs and DTX were combined. | Breast cancer | [144] |
Antimicrobial Effects | |||||
Gold-chitosan hybrid NPs (16.9 nm) | Tested against the S. aureus (Gram-positive) P. aeruginosa (Gram-negative) bacteria | 0.25 mg/mL | The action is still not clear. | Bacterial infection | [145] |
Au-NPs (17 nm) | HIV-1 | 0.05–0.12 mg/mL | Au-NPs inhibits HIV-1 but its mechanism is unknown. | Viral infection | [146] |
Au-NPs (25 nm) | Candida sp | 16–32 μg/mL | Cell death for intracellular acidification by the inhibition of H+ ATPase. | Fungal infection | [147] |
IgG-Au-NPs (32 nm) | MRSA cultures | 1–50 mg/L | 6.25% minimum inhibition concentration (MIC) for the Ig-Au-NPs, while 25% MIC was found for Au-NPs alone. | Methicillin-resistant Staphylococcus aureus (MRSA) infection | [148] |
Miscellaneous Effects | |||||
Au-NPs/chalcones conjugate (2 to 12 nm) | HEK293 cells | 20–100 µg/mL | Therapeutic development of antidiabetic drug, which is derived from H. foetidum by increasing glucose uptake and no particle shows cytotoxicity against HaCaT keratinocytes. Helichrysetin is a potential compound for antidiabetic effect. | Antidiabetic | [149] |
Au-NPs/chalcones conjugate (2 to 12 nm) | α-amylase and α-glucosidase enzyme | 20–100 µg/mL | Potential enzyme inhibitory activities against α-amylase and α-glucosidase enzymes. | Enzyme inhibition | [149] |
Au-NPs | pBR322 (plasmid DNA) | 64 ng/mL (nanogram) | γ-ray radiation applied by HDR brachytherapy, ROS (reactive oxygen species) formation and DNA breaks occurred in positive charged Au-NPs but not in negative charged Au-NPs. | Plasmid DNA damage | [150] |
SPIO-Au-NPs (FeO-Au) core-shell NPs | PC-12 cells (Neuron like cell) | 127 μg of SPION-Au-NPs | Shows higher intracellular interaction with PC-12 neuron-like cells. | Neuroregenaration | [151] |
Synergistic Immuno Photothermal Nanotherapy (SYMPHONY) 30, 60 nm | Tumor cell treated | 0.05 nM NPs with radiation | In murine animal models, it provides a ‘cancer vaccine’ effect that leads to immunologic memory and inhibits cancer recurrence. | Photoimmunotherapy | [152] |
Peptide-coated Au-NPs | Human peripheral blood mononuclear cells | 12.5–50 µg/mL | Efficiently suppressed TLR signaling and shielded mice from LPS-induced acute lung injury. PPIs and the recently found that Au-NPs-based TLR inhibitors have comparable modes of action. | Acute Lung Injury | [153] |
2.2. Therapeutic Interventions of Silver Nanoparticles (Ag-NPs)
- Nanotherapeutic Application of Silver
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effects | |||||
Ag-NPs (5–20 nm) | MCF7-FLV cell line | 136 µM | Cytotoxic effects against breast cancer. | Breast Cancer | [70] |
Ag-NPs (26.18 nm) | Human alveolar cancer cell line: A549 | 87 and 41 µg/mL | Activity against the A549 cell line without showing any damage in noncancer cells. | Alveolar cancer | [162] |
Ag-NPs (50–70 nm) | Human acute T cell leukemia cell line | 10 to 50 µM | Cytotoxic activity against leukemia. | Leukemia | [163] |
Ag-NPs (33 nm) | Human cervical cancer cells (HeLa) | 10 to 50 µg/mL | Induced cytotoxicity in HeLa cells in a concentration-dependent manner. | Cervical cancer | [164] |
Ag-NPs (24–150 nm) | HCT-116 cells colon cancer cell | 100 µg/mL | The sub-G1 phases of the cell cycle were changed, and larger levels of fragmented DNA were discovered. | Colon cancer | [165] |
Ag-NPs (6 nm) with gemcitabine (GEM) | Human ovarian cancer cell line A2780 | 50% inhibitory concentration (IC50) of GEM and Ag-NPs after a 24 h exposure was 100 and 90 nM | Lowering cell viability and proliferation, as well as increasing LDH leakage and ROS production. | Ovarian cancer | [166] |
Ag-NPs (2.8 and 18 nm) | PANC-1 and hTERT-HPNE | 1.67 μg/mL for 2.8 nm size and 26.81 μg/mL for 18 nm size | Ag-NPs triggered programmed cell death in PANC-1 cells, including apoptosis and necroptosis, as well as autophagy and mitotic catastrophe, in a concentration- and size-dependent manner. | Pancreatic ductal adenocarcinoma | [167] |
Ag-NPs (60 nm) | MG63 osteosarcoma cell line | 81.8 ± 2.6 and 75.5 ± 2.4 µg/mL | Chromatin condensation causes dose-dependent cytotoxicity and ultimately cell death. | Osteosarcoma | [168] |
Ag-NPs (lesser than 50 nm) | Pleomorphic hepatocellular carcinoma (SNU-387), hepatic ductal carcinoma (LMH/2A), morris hepatoma (McA-RH7777), and novikoff hepatoma (N1-S1 Fudr) cell lines | 477, 548, and 605 µg/mL | In the presence of Ag nanoparticles, the liver malignant cells viability decreased. | Liver cancer | [169] |
Ag-NPs (30 to 90 nm) | A431 human skin cancer cells | 64.2 µg/mL | Showed a high level of cytotoxicity against the A431 cell line. | Skin cancer | [170] |
Ag-Cys-NPs | Glioma and neuroblastoma cells | 100 and 1000 ng/mL | Ag-Cys-NPs is about 10-fold potent than the Cu-NPs for SH-EP 1 cells and Ag-Cys-NPs is 20 folds more potent than Cu-NPs for glioma cells. | Anticancer | [171] |
Antibacterial Effects | |||||
Ag-NPs (10 nm) | Vibrio cholerae | 40 μg/mL | Antibacterial efficacy of microbial GLP-capped Ag-NPs against V. cholerae. | Cholera | [172] |
Ag-NPs (70 nm) | Microbacterium tuberculosis, H37Rv | 6.25–50 mM | Mild growth-inhibitory effect. | Tuberculosis | [173] |
Ag-NPs (12.62–27.45 nm) with imipenem | Klebsiella pneumoniae clinical strain | Concentration below 3 mg/L | The antibacterial properties of AgNPs in conjunction with imipenem were extended against IRKP infection. | Pneumoniae | [174] |
Antiviral Effects | |||||
Ag-NPs (10 nm) | SARS-CoV-2 | 1–10 ppm | Inhibiting extracellular activity of SARS-CoV-2. | COVID-19 | [154] |
Ag-NPs (30–50 nm) | HeLa-CD4-LTR-β-gal cells, MT-2 cells, human PBMC | 3.9 ± 1.6 mg/mL against HeLa-CD4-LTR-β-gal cells, as 1.11 ± 0.32 mg/mL applied against human PBMC, and 1.3 ± 0.58 mg/mL used against MT-2 cells. | HIV particles are turned inactive quickly, allowing for early disruption of the viral replication cycle. | HIV | [155] |
Ag-NPs (3.5, 6.5, 12.9 nm)/Ch composite | H1N1 influenza A virus | 250 μL Ag NP/Ch composite suspension | Antiviral activity against H1N1 influenza. Provides a concentration-dependent effect. | Influenza | [175] |
Ag-NPs (13, 33 and 46 nm) | HSV-1 and HSV-2 | 2.5 µL | Vero cell infection by HSV-1 and HSV-2 is downregulated in a dose-dependent manner. | Herpes | [176] |
Ag-NPs (10 nm) | HepAD38 cell line | 5 to 50 µM | Suppressing HBV RNA and extracellular virions generation in vitro. | Hepatitis B | [177] |
Ag-NPs (70–95 nm) | Chikungunya virus (CHIKV) | 31.25 μg/mL | By inhibiting the cytopathic impact, showing excellent efficacy against CHIKV. | Chikungunya | [178] |
Ag-NPs (100 nm) | Serotype DEN-2 | 20 μL/mL | Plaque assay estimates of dengue virus output were lowered. | Dengue | [179] |
Miscellaneous Effects | |||||
Ag-NPs (37 nm) | Propionibacterium acnes | 3.1 µg/mL | The mechanism of silver colloid particles bactericidal action on bacteria is still being investigated. | Acne | [180] |
Ag-NPs (37 nm) | Malassezia furfur | 25 µg/mL | Antifungal activity was highest against M. furfur. | Dandruff | [180] |
Ag-NPs (53 nm) | α-amylase and α-glucosidase | 54.56 and 37.86 mg/mL | Inhibition of carbohydrate digestion enzymes, for example α-amylase and α-glucosidase, was effective. | Diabetes | [181] |
FA-Ag-NPs | Murine macrophage cells (RAW264.7), mice, age: 7–8 weeks. | 0.652 nmol/kg | Rheumatoid arthritis treatment was performed by simultaneously M1 macrophage apoptosis and M1-to-M2 macrophage re-polarization. | Rheumatoid arthritis | [182] |
Ag-NPs-PADM hydrogel (PADM = porcine dermal extracellular matrix), 5 and 50 nm | Rat, age: 6-month, weight: 200–300 g | 20, 50, and 80 µg/mL | In vivo, Ag-NPs-PADM hydrogel enhanced angiogenesis and repaired infected skin defects. | Skin infection defect | [183] |
Ag-NPs 20–35 nm | Rat model | Orally administered Ag-NPs concentrations of 175 and 350 ppm | Ag NPs have a gastroprotective effect in rats against ethanol-induced gastric ulcer. Superoxide dismutase (SOD) and catalase (CAT) activities were increased by Ag NPs. | Gastroprotective | [184] |
2.3. Therapeutic Interventions of Copper Nanoparticles (Cu-NPs)
- Nanotherapeutic Application of Copper
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effect | |||||
Cu-NPs/CS-Starch (5–7 nm) | TPC1, BCPAP and FTC133 | 207 µg/mL | TPC1, BCPAP, and FTC133 cell lines shown substantial antihuman thyroid activity. | Thyroid cancer | [95] |
Cu-NPs (62.7 nm) with albumin | MDA-MB 231 cell line | 70 µM | Suppressed cancer cell viability while being less harmful to normal cells. | Breast cancer | [190] |
Cu-NPs (4.7 to 17.4 nm) | HepG2 cells | 19.88 µg | HepG2 cells have a high cytotoxic activity. | Hepatic cancer | [193] |
Cu-NPs (4.7 to 17.4 nm) | Caco-2 cells | 11.21 µg | Inhibition of Caco-2 cell growth. | Colon cancer | [193] |
Cu-NPs (10–20 nm) with chitosan | UM-UC-3 (Transitional cell carcinoma), SCaBER (Squamous cell carcinoma), and TCCSUP (Grade IV, transitional cell carcinoma) | 238, 404, and 569 µg/mL | Cytotoxic activity against common bladder cancer cell lines in humans. | Bladder cancer | [195] |
Cu-NPs (39.3 ± 5.45 nm) | Human skin carcinoma cells (B16F10) and mouse embryonic fibroblast cell line (NiH3T3) | 40 and 120 μg/mL | Mice showed potential suppression of B16F10 melanoma cell proliferation and tumor development inhibition. | Melanoma | [196] |
Cu-NPs (12–16 nm) | Human lung carcinoma cells (A549) | 20–100 µg/mL | In a dose-dependent way, lung cancer cells showed extensive structural damages and increased oxidative stress indicators. | Lung carcinoma | [197] |
Bimetallic CuFe (copper–iron) PBA and CoFe (cobalt–iron) PBA NPs | Tumor tissues for in vitro and BALB/c mice for in vivo test | 5, 10, 20, 40, 80, and 160 μg/mL | Prussian blue analogs (PBA-DDSs) prepared with metal NPs doxorubicin (DOX) delivery and pH-controlled release development. | Breast cancer | [198] |
Cu-NPs (15 ± 1.7 nm) | HeLa, A549, and BHK21 cell lines | 120 µM | Caused the death of tumor/cancer cells through apoptosis. | Antitumor | [199] |
Cu-NPs with chitosan (˂20 nm) | CHO cells and MC3T3-E1 preosteoblast cells | 1–1000 µg/mL | A higher degree of mitochondrial ROS production. | Osteosarcoma | [200] |
CuHARS (20–80 nm) | Cell line of a glioma tumor | 20 μg/mL | CuHARS decreases the glioma cell and BMVECs viability 20% and 200% respectively. Immune supportive by the production of NO. | Antitumor and immunomodulatory | [201] |
Antiviral Effects | |||||
Cu-NPs (20 nm) | SARS-CoV-2 | 500 μL | By putting virus-containing media onto copper-coated PP filters and then adding Vero cells, inactivation was assessed. | COVID-19 | [189] |
Cu-NPs (13.5 ± 0.6 nm) | Culex quinquefasciatu, Anopheles stephensi, and Aedes aegypti | 500 µg/mL | A mortality rate that was dosage and time dependent. | Chikungunya | [191] |
Cu-NPs (132 nm) | Aedes aegypti larvae | 55.12 mg/mL | Assessing the larvicidal efficacy of Aedes aegypti. | Dengue | [192] |
Miscellaneous Effects | |||||
Cu-Epigallocatechin-3-gallate (Cu-EGCG) | Female Sprague rats | 50, 100, 200 μg/mL | Inhibited bacteria such as E. coli and S. aureus to protect from wound infection. | Wound healing | [56] |
Cu-NPs (30 and 50 nm) | Streptomyces griseus | - | Nanocopper has the potential to be an effective new fungicide. | Red root-rot disease | [185] |
Cu-NPs (12–16 nm) | - | 10 µg/mL | Inhibitory actions of glycosidase in vitro. | Antidiabetic | [188] |
Cu-NPs (100 nm) | Fusarium equiseti F. oxysporum and F. culmorum | 25, 20 and 19 mm | Exhibited antifungal efficacy against F. oxysporum. | Crop diseases | [194] |
Cu-NPs (spherical 2.88 ± 0.94, triangular 1.27 ± 0.37 and hexagonal 1.81 ± 0.52 nm) | Cultured porcine ovarian granulosa cells | 1, 10, or 100 ng/mL | The ability to influence viability, proliferation, apoptosis, and the release of steroid hormones. | Reproductive disorders | [202] |
Cu-NPs (17 and 41 nm) | T. gondii tissue cysts | 0.2 and 0.3 mL/kg and in combined with atovaquone (100 mg/kg) | Infected mice with T. gondii had substantial prophylactic effects when combined with atovaquone. | Toxoplasmosis | [203] |
CuHARS (polymer-coated copper cystine high-aspect ratio structures); 60–100 nm | Escherichia coli and Staphylococcus epidermidis | 5 μg | NO production facilitates antimicrobial action of CuHARS. | Antibacterial | [204] |
CuO.MBGs; Mesophorus bioactive glasses (MBGs) (10–20 nm) | In vitro simulated body fluid (SBF) | 5% of CuO NPs in MBG | Outstanding biomaterial for bone regeneration. MBGs released therapeutic amounts of Ca2+ and Cu2+ ions. | Bone defect | [205] |
CuS incorporated hyaluronic acid (injectable hydrogel); average 35 nm | SD male rats; weight range 200∼220 g | 200, 100, 50, 20, and 10 μg/mL | Improved wound healing and angiogenesis occur. | Wound healing | [206] |
2.4. Therapeutic Interventions of Zinc Nanoparticles (Zn-NPs)
- Nanotherapeutic Application of Zinc
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effects | |||||
ZnO-NPs (16–19 nm) | Breast cancer cell (MCF7), and Lung Cancer cell (A549) | 31.2 μg/mL | The cell viability is reduced by NPs, which induces cytotoxicity in cancerous cells. | Anticancer | [213] |
ZnO-NPs (100 nm) | Human Breast Cancer (MCF-7) cells | 10 μg/mL | Apoptosis is provoked and induced through an intrinsic mitochondrial pathway, depending on caspase activation. | Anticancer | [214] |
ZnO (36.91 ± 1.21 nm), ZnO@Ce6 (47.75 ± 0.05 nm) and ZnO@Ce6-PDA (51.92 ± 1.96 nm) | HeLa cells | 30 μg/mL | Photothermal and photodynamic action, and increased the cell viability by more than 90%. | Anticancer | [215] |
ZnO-NPs (30.4–40.8 nm) | MCF-7 cell line; (Breast cancer cell line) | 25 μg/mL | The growth of Gram-positive Bacillus licheniformis is inhibited, reducing the viability of MCF-7 cells. | Breast cancer | [216] |
ZnO-NPs (30.4–40.8 nm) | MCF-7 cell line; (Breast cancer cell line) | 25 μg/mL | The growth of Gram-positive Bacillus licheniformis is inhibited, reducing the viability of MCF-7 cells. | Breast cancer | [216] |
ZnO-NPs (66.25 nm) | MDA-MB 231 and MCF-7 breast cancer cell lines. | 0.1, 0.05 and 0.01 M | The activity of MDA-MB 231 cells is inhibited with increased concentration. | Breast cancer | [217] |
ZnO-NPs (10–15 nm) | MCF-7 cell lines | 15.88 μg/mL | Inducing apoptosis in MCF-7 cell line via the Caspase-8 and p53 pathway. Cancer cells may develop and spread throughout the body as a result of mutations (changes) in the p53 gene. | Breast cancer | [218] |
PBA-ZnO (<40 nm) | MCF-7 cell lines | 35 and 50 μg/mL | Cell death by apoptosis was induced in the MCF-7 cell line by enhancing oxidative stress and mitochondrial damage. | Breast cancer | [219] |
ZnO-NPs (10–70 nm) | MCF-7 cell lines | 50 μg/mL | Inhibiting apoptosis. | Breast cancer | [220] |
Zn-Fe2O4-NPs (17.12 nm) | MCF-7 cell lines | 25–500 µg/mL | Decrease in cell viability by cytotoxic activity. | Breast cancer | [221] |
ZnO-NPs (31.5 nm) | MCF-7, MDA-MB-231, and HFF cell lines. | 11.16 μg/mL | Reduction of the expression of micro-RNAs. | Breast cancer | [222] |
Triton-X modified ZnO-NPs (13.45 ± 1.42 nm) | Breast cancer cell line (MDA-MB-231) and normal cell line (NIH 3T3) were used. | 55.24 μg/mL | Cytotoxicity is enhanced through surface modification. | Breast cancer | [223] |
PEG-ZnO-NPs (150 nm) | DMEM medium (HiMedia) | 6.25–37.5 μg/mL | The impairment of DNA damage repair enzyme NEIL2 by inducing apoptosis in breast cancer cells through ROS. | Anticancer | [224] |
MSN-ZnO-Au-NPs (76.5 ± 11.8 nm) | Breast cancer cells (MCF-7: estrogen receptor-positive, CAL51: triple-negative). | 25 µg/mL | The viability of all cell lines is reduced. | Resistant breast cancer | [225] |
ZnO-NPs (12–14 nm) | MDA-MB 231 cancer cells. | 7.103 μg/mL | Decreasing cell viability by cytotoxic impact. | Breast cancer | [226] |
ZnONPs (25–40 nm) | Michigan Cancer Foundation-7 [MCF7], and murine (TUBO) breast cancer cell lines | 8, 4, and 2 µg/mL | Inducing apoptosis by increasing the concentration of ZnO-NPs. | Antitumor | [227] |
Zn-NPs (9–17 nm) | MCF-7 (breast carcinoma cell line), HCT-116 (colon carcinoma cells) | 3.9, 7.8, 15.6, 31.25, 62.5, 125, 250 and 500μg/mL were used. | For MCF-7, concentrations of 373 μg/mL and >500 μg/mL and for HCT-116, concentrations of 226 and 317 μg/mL were found effective in the in vitro test. | Antitumor | [228] |
Antibacterial Effects | |||||
ZnO-NPs (2–28 nm) | Psedomanas sp., Fusarium sp. | 0.1 M | Bacterial membranes are disrupted by the formation of ROS, for example superoxide and hydroxyl radicals. | Bacterial and fungal infection | [229] |
ZnO-NPs (45–150 nm) | Helicobacter pylori and human mesenchymal stem cells (hMSc) | 3.125–100 μg/mL | Biocompatibility to hMSC and described as safe in mammalian cells and can be used as antibiotics. | Antibacterial | [230] |
RF-contained Zn2+ ion-cross-linked SA-g-AA-M PNPs. <300 nm | Vero cells | 100 µg/mL | The gene transcription is inhibited by inhibiting the β-subunit of the bacterial RNA polymerase. | Tuberculosis | [231] |
ZnO-NPs (125 nm) | Streptococcus mutans | 3.90–4000 μg/mL | Bacteriostatic and bactericidal effects. | Microbial infection | [232] |
ZnO-NPs (12 nm) | Staphylococcus aureus and Escherichia coli | 5.6 µg/mL | The ROS production was increased, while the cellular function and cell membrane were disrupted. | Bacterial infection | [233] |
MgZnO-NPs/PU (52.65 ± 2.58 nm) | E. coli, DH5α strain | 9 × 10−5 CFU/mL | The damage of the structure and function of cell originals (mesosome), consequently affecting the deoxyribonucleic acid (DNA) replication by promoting ROS. | Bacterial infection | [234] |
ZnO-NPs (20–45 nm) | Ciprofloxacin | 500, 1000, and 2000 µg/mL | Increasing antimicrobial activity of ciprofloxacin. | Bacterial infection | [235] |
ZnO-NPs (80.1–90 nm) | Staphylococcus aureus, Salmonella Typhimurium, Bacillus cereus and Pseudomonas aeruginosa | 0.05 and 0.5 mg/L | ZnO NPS were used in packaging that increased safety against microbes as well as food shelf-life by inhibiting bacterial growth. | Bacterial infection | [236] |
ZnO-NPs (30 nm) | Campylobacter jejuni | 0.025, 0.03, 0.04, 0.05, and 0.10 mg/mL | Damaging membrane integrity by increasing cell membrane permeability. | Bacterial infection | [237] |
ZnO-NPs (60–70 nm) | S. aureus and P. aeruginosa and standard strain of E. coli. | 1028, 516, 256, and 125 µg/mL were used. | Producing of reactive oxygen species (ROS) is caused disruption of bacterial membranes. | Bacterial infection | [238] |
ZnO-NPs (≈66 nm) | Eel kidney cell line (EK-1). | 15.75, 31.5, and 3.15 µg/mL | Decreasing cell viability and growth rate of microorganism. | Microbial infection | [239] |
ZnO-NPs (15 nm) | S. pneumoniae | 12 μg/mL | Reducing in microbial biofilm formation. | Bacterial infection | [240] |
Antifungal Effects | |||||
ZnO-NPs (12–14 nm) | Aspergillus and Penicillium | 5, 10, 15, 20, and 25 g/mL | Cell membrane is damaged and growth rate is inhibited by interaction of zinc ion with cell membrane. | Fungal infection | [226] |
ZnO-NPs (35–129 nm) | Candida parapsilosis | 15.65 µg/mL | Growth is inhibited and surface damage is pronounced. | Fungal infection | [236] |
ZnO-NPs (70 ± 15 nm) | Botrytis cinerea and Penicillium expansum | 0, 3, 6, and 2 mmol/L | Fungal hyphae is deformed, while development of conidiophores and conidia are prevented. | Fungal infection | [241] |
ZnO-NPs (430 nm) | Candida albicans, A. niger and A. terreus. | 30, 60, and 90 µL | Leading to the death of fungal hyphae by deforming of fungal hyphae. | Candidiasis, athlete’s foot, mycosis, and ring worm | [242] |
ZnO-NPs | Candida albicans | 5, 10, 15, and 20 mg/mL | Producing reactive oxygen species (ROS), for example hydrogen peroxide, superoxide anion, hydroxyl radical, and hydroxyl ion. | Fungal infection | [243] |
ZnO-NPs (76.15 nm) | Alternaria alternata, Botrytis cinerea, Aspergillus niger, Penicillium expansum, and Fusarium oxysporum. | 256 µg/mL | Disruption of fungal membrane and inhibition of fungal growth. | Fungal infection | [244] |
ZnO-NPs (27 ± 5 nm) | Aspergillus flavus and Aspergillus niger | 25 μg/mL | Inhibiting the growth of fungus. | Fungal infection | [245] |
ZnO-NPS (60 nm) | Trichophyton mentagrophyte, Microsporum canis, Candida albicans, and Aspergillus fumigatus | 40 mg/mL | Inhibiting the growth of fungus. | Ring worm | [246] |
ZnO-NPs (≤50 nm) | Aspergillus fumigatus Fungus and Candida Albicans | 3, 6, and 12 mL/L | Lowering the growth rate of fungus. | Fungal infection | [247] |
ZnO-NPs (13.92 nm) | Alternaria alternata | 20–160 mg/L | The mycelia growth is inhibited. | Early blight disease | [248] |
CS–Zn-CuNCs (16.6–100 nm) | A. alternata, R. solani, and B. cinerea | 90 µg/mL | Inhibiting growth by in vitro application. | Fungal infection | [249] |
Antidiabetic Effects | |||||
ZnO-NPs (≤10 nm) | Streptozotocin-induced type 1 and 2 diabetic rats | 1, 3, and 10 mg/kg | Glucose tolerance was improved, higher serum insulin (70%) and blood glucose (29%) was reduced. Nonesterified fatty acids and triglycerides was also reduced. | Diabetes | [250] |
ZnO-NPs (80–100 nm) | Diabetic rats | 1, 3, and 10 mg/kg | Glucose disposal, insulin levels, and zinc status are increased. | Diabetes | [251] |
ZnO-NPs (10 to 20 nm) | Alpha-amylase | 13.085434 μg/mL | The activity of α-amylase is inhibited. | Diabetes | [252] |
ZnO-NPs (<100 nm) | Mice | 8 and 14 mg/kg | Decreasing blood glucose. | Diabetes | [253] |
ZnO-NPs (22.6 nm) | Wistar rats | 70 mg/kg | Hyperlipidemia is controlled through lowering the levels of lipids and lipoproteins in the blood plasma. | Diabetes | [254] |
ZnO-NPs | Albino rats | 10 mg/kg | Ameliorative effect. | Diabetes | [255] |
Miscellaneous Effects | |||||
Zn-NPs (1–100 nm) | Layer chicks | 30 ppm | Increasing the level of serum glucose and alkaline phosphate, while decreasing alanine transferase. | Increased chicken growth rate | [212] |
ZnO-NPs (48.2 nm) | Xanthomonas oryzae | 16.0 µg/mL | The bacterial membrane is collapsed and ruptured by interacting with ZnO NPs and as a result in the leakage of bacterial cytoplasm. | Leaf blight | [256] |
ZnO-NPs (≤40 nm) | Rats | 10 mg/kg | Heart injury is induced by ionizing radiation (IR). | Cardiovascular disorders | [257] |
Zn-NPs (50–100 nm) | Swiss albino rats | 10 mg/kg | Controlling blood glucose level. | Testicular diabetic complications | [258] |
Vacuoles-ZnAA-NPs (AA = ascorbic acid) | B16F10 (KCLB 80080) cells. Used African–American, Asian, White donors’ tissues. | ZnAA-Vac treated for 12 days at 100 and 1000 ppm | It had a stronger depigmenting impact, reducing the melanin hue by 75%. | Melanin treatment | [259] |
2.5. Therapeutic Interventions of Nickel Nanoparticles (Ni-NPs)
- Nanotherapeutic Application of Nickel
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effect | |||||
DPMC-Ni-NPs (55 nm) | MCF-7, HepG2, A549, NHDF, and MTT cell lines | 25, 22.47, 25.11 and 64.23 μg/mL concentration were used. | Cytotoxicity against breast cancer cell line (MDA-MB-231) was concentration dependent. | Breast cancer | [224] |
Ni-NPs (1–100 nm) | Leukemia cancer cells | - | Increasing cell membrane permeability and promoting intracellular absorption in cancer cells. | Anticancer | [261] |
Qu–PEG–Ni-NPs (48–72 nm) | MCF–7 cells | 6.25 and 50 µg/mL | Mitochondrial-mediated apoptosis is induced through ROS overproduction. | Breast cancer | [262] |
Ni-NPs@F. officinalis (16.85–49.04 nm) | PA-1, SK-OV-3, Caov-3, and SW-626 cell lines were used | 375, 225, 246, and 279 µg/mL | Reducing viability of malignant ovarian cell line. | Ovarian cancer | [265] |
NiO-NPs (5.46 nm) | Human lung cancer cell line (A549) | 93.349 μg/mL | Cytotoxicity is exhibited. | Lung cancer | [267] |
Nickel-Ferrite (NiFe2O4) nanorod, rosemary leaves used to prepare NPs, 40–200 nm | Human breast cancer (MCF-7) cell lines were used. | 2, 4, 8, 16, 32, 64, 128, 256 and 512 μg/mL | NiFe2O4 NP had cytotoxicity effect on MCF-7. | Anticancer | [272] |
Antibacterial Effects | |||||
Ni-NPs (30 nm) | Pseudomonas aeruginosa, Staphylococcus aureus, and Klebsiella sp. | 2.5, 5, 10, 15 and 20 μg/mL | Penetrating the bacteria and damaging them by interacting with phosphorous- and sulphur-containing compounds such as DNA. | Bacterial infection | [263] |
NMMNPs (300 to 800 nm) (NMMNPs = nickel magnetic mirror nanoparticles) | S. aureus and E. coli in S. aureus | 0.01 g | Bacterial growth is inhibited and bacteria are killed. | Bacterial infection | [264] |
NiGs-NPs (12–36 nm) Gs:green synthesized | K. pneumoniae, E. coli, S. typhi, B. subtilis, and S. epidermidis | 25–100 μg/mL | Induced ROS generation. | Bacterial infection | [270] |
Ni-NPs (0.5 nm) | Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, Vibrio cholerae, and Proteus vulgaris. | 1–0.125 mg/mL | Microbial growth inhibition. | Bacterial infection | [273] |
Ni-NPs (40–80 nm) | Escherichia coli | 21, 29 and 36 μΜ | Growth is inhibited. | Bacterial infection | [274] |
Ni-NPs (10 nm and 50 nm) | Staphylococcus aurous and Escherichia coli were used. | 0.42 and 0.21 µg/mL, 0.84 and 0.42 µg/mL | Destroyed bacterial cells. | Bacterial infection | [275] |
Ni-NPs (<100 nm) | S. aureus and Escherichia coli | 0.05, 0.1, and 1 mg/mL | Inhibited the growth of bacterial bioflim. | Bacterial infection | [276] |
Miscellaneous Effects | |||||
DPMC-Ni-NPs (55 nm) | DPPH, hydrogen peroxide, and super oxide | - | - | Oxidative stress | [260] |
Ni-NPs@F. officinalis (16.85–49.04 nm) | DPPH free radicals | 253, 145, and 107 µg/mL | DPPH is inhibited by adding radical species. | Oxidative stress | [265] |
Ni-NPs (50 nm) | Sprague Dawley rats | 1, 10, and 20 mg/kg concentrations were used. | Increasing number of WBC. | Liver and spleen injury, lung inflammation | [266] |
NiO-NPs (5.46 nm) | α-amylase enzyme | 268.13 µg/mL | Inhibited α-amylase enzyme and produced a hypoglycemic effect. | Diabetes | [267] |
Ni-NPs (80–100 nm) | Culex quinquefasciatus. | 250, 500, and 1000 ppm | Larvicidal effect. | Lymphatic filariasis | [268] |
Ni-NPs (150 nm) | Larvae of R. (B.) microplus, H. a. anatolicum, C. quinquefasciatus, A. subpictus, and C. gelidus. | 10.17, 10.81, 4.93, 5.56, and 4.94 mg/L | Caused larvae death. | Parasitosis | [269] |
NiFe2O4/C nanocomposite. | In vitro: C540 (B16/F10) cells; in vivo: mice model (intratumorally injected) | 1.0-MHz radiation was applied with 100 μg/mL NPs | NPs and radiation can recover tumor cells and necrosis, up to 60%. | Sonodynamic therapy | [277] |
NiO-NPs preparation with Neem leaf extract. (12 nm) | S. aureus and E. coli | - | Antibacterial effect was found concentration dependent. | Antibacterial | [278] |
NiFe2O4 nanoparticles (chitosan- and PEG-coated nickel ferrite), 2–58 nm | Mössbauer spectroscopy | Temperature value from 200–800 °C | Hyperthermia heating requires specific particle size, shape, magnetism, and solution concentration. | Hyperthermia heating | [279] |
Nickel silicate nanoplatforms (LNS NPs) | Mouse model | - | LNS NPs may produce enough superoxide radicals when exposed to a 660 nm laser; it may simultaneously form oxygen and create superoxide radicals (O2−•). | Hypoxic tumor therapy | [280] |
2.6. Therapeutic Interventions of Iron Nanoparticles (Fe-NPs)
- Nanotherapeutic Application of Iron
Nanoparticles (Diameter) | Test Medium | Concentration | Effect/Result | Disease Against | References |
---|---|---|---|---|---|
Anticancer Effects | |||||
Superparamagnetic iron oxide nanoparticles (SPIONs (7.3, 15.1, and 30.0 nm | Human breast cancer cell MCF7 | 80 μg/mL | Higher measurements and more reasonable size of SPIONs upgraded the take-up sum into MCF7 cells. | Breast cancer | [162] |
SPIONs | Liver cancer cells (HepG2) (in vitro) | 100 μg/mL | A potent cytotoxicity on HepG2 under hyperthermia condition. | Cancer | [287] |
Zero valent iron NPs (ZVI-NPs) (97.1–55.77 nm) | BALB/c mice, age: 5–6 week | 5 and 10 μg/mL | Lung cancer cells died by ferroptosis as a result of ZVI-NP-induced mitochondrial malfunction, intracellular oxidative-stress, and lipid-peroxidation. | Lung cancer | [288] |
CA-coated Fe3O4 NPs (50 nm) | 4T1 cells | 10 μg/mL | Induced tumor cell ferroptosis. | Breast cancer | [297] |
SPION-deferasirox | AS1411 DNA aptamer | 100 mg | In vivo tumor growth inhibitory effect. | Antitumor | [298] |
Rosemary-Fe-NPs (100 nm) | 4T1 and C26 cancer cell lines | 3.12 to 200 µg/mL | Rosemary-Fe-NPs exerted more cytotoxic effect. | Anticancer | [299] |
CAP and iron oxide-based magnetic NPs (MNPs) | A549 cells in vitro | 50 emu/g | Potentially inhibited tumor growth. | Lung cancer | [300] |
SPIONs (44.6 nm) | Breast cancer cell lines T-47D, BT-474, MCF7, and MDA-MB-231 | 25, 50 and 75 µg/mL | Extremely moderate molecule take-up and low cytotoxicity, while SPIONLA meaningfully affected cell take-up and cell harmfulness. | Breast cancer | [301] |
Fe3O4@PEI-Pt(IV)-PEG-LHRH@siEZH2 nanoparticles | A2780/DDP cells (cisplatin resistant) | 0.78 to 50 µM | Killing performance to A2780/DDP cells. | Anticancer | [302] |
34DABA coated SPIOs (less than 20 nm) | HepG2 liver cancer cells | 5, 10, 15, 20, and 25 μg | Good cytocompatibility and higher killing efficiency. | Liver cancer | [303] |
Fe-NP nanopowder (35–45 nm) | PC12 cell nervous system (in vitro) | 100 μg/mL | Fe-NPs induced apoptotic cytotoxicity. | Cancer | [304] |
Au-Fe3O4 -NPs (20.8 nm) | MCF-7 cells | 50 μg/mL | Effective and promising photothermal therapy. | Breast cancer | [304] |
Iron oxide nanoparticles (Fe2O3-NPs) (20 to 60 nm) | Lung cancer cell (A549) lines | Highest concentration of adsorbent (50 mg/L) | No toxicity against A549 cell lines. | Lung cancer | [305] |
Miscellaneous Effects | |||||
Magnetic Fe2O3-NPs (50–110 nm) | S. aureus | DMF arrangement with 40 and 60 MJ laser fluencies showed the most noteworthy antibacterial action. | ROS disrupting bacterial cell membrane. | Bacterial infection | [289] |
Fe2O3-NPs (10–15 nm) | A/Puerto Pico/8/1934H1N1 influenza virus strain (PR8-H1N1) | 1.1 pg | Inactivation of cell protein through the communication of nanoparticles and -SH bunch (proposed, not examined at this point). | Viral infection | [291] |
Fe2O3-NPs (10–15 nm) | H1N1 Influenza A | 4.25 ± 0.2 pg | Change in viral RNA transcripts within 24 h, eight-fold reduction when treated with iron oxide. | Viral infection | [291] |
Fe2O3-NPs (10–30 nm) | Trichothecium roseum, Cladosporium herbarum, Penicillium chrysogenum, Alternaria alternate, and Aspergillus niger | 0.063–0.016 mg/mL | Development of ROS, protein and DNA damage oxidative stress was the way of producing antifungal effect. | Fungal infection | [292] |
Zero-valent iron (Fe0) NPs, spherical (31.1 nm) | Staphylococcus aureus (Gram-positive) and E. coli (Gram-negative) | MIC at 30 μg/mL and complete growth inhibition concentration at 60 μg/mL | Oxidative stress generation via ROS and visible damage to bacterial protein and DNA. | Bacterial infection | [298] |
4 nm core Fe2O3 coated with tartaric/adipic acid | Mitochondrial DNA (mtDNA), mitochondrial function, and autophagy in colorectal cell lines (HT-29) | 0.5 mM/L | Reduced the number of mtDNA copies (indicative of a reduction in the number of mitochondria in these tumor cells). | Mitochondrial dysfunction | [306] |
3. Metal Nanoparticles Elimination from Body
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Metals | Liver (ppm) | Kidney (ppm) | Lung (ppm) | Heart (ppm) | Brain (ppm) | Muscle (ppm) |
---|---|---|---|---|---|---|
Iron | 16,769 | 7168 | 24,967 | 5530 | 4100 | 3500 |
Manganese | 138 | 79 | 29 | 27 | 22 | <4–40 |
Nickel | <5 | <5–12 | <5 | <5 | <5 | <15 |
Zinc | 5543 | 5018 | 1470 | 2772 | 915 | 4688 |
Cobalt | <2–13 | <2 | <2–8 | - | <2 | 150 |
Copper | 882 | 379 | 220 | 350 | 401 | 85–305 |
Nanoparticles Name | Site of Action | Application | References |
---|---|---|---|
Au-NPs | Cancer gliblastoma-based multiforme | Radiosensitizer applications | [94,95] |
Au-NPs | Cancer cell | Radiosensitizer application | [96] |
Ag-NPs | Skin | Skin penetration evaluation | [97] |
Pt-NPs lined with polyvinyl alcohol | Brain | Toxicity evaluation | [98] |
Ag-NPs | Antimicrobial agent | Antimicrobial assessment | [99] |
Au-NPs/Ag-NPs | Cancer cell | Photothermal therapy, imaging therapy | [100] |
Au-branched shell nanostructure | Breast cell | Imaging therapy, photothermal therapy, chemotherapy. | [101] |
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Islam, T.; Rahaman, M.M.; Mia, M.N.; Ara, I.; Islam, M.T.; Alam Riaz, T.; Araújo, A.C.J.; de Lima Silva, J.M.F.; de Lacerda, B.C.G.V.; de Andrade, E.M.; et al. Therapeutic Perspectives of Metal Nanoformulations. Drugs Drug Candidates 2023, 2, 232-278. https://doi.org/10.3390/ddc2020014
Islam T, Rahaman MM, Mia MN, Ara I, Islam MT, Alam Riaz T, Araújo ACJ, de Lima Silva JMF, de Lacerda BCGV, de Andrade EM, et al. Therapeutic Perspectives of Metal Nanoformulations. Drugs and Drug Candidates. 2023; 2(2):232-278. https://doi.org/10.3390/ddc2020014
Chicago/Turabian StyleIslam, Tawhida, Md. Mizanur Rahaman, Md. Nayem Mia, Iffat Ara, Md. Tariqul Islam, Thoufiqul Alam Riaz, Ana C. J. Araújo, João Marcos Ferreira de Lima Silva, Bruna Caroline Gonçalves Vasconcelos de Lacerda, Edlane Martins de Andrade, and et al. 2023. "Therapeutic Perspectives of Metal Nanoformulations" Drugs and Drug Candidates 2, no. 2: 232-278. https://doi.org/10.3390/ddc2020014
APA StyleIslam, T., Rahaman, M. M., Mia, M. N., Ara, I., Islam, M. T., Alam Riaz, T., Araújo, A. C. J., de Lima Silva, J. M. F., de Lacerda, B. C. G. V., de Andrade, E. M., Khan, M. A., Coutinho, H. D. M., Husain, Z., & Islam, M. T. (2023). Therapeutic Perspectives of Metal Nanoformulations. Drugs and Drug Candidates, 2(2), 232-278. https://doi.org/10.3390/ddc2020014