Gold and silver nanoparticles are nanoparticles that have been widely used in various fields and have shown good benefits. The method of nanoparticle biosynthesis utilizing plant extracts, also known as green synthesis, has become a promising method considering the advantages it has compared to other synthesis methods. This review aims to give an overview of the phytochemical compounds in plants used in the synthesis of gold and silver nanoparticles, the nanoparticle properties produced using plant extracts based on the concentration and structure of phytochemical compounds, and their applications. Phytochemical compounds play an important role as reducing agents and stabilizers in the stages of the synthesis of nanoparticles. Polyphenol compounds, reducing sugars, and proteins are the main phytochemical compounds that are responsible for the synthesis of gold and silver nanoparticles. The concentration of phytochemical compounds affects the physical properties, stability, and activity of nanoparticles. This is important to know to be able to overcome limitations in controlling the physical properties of the nanoparticles produced. Based on structure, the phytochemical compounds that have ortho-substituted hydroxyl result in a smaller size and well-defined shape, which can lead to greater activity and stability. Furthermore, the optimal condition of the biosynthesis process is required to gain a successful reaction that includes setting the metal ion concentration, temperature, reaction time, and pH.

/pdf/biosynthesis-of-gold-and-silver-nanoparticles-using-u27no8ag.pdf

Biosynthesis of Gold and Silver Nanoparticles Using Phytochemical Compounds

Cancer is a global health burden responsible for an exponentially growing number of incidences and mortalities, regardless of the significant advances in its treatment. The identification of the hallmarks of cancer is a major milestone in understanding the mechanisms that drive cancer initiation, development, and progression. In the past, the hallmarks of cancer have been targeted to effectively treat various types of cancers. These conventional cancer drugs have shown significant therapeutic efficacy but continue to impose unfavorable side effects on patients. Naturally derived compounds are being tested in the search for alternative anti-cancer drugs. Steroidal saponins are a group of naturally occurring compounds that primarily exist as secondary metabolites in plant species. Recent studies have suggested that steroidal saponins possess significant anti-cancer capabilities. This review aims to summarize the recent findings on steroidal saponins as inhibitors of the hallmarks of cancer and covers key studies published between the years 2014 and 2024. It is reported that steroidal saponins effectively inhibit the hallmarks of cancer, but poor bioavailability and insufficient preclinical studies limit their utilization. 

Steroidal Saponins: Naturally Occurring Compounds as Inhibitors of the Hallmarks of Cancer

Improving the precise accumulation and retention of nanomedicines in tumor cells is one of the keys to effective therapy of tumors. Herein, supramolecular peptides capped Au nanocages (AuNCs) that may self-aggregate into micron-sized clusters intracellularly in response to spermine (SPM), leading to specific accumulation and retention of AuNCs in SPM-overexpressed tumor cells, are developed. In this design, polydopamine (PDA) is in situ coated on the surface of AuNCs with doxorubicin (DOX) encapsulated. A small peptide, Phe-Phe-Val-Leu-Lys (FFVLK), is conjugated with PDA via esterification, and cucurbit[7]uril (CB[7]) is threaded onto the N-terminal Phe via host-guest interactions. Once the supramolecular peptide (CB[7]-FFVLK) capped AuNCs are internalized in SPM-overexpressed breast cancer cells, CB[7] can be competitively removed from FFVLK by SPM, due to the much higher binding affinity between CB[7] and SPM than that between CB[7] and Phe, leading to exposure of free FFVLK, which can subsequently self-assemble and induce the aggregation of AuNCs to micron-sized clusters, resulting in the significantly enhanced accumulation and retention of DOX-loaded AuNCs in tumor cells. Under NIR laser irradiation, the enhanced photothermal conversion of AuNCs aggregates, together with photothermia-induced release of DOX leads to synergistic photothermal therapy and chemotherapy against breast cancer.

Spermine-Responsive Intracellular Self-Aggregation of Gold Nanocages for Enhanced Chemotherapy and Photothermal Therapy of Breast Cancer.

DNA damage is a double-edged sword in cancer cells. On the one hand, DNA damage exacerbates gene mutation frequency and cancer risk. Mutations in key DNA repair genes, such as breast cancer 1 (BRCA1) and/or breast cancer 2 (BRCA2), induce genomic instability and promote tumorigenesis. On the other hand, the induction of DNA damage using chemical reagents or radiation kills cancer cells effectively. Cancer-burdening mutations in key DNA repair-related genes imply relatively high sensitivity to chemotherapy or radiotherapy because of reduced DNA repair efficiency. Therefore, designing specific inhibitors targeting key enzymes in the DNA repair pathway is an effective way to induce synthetic lethality with chemotherapy or radiotherapy in cancer therapeutics. This study reviews the general pathways involved in DNA repair in cancer cells and the potential proteins that could be targeted for cancer therapeutics.

/pdf/dna-damage-and-its-role-in-cancer-therapeutics-3tlup8um.pdf

DNA Damage and Its Role in Cancer Therapeutics

Despite many efforts, breast cancer remains one of the deadliest cancers and its treatment faces challenges related to cancer drug side effects and metastasis. Combining 3D printing and nanocarriers has created new opportunities in cancer treatment. In this work, 3D-printed gelatin-alginate nanocomposites containing doxorubicin-loaded niosomes (Nio-DOX@GT-AL) were recruited as an advanced potential pH-sensitive drug delivery system. Morphology, degradation, drug release, flow cytometry, cell cytotoxicity, cell migration, caspase activity, and gene expression of nanocomposites and controls (Nio-DOX and Free-DOX) were evaluated. Results show that the obtained niosome has a spherical shape and size of 60-80 nm. Sustained drug release and biodegradability were presented by Nio-DOX@GT-AL and Nio-DOX. Cytotoxicity analysis revealed that the engineered Nio-DOX@GT-AL scaffold had 90 % cytotoxicity against breast cancer cells (MCF-7), whereas exhibited <5 % cytotoxicity against the non-tumor breast cell line (MCF-10A), which was significantly more than the antitumor effect of the control samples. Scratch-assay as an indicator cell migration demonstrated a reduction of almost 60 % of the covered surface. Gene expression could provide an explanation for the antitumor effect of engineered nanocarriers, which significantly reduced metastasis-promoting genes (Bcl2, MMP-2, and MMP-9), and significantly enhanced the expression and activity of genes that promote apoptosis (CASP-3, CASP-8, and CASP-9). Also, considerable inhibition of metastasis-associated genes (Bax and p53) was observed. Moreover, flow-cytometry data demonstrated that Nio-DOX@GT-AL decreased necrosis and enhanced apoptosis drastically. The findings of this research can confirm that employing 3D-printing and niosomal formulation can be an effective strategy in designing novel nanocarriers for efficient drug delivery applications. 

Doxorubicin-loaded Niosomes functionalized with gelatine and alginate as pH-responsive drug delivery system: A 3D printing approach.

Simple Summary The number of children and adults with cancer that are completely cured is still increasing thanks to effective anti-cancer therapy, but they may be confronted with the negative lasting effects of the treatment later in life. In this review, we provide an overview of major clinical symptoms and toxic side-effects observed in cancer survivors. We describe which types of anti-cancer treatments—primarily DNA-damaging chemotherapeutics—might cause these toxicities and what the (potential) underlying mechanisms are. These treatments not only damage cancer cells in their attempt at tumor killing but also harm healthy cells and tissues. Observations of side-effects in cancer patients and survivors strengthen the hypothesis that the primary induced DNA damage can lead to varying toxicities while also accelerating features of aging, depending on type and dose of chemotherapeutic, clearing method, and affected organ. Abstract Recent advances have increased survival rates of children and adults suffering from cancer thanks to effective anti-cancer therapy, such as chemotherapy. However, during treatment and later in life they are frequently confronted with the severe negative side-effects of their life-saving treatment. The occurrence of numerous features of accelerated aging, seriously affecting quality of life, has now become one of the most pressing problems associated with (pediatric) cancer treatment. Chemotherapies frequently target and damage the DNA, causing mutations or genome instability, a major hallmark of both cancer and aging. However, there are numerous types of chemotherapeutic drugs that are genotoxic and interfere with DNA metabolism in different ways, each with their own biodistribution, kinetics, and biological fate. Depending on the type of DNA lesion produced (e.g., interference with DNA replication or RNA transcription), the organ or cell type inflicted (e.g., cell cycle or differentiation status, metabolic state, activity of clearance and detoxification mechanisms, the cellular condition or micro-environment), and the degree of exposure, outcomes of cancer treatment can largely differ. These considerations provide a conceptual framework in which different classes of chemotherapeutics contribute to the development of toxicities and accelerated aging of different organ systems. Here, we summarize frequently observed side-effects in (pediatric) ex-cancer patients and discuss which types of DNA damage might be responsible.

/pdf/chemotherapy-side-effects-not-all-dna-damage-is-equal-2vpuuk6u.pdf

Chemotherapy Side-Effects: Not All DNA Damage Is Equal

Obesity can disturb spermatogenesis and subsequently affect male fertility and reproduction. In our study, we aim to elucidate at which cellular level of adult spermatogenesis the detrimental effects of obesity manifest. We induced high fat diet (HFD) obesity in low-density lipoprotein receptor knock-out Leiden (Ldlr-/-.Leiden) mice, and studied the morphological structure of the testes and histologically examined the proportion of Sertoli cells, spermatocytes and spermatids in the seminiferous tubules. We examined sperm DNA damage and chromatin condensation and measured plasma levels of leptin, testosterone, cholesterol and triglycerides. HFD-induced obesity caused high plasma leptin and abnormal testosterone levels and induced an aberrant intra-tubular organisation (ITO) which is associated with an altered spermatids/spermatocytes ratio (2:1 instead of 3:1). Mice fed a HFD had a higher level of tubules in stages VII + VIII in the spermatogenic cycle. The stages VII + VII indicate crucial processes in spermatogenic development like initiation of meiosis, initiation of spermatid elongation, and release of fully matured spermatids. In conclusion, HFD-induced obese Ldlr-/-.Leiden mice develop an aberrant ITO and alterations in the spermatogenic cycle in crucial stages (stages VII and VII). Thereby, our findings stress the importance of lifestyle guidelines in infertility treatments. 

/pdf/high-fat-diet-induced-obesity-prolongs-critical-stages-of-2wt5w9rd.pdf

High fat diet-induced obesity prolongs critical stages of the spermatogenic cycle in a Ldlr−/−.Leiden mouse model

Childhood renal tumors account for around 6% of all childhood cancers and 90% of these cases are Wilms tumor. In Europe, the SIOP-RTSG approach is considered standard of care and has resulted in five-year survival rates of over 90%. Efforts to decrease toxicity are now being pursued. Short-term fasting (STF), a short but strong reduction in calorie-intake, is associated with improved fitness, enhanced coping with acute physical stress and a lower risk of age-associated diseases. STF temporarily reduces growth to boost resilience, maintenance, and defense-mechanisms, by which toxic side-effects of (oxidative) damage and inflammation are largely prevented. Renal surgery for Wilms tumor carries a risk of acute kidney injury (AKI) and pediatric patients that had an episode of AKI are at increased risk for developing chronic renal disease. STF could mitigate surgery-induced stress and could further improve outcomes. We aim to investigate the effect of STF on renal function recovery after renal tumor surgery by conducting a single-center, prospective, randomized, non-blinded, intervention study. Children diagnosed with a unilateral renal tumor and opting for curative treatment are eligible for inclusion. The main study objective is to investigate the potential decrease in occurrence of AKI due to STF. Secondary objectives include renal function recovery, child's wellbeing, physical functioning, and feasibility of and adherence to STF in children with cancer.

/pdf/fasting-intervention-for-children-with-unilateral-renal-7vh764s2.pdf

Fasting Intervention for Children With Unilateral Renal Tumors to Reduce Toxicity

Short-term fasting before living kidney donation has an immune-modulatory effect

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Chemotherapy Side-Effects: Not All DNA Damage Is Equal

High fat diet-induced obesity prolongs critical stages of the spermatogenic cycle in a Ldlr−/−.Leiden mouse model

Fasting Intervention for Children With Unilateral Renal Tumors to Reduce Toxicity

Short-term fasting before living kidney donation has an immune-modulatory effect