Essential oil-derived compounds such as eugenol, thymol, cinnamaldehyde, and carvacrol exhibit potent antimicrobial and anti-inflammatory properties, making them promising candidates for therapeutic and industrial applications. This review examines the current evidence regarding the mechanisms of action, efficacy, and ability to disrupt quorum sensing and biofilm formation of essential oil-derived compounds against a broad spectrum of Gram-positive and Gram-negative bacteria, including multidrug-resistant (MDR) strains. The anti-inflammatory activity of these compounds is also highlighted, with emphasis on their modulation of key signaling pathways such as nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs), and their ability to downregulate pro-inflammatory cytokines. However, challenges persist, including cytotoxicity at high concentrations, chemical instability, poor water solubility, and variable pharmacokinetics. Advanced delivery systems such as nano encapsulation and synergistic formulations offer potential strategies to overcome these limitations. This review highlights both the therapeutic potential and the current limitations of these natural compounds, emphasizing the need for continued research to translate preclinical findings into clinical applications.

Essential oils (EOs) and their bioactive constituents have attracted growing interest as potential anticancer agents because they can target multiple pathways involved in tumor progression. However, the literature on their anticancer activity is highly heterogeneous and often limited by methodological weaknesses that reduce the reliability and translational value of the reported findings. This systematic review critically assessed the anticancer activity of EOs and EO-derived compounds by considering only studies that met defined methodological criteria. A PubMed search identified 872 articles published between 2015 and 2026, of which 97 were retained after screening based on EO chemical characterization, evaluation of cancer selectivity using non-tumoral control cells, and direct assessment of EO-driven anticancer effects. Across different tumor models, EOs and their constituents consistently showed selective cytotoxic or antiproliferative activity, commonly associated with oxidative stress, mitochondrial dysfunction, apoptosis, cell-cycle arrest, and modulation of oncogenic pathways. Some studies also reported reduced migration, invasion, and tumor-promoting signaling, while nanoformulation improved stability and efficacy in selected models. Overall, despite encouraging preclinical evidence, the translational potential of EO-based anticancer strategies remains limited by recurrent methodological shortcomings and insufficient in vivo validation. Standardized experimental criteria will be essential to improve reproducibility and support future clinical development.

Essential oils (EOs) are complex mixtures of volatile secondary metabolites produced by medicinal and aromatic plants (MAPs), mainly including terpenes, terpenoids and phenylpropanoid/benzenoid derivatives. Their composition depends on the plant species, chemotype, organ, developmental stage, environmental conditions and post-harvest processing, and directly affects EO yield, EO profile, biological properties, standardization and industrial value. This narrative and conceptual review connects plant biosynthesis, environmental regulation, matrix selection and extraction strategy as interdependent determinants of EO quality. Terpenoid constituents originate mainly from the mevalonate (MVA) and methylerythritol phosphate (MEP) pathways, whereas phenylpropanoid and benzenoid volatiles derive largely from the shikimate/phenylalanine pathway. Conventional extraction methods, such as hydrodistillation and steam distillation, remain widely used, while intensified and complementary approaches, including microwave-assisted methods, ultrasound pretreatment, supercritical CO₂ extraction and solvent-free methods, are increasingly investigated to improve selectivity and reduce extraction time, solvent use, water demand and energy consumption. Rather than ranking extraction methods only by yield, this review emphasizes that EO quality should be interpreted through an integrated plant-to-extraction framework, in which botanical raw material, target chemical classes, matrix properties, compound stability and intended application jointly guide the selection of an extraction strategy. This integrated perspective may support more reproducible, application-oriented and sustainable EO production.

Colorectal cancer is one of the leading causes of cancer-associated mortality, and multifactorial resistance remains one of the main challenges in its treatment. Essential oils and their main compounds show interesting anticancer properties, but their mechanism of action is yet to be defined. This study aims to assess the cytotoxic effects of eugenol (EU) and cinnamaldehyde (CN) on colorectal cancer (CRC) cells, highlighting possible mechanisms of action. These compounds were tested on normal immortalized colonocytes (NCM-460) and two CRC cell lines: Caco-2, a human colon epithelial adenocarcinoma cell line, and SW-620, colon cancer cells derived from a lymph node metastatic site. The efficacy of EU and CN was evaluated through CellTiter-Glo^® and clonogenic assays and by determining proinflammatory cytokine secretion. Transcriptome analysis was used to identify possible pathways affected by EU and CN treatments. The results confirmed that EU and CN were selectively cytotoxic and pro-apoptotic against CRC cells, with different putative mechanisms. While EU drove cytotoxicity through robust transcriptional remodeling, CN yielded a stronger anti-inflammatory action. We confirmed that EU and CN are promising natural candidates in CRC prevention and treatment, even in association with chemotherapeutic drugs.

Purpose Oral iron supplementation is frequently limited by gastrointestinal side effects and reduced absorption associated with hepcidin-mediated regulation. This randomized, parallel-group, active-controlled study evaluated whether a reduced-dose alternate-day oral iron supplementation strategy could improve iron status in women with iron deficiency. Methods Sixty-six iron-deficient women of reproductive age (18–50 years; serum ferritin < 30 ng/mL) were randomized to receive, for 42 days, either micronized, dispersible ferric pyrophosphate providing 21 mg of elemental iron every 48 h combined with a daily gut microbiota modulator, or sucrosomial ferric pyrophosphate providing 30 mg of elemental iron per day. The primary endpoint was serum ferritin, while secondary endpoints included serum iron, transferrin, transferrin saturation (TSAT), total iron-binding capacity (TIBC), hemoglobin, and red blood cell count. Results Serum ferritin increased significantly over time in both groups (p < 0.001), with no significant differences between treatments. Comparable improvements were observed for serum iron, transferrin, TSAT, and TIBC, while hemoglobin remained stable throughout the study. Both interventions were generally well tolerated, with only mild transient gastrointestinal adverse events and no clinically relevant changes in inflammatory markers. Conclusion A reduced-dose alternate-day oral iron supplementation strategy achieved improvements in iron status comparable to standard daily supplementation despite lower cumulative iron exposure. These findings support the potential clinical relevance of physiologically informed low-dose iron supplementation strategies in women with iron deficiency.

Microplastics (MPs), defined as plastic particles smaller than 5 mm, either intentionally manufactured or generated through the degradation of larger plastic materials, have infiltrated the food chain and have been detected in various human biological samples. Among the possible exposure routes, ingestion appears to be the primary one; however, the mechanisms by which MPs may cross the intestinal barrier-such as transcytosis, uptake by Microfold Cells, persorption, and barrier dysfunction-and disseminate throughout the body remain poorly understood. In addition to their potential direct toxicity, stemming from their ability to carry plastic additives and adsorbed environmental pollutants, an increasing body of evidence indicates that MPs can disrupt intestinal physiology through multiple mechanisms once they reach the intestinal lumen. The aim of this narrative review is to gather and critically analyze current evidence regarding the effects of MPs on gut homeostasis, with particular focus on the mechanisms underlying their interactions with the gut microbiota and the intestinal epithelial barrier. The findings indicate that MPs pose an emerging challenge to intestinal physiology, being capable of disrupting gut homeostasis by reducing short-chain fatty acid-producing bacteria while promoting proteolytic and pro-inflammatory taxa. These alterations ultimately compromise intestinal barrier integrity.