Achillea nobilis represents a species of considerable medicinal importance within the Asteraceae family, historically employed in Central Asia and various Eurasian territories for the management of inflammatory, microbial, and gastrointestinal ailments. Notwithstanding its extensive ethnopharmacological significance, the phytochemical profile and pharmacological attributes of its various anatomical components have not been comprehensively investigated. This research endeavor sought to delineate the phytochemical constituents and evaluate the antimicrobial efficacy of ethanol extracts derived from both the aerial and root segments of A. nobilis. Qualitative phytochemical analysis and GC–MS characterization unveiled a diverse array of bioactive compounds, encompassing flavonoids, phenolic compounds, organic acids, lactones, alcohols, and heterocyclic derivatives. In particular, the aerial oil extract exhibited the presence of terpenoids, fatty acids and their esters, sterols, hydrocarbons, and minor organosilicon and cyclobutanone derivatives, with notable compounds such as linoleic acid (8.08%), 6-tetradecyne (14.99%), isopropyl linoleate (14.64%), and E,Z-1,3,12-nonadecatriene (22.25%). In vitro antimicrobial activity was assessed against eight clinically relevant microbial strains employing the broth microdilution technique. The aerial ethanol extract exhibited pronounced antimicrobial properties, particularly against MRSA and C. albicans, with MICs ranging from 0.5 to 2 mg/mL, whereas the root ethanol extract displayed MICs of 1 to 3 mg/mL. Additionally, the aerial oil extract showed moderate inhibitory activity, with MIC values ranging from 1.5 to 3 mg/mL, demonstrating effectiveness particularly against C. albicans, C. neoformans, and MRSA. These findings underscore the therapeutic potential of A. nobilis, particularly its aerial component, as a viable natural source of antimicrobial agents.

Hearing loss is a major global health burden, and increasing evidence indicates that environmental and occupational exposure to neurotoxic metals may contribute to auditory dysfunction. This narrative review aimed to synthesize experimental evidence on metal-induced neuro-ototoxicity, with particular emphasis on morphological and functional alterations affecting peripheral and central components of the auditory system. A structured literature search was conducted in PubMed/MEDLINE, Web of Science, Scopus, and Google Scholar, focusing on animal studies investigating lead, mercury, cadmium, arsenic, and chromium exposure and auditory outcomes. Experimental evidence demonstrates that these metals can induce cochlear hair-cell injury, particularly involving outer hair cells and basal cochlear regions, as well as ribbon synapse loss, spiral ganglion dysfunction, and alterations of the stria vascularis. Central auditory effects include disrupted neural conduction, altered auditory brainstem responses, glial activation, synaptic dysfunction, and changes within the cochlear nucleus and inferior colliculus. Across metals, oxidative and nitrative stress, mitochondrial dysfunction, neuroinflammation, calcium dysregulation, and regulated cell death emerge as interconnected mechanisms. Notably, auditory synaptopathy and central auditory dysfunction may occur with limited overt hair-cell loss. These findings support a multisite model of metal-induced neuro-ototoxicity and highlight the importance of evaluating both peripheral and central auditory pathways in experimental toxicology and environmental health research.