Lithium chloride at environmental concentrations impairs microtubule function and promotes genotoxicity in Allium cepa.

The growing demand for lithium, driven by the energy transition and widespread use of rechargeable batteries, has raised concerns about its environmental release. This study assessed the toxicological effects of lithium chloride (LiCl) at environmentally relevant concentrations using the Allium cepa bioassay. While lithium's genotoxicity at high concentrations is known, its effects at levels typical of aquatic systems (up to 4 mg/L) remain poorly understood. A set of biomarkers was applied to evaluate cytotoxicity, genotoxicity, oxidative stress, and in silico molecular interactions. LiCl exposure significantly reduced the mitotic index, indicating cytotoxic effects via impaired cell division. Increased chromosomal aberrations and nuclear abnormalities were observed, particularly at 4 mg/L, suggesting genotoxicity. However, the Comet assay revealed minimal DNA strand breaks, pointing to an aneugenic mechanism likely caused by mitotic spindle disruption rather than clastogenic effects. Cell cycle analysis showed reduced metaphase and increased anaphase frequencies, reinforcing the hypothesis of chromosomal missegregation. In silico modeling demonstrated strong interactions between Li+ ions and tubulin, potentially affecting spindle stability. Additionally, altered superoxide dismutase (SOD) activity indicated oxidative stress involvement. Overall, lithium at environmentally realistic concentrations induces cytotoxic and genotoxic effects in A. cepa, primarily through aneugenic mechanisms linked to oxidative stress and microtubule disruption.