Abstract
In this study, the toxicological effects of elevated concentrations of iron (FeSO(4)), an essential trace element, were systematically investigated in Allium cepa L. A comprehensive set of biomarkers were employed, encompassing cytogenetic parameters (mitotic index, micronucleus frequency, chromosomal aberrations), physiological indicators (germination rate, root length, biomass accumulation), biochemical markers (malondialdehyde, proline content, chlorophyll concentration, superoxide dismutase and catalase activities), and anatomical assessments of root meristem cell integrity. Additionally, the Comet assay was utilized to quantify DNA damage. Four experimental groups were established: one control group and three treatment groups, each exposed to FeSO(4) concentrations of 50, 100, and 200 mg/L, respectively. At the conclusion of the experimental period, root tips and leaf tissues were collected and processed using standardized protocols for subsequent analyses. The results demonstrated that the control group exhibited superior physiological performance, with the highest values recorded for germination, root elongation, MI percentage and chlorophyll content. Conversely, FeSO(4) treatments induced a concentration-dependent decline in these parameters, accompanied by a significant increase in MN frequency, chromosomal aberrations, MDA and proline levels, and SOD and CAT enzyme activities. The most pronounced effects were observed at 200 mg/L FeSO(4,) where the MI was reduced by 36% and the DNA tail percentage-a marker of DNA fragmentation-elevated by 57.3% compared to the control. Additionally, FeSO(4) exposure induced dose-dependent anatomical damage in A. cepa root meristem cells, particularly causing epidermis and cortex cell damage, nucleus flattening, and conduction tissue thickening, likely due to oxidative stress and mechanical pressure. These findings reveal that excessive FeSO(4) exposure triggers severe genotoxic, biochemical, and anatomical disruptions in Allium cepa, driven by oxidative stress and cellular damage. This underscores the potential ecological risks of iron pollution in terrestrial and aquatic environments.