Multi-Endpoint Toxicity Assessment of a Commercial Aclonifen-Based Herbicide Formulation Using Allium cepa and MDBK Cells

Commercial pesticide formulations can affect non-target organisms, yet marketed aclonifen products remain insufficiently characterized across complementary test systems. This study assessed a commercial suspension concentrate containing 600 g/L aclonifen using Allium cepa L. root meristems and Madin–Darby bovine kidney (MDBK) cells. Both models were exposed for 24, 48, or 72 h to 50, 100, or 200 mg/L nominal aclonifen-equivalent concentrations selected around an approximate EC50 identified in preliminary root-growth testing. Root elongation, mitotic index (MI), micronucleus (MN) frequency, chromosomal aberrations (CA), comet tail DNA and tail moment, and MTT-derived relative metabolic viability were evaluated. The formulation significantly reduced root elongation and MI and increased MN, total CA, tail DNA, and tail moment at all tested concentrations within each exposure period. At 72 h and 200 mg/L, MN increased from 0.12% to 2.86%, total CA from 1.41% to 18.20%, and tail DNA from 5.50% to 47.48%; chromosome stickiness was the predominant mitotic abnormality. In MDBK cells, relative metabolic viability declined to 30.11% at 200 mg/L after 72 h. These findings show that, under the experimental conditions, the tested commercial formulation produced growth and mitotic inhibition, cytogenetic alterations, primary DNA damage, and reduced MTT-derived relative metabolic viability in MDBK cells, providing a multi-endpoint basis for formulation-level biological hazard characterization.