ArticleNeurotoxicity research2026
Trifloxystrobin-Induced Neurotoxicity in Wistar Rats: Biomarkers of Oxidative Stress, Cholinergic Dysfunction, and DNA Damage.
Article in Neurotoxicity research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Trifloxystrobin (TFX), a broad-spectrum fungicide, inhibits mitochondrial Complex III. While widely used, its neurotoxic mechanisms in mammalian systems remain poorly characterized. This study investigated TFX-induced neurotoxicity in male Wistar rats following 28-day oral exposure to 3, 6, 12, and 24 mg/kg/bw (corresponding to NOAEL/2, NOAEL, NOAEL × 2, and NOAEL × 4). We evaluated dose-dependent effects on brain histopathology, cholinergic function, lipid metabolism, oxidative stress, and DNA integrity. TFX exposure induced significant histopathological alterations, including neurodegeneration, cellular infiltraion, and blood congestion. It also produced a dose-dependent impairment of cholinergic neurotransmission, indicated by suppressed acetylcholinesterase activity, which correlated with observed reduced motor activity and hindlimb strength. Furthermore, TFX disrupted lipid homeostasis by elevating total cholesterol, LDL-C, and HDL-C, while reducing triglycerides. Oxidative stress was evident through increased lipid peroxidation and protein carbonylation, accompanied by altered activities of key antioxidant enzymes (SOD, CAT, GPx, GST). The Comet assay confirmed dose-dependent DNA fragmentation, demonstrating TFX's genotoxic potential. These findings elucidate multiple pathways of TFX-induced neurotoxicity and highlight the need for further investigation into the long-term neurological risks of this fungicide.
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