Trifloxystrobin (TRI) and kresoxim-methyl (KRE), as quinone outside inhibitor fungicides (QoIs), have broad applications due to their effective activity against fungi. Excessive usages of agrochemicals trigger environmental risks, such as aquatic organisms (fish). Research performed in recent years has focused on the ecotoxicology of TRI and KRE in fish containing histologic morphology, enzyme activity, protein and gene expression under chronic toxicity conditions, whereas less is known about the underlying mechanisms of toxicity and differences between TRI and KRE in fish under acute toxicity conditions. In the present study, in comparison to different exposure routes [whole-body exposure (WBE), head exposure (HE), trunk exposure (TE), and Oral administration (OA)], the external substances TRI and KRE entered the fish body mainly via gill organs and led to fish toxicity. Furthermore, gill organs and gill cells were vulnerable to TRI and KRE exposure, which indicated that the gill is a vital impaired organ. The 96 h-LC50 (sublethal concentration) value of KRE was 289.8 μg L-1 (R2 = 0.9855) with an approximate 10-fold difference in TRI toxicity. The cytotoxicity exposed to TRI was higher than that in KRE at the same concentration. The potential mechanisms of toxic differences could be various toxic effects in terms of MCIII (mitochondrial complex III) activity, ATP (Adenosine triphosphate) content, MA (mitochondrial activity), ROS (reactive oxygen species) levels, and cellular respiration. Furthermore, the disorder in MCIII activity was probably the main potential mechanisms of toxic differences. To some extent, this research provides not only new insight into the underlying toxic mechanism of TRI and KRE in fish but also a basis for the guidance of agrochemicals considering aquatic risks.
Keywords: Exposure routes; Gill; Kresoxim-methyl; Toxicological differences; Trifloxystrobin.
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