ArticleToxics2025
New Insights into Biochemical, Genotoxic, and Analytical Aspects of Low-Level Imidacloprid Exposure in Liver and Kidney Tissue of Adult Male Wistar Rats.
Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Besides its neurotoxic action and selective toxicity on insecticidal nicotinic acetylcholine receptors, recent studies have shown that imidacloprid may cause other adverse effects in mammals. In the present study, cholinesterase activity, oxidative stress response, genotoxicity in the liver and kidney, and imidacloprid levels in the urine, liver, and kidney of male Wistar rats orally administered with 0.06, 0.8, and 2.25 mg imidacloprid/kg bw/day for 28 days were evaluated. Imidacloprid urine mass concentrations in treated rats increased dose-dependently. Exposure to 0.8 mg imidacloprid/kg bw/per day significantly decreased cholinesterase activities in the liver and kidney. Reactive oxygen species levels decreased significantly in the liver at the same dose. Lipid peroxidation was significantly reduced in the liver at two higher doses. No significant changes in glutathione levels or the activities of superoxide dismutase and catalase were observed. A significant decrease in the activity of glutathione peroxidase was detected in the liver at the highest dose. DNA damage was low in both liver and kidney. Exposure to imidacloprid at studied experimental conditions did not cause a significant oxidative stress response and resulted in low genotoxic effects in the liver and kidney of rats, indicating that these organs are less susceptible to adverse imidacloprid effects at such low doses.
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Registered trials
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