Although considered a good alternative to organophosphate pesticides, there are reports indicating adverse effects of neonicotinoid insecticides on reproduction. Our aim was to assess the effects of exposure to low doses of imidacloprid on antioxidant state, DNA damage, and concentration of essential elements in the testes and epididymis using a rat model. Adult male Wistar rats were orally treated with doses comparable to currently proposed health-based reference values: 0.06 (ADI), 0.80 (10× AOEL), or 2.25 (1/200 LD₅₀) mg/kg b.w./day for 28 consecutive days. Exposure to 2.25 mg/kg b.w./day of imidacloprid resulted in a significantly lower testis weight (1.30 ± 0.17 g compared to 1.63 ± 0.15 g in controls). Treatment with 0.06 mg/kg b.w./day increased the level of reduced glutathione in the epididymis (73%), while the activities of epididymal glutathione peroxidase and superoxide dismutase significantly increased in all treated rats (74–92% and 26–39%, respectively). Exposure to imidacloprid resulted in a low, but significant, level of DNA damage in testicular sperm cells regardless of the concentration applied (<28% compared to the negative control). Higher concentrations of Mo were measured in the testes of rats treated with 0.80 and 2.25 mg/kg b.w./day (72.9 ± 7.9 and 73.9 ± 9.1 mg/g, respectively) compared to the control animals (60.5 ± 7.8 mg/g). Higher concentrations of Na were measured in the testes of rats treated with 2.25 mg/kg b.w./day (1679 ± 82 mg/g compared to 1562 ± 56 mg/g in controls). The fact that such low doses of imidacloprid were able to produce measurable biological effects calls for the further evaluation of this widely used insecticide.

In agricultural activities, pest control is essential, and the most effective method is the use of chemical agents that also represent an important source of exposure to potentially toxic compounds. Pesticides constitute a heterogeneous group of compounds designed specifically to control different pests. Besides measuring their levels or that of their metabolites in air, plasma, serum, blood, urine, etc., some studies reported increased DNA damage levels after occupational or environmental pesticides exposure, evidenced by several cytogenetic biomarkers such as chromosomal aberrations (CA), sister chromatid exchanges (SCE), micronuclei frequency (MN) together with other nuclear abnormalities (NA), alkaline comet assay, but also changes in oxidative stress parameters and miRNA levels. Single or combined, these techniques have also been used in genotoxic biomonitoring studies of workers occupationally exposed to pesticides in Mexico. Despite being a country with great agricultural activity and reported excessive pesticide use, genotoxic studies have been relatively few and, in some cases, contradictory. A review was made of the studies available (published until the end of 2020 on PubMed, Web of Science, Redalyc and Scielo, both in English and Spanish) in the scientific literature that evaluated occupational exposure of human samples to pesticides assessed with DNA damage and related biomarkers in Mexico.

To contribute new information to the pyrethroid pesticide α-cypermethrin toxicity profile, we evaluated its effects after oral administration to Wistar rats at daily doses of 2.186, 0.015, 0.157, and 0.786 mg/kg bw for 28 days. Evaluations were performed using markers of oxidative stress, cholinesterase (ChE) activities, and levels of primary DNA damage in plasma/whole blood and liver, kidney, and brain tissue. Consecutive exposure to α-cypermethrin affected the kidney, liver, and brain weight of rats. A significant increase in concentration of the thiobarbituric acid reactive species was observed in the brain, accompanied by a significant increase in glutathione peroxidase (GPx) activity. An increase in GPx activity was also observed in the liver of all α-cypermethrin-treated groups, while GPx activity in the blood was significantly lower than in controls. A decrease in ChE activities was observed in the kidney and liver. Treatment with α-cypermethrin induced DNA damage in the studied cell types at almost all of the applied doses, indicating the highest susceptibility in the brain. The present study showed that, even at very low doses, exposure to α-cypermethrin exerts genotoxic effects and sets in motion the antioxidative mechanisms of cell defense, indicating the potential hazards posed by this insecticide.