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We previously showed that farmers in Bolivia are exposed to many pesticides, some at elevated levels, and that this was associated with increased risk of genetic damage. To improve the understanding of possible mixture effects, the cytotoxicity and genotoxicity of pesticides were studied in vitro using human liver HepG2 cells. The studied pesticides were 2,4‐D, chlorpyrifos, cypermethrin, glyphosate, methamidophos, paraquat, profenofos, and tebuconazole. Three mixtures (U1, U2, and U3) were based on profiles of urinary pesticide metabolites and one mixture on the most frequently used pesticides (S1). The results showed that paraquat and methamidophos were the most cytotoxic pesticides (EC50 ≤0.3 mM). Paraquat, chlorpyrifos, tebuconazole, and the U1, U2, and U3 mixtures, which contained a large proportion of either chlorpyrifos or tebuconazole, significantly increased intracellular ROS levels. Most pesticides activated DNA damage signaling through proteins Chk1 and H2AX. Strongest responses were elicited by paraquat, profenofos, chlorpyrifos, cypermethrin, and the S1 mixture, which contained 25% paraquat. Comet assay revealed significant increases of DNA damage in response to paraquat, cypermethrin, and U2 and S1 mixtures, which contained high levels of cypermethrin and paraquat, respectively. In summary, we showed that the tested pesticides, alone or in mixtures, in general induced oxidative stress and that most pesticides, and especially paraquat and cypermethrin, were genotoxic in HepG2 cells. We could also show that mixtures dominated by these two pesticides displayed a marked genotoxic potency, which agreed with our previous population studies.

Dimethoate is an organophosphorus pesticide used against agricultural insects, which causes oxidative stress and damage in many organs, including the reproductive ones. Cherry laurel (Laurocerasus officinalis Roem.) fruit is rich in vitamins and phenolic compounds with antioxidant effect. The aim of this study was to investigate how effective its extract would be against dimethoate-induced testis and sperm damage in rats. Sixty animals were divided in six groups of 10. Group 1 (control) received only 1 mL of saline (0.9 % NaCl). Group 2 received 7 mg/kg of dimethoate in 1 mL of saline. Group 3 received 4 mg/kg of extract in 1 mL of saline. Group 4 received the extract 30 min before dimethoate administration. Group 5 received vitamin C (positive control, 100 mg/kg in 1 mL of saline) 30 min before dimethoate administration. Group 6 received only dimethoate for the first four weeks and then a combination of dimethoate and extract for another four weeks. All doses were administered daily by oral gavage. After eight weeks of treatment, the rats were euthanised and their reproductive organs removed. We took their body and reproductive organ weights and evaluated testicular oxidative stress, semen characteristics, sperm DNA damage, testicular apoptosis, and histopathological changes. Dimethoate significantly decreased body and reproductive organ weights, sperm motility and concentration, testicular superoxide dismutase, and glutathione-peroxidase activities and significantly increased lipid peroxidation, abnormal sperm rate, sperm DNA damage, testicular apoptosis, and caused histopathological lesions. Cherry laurel extract significantly countered many dimethoate-induced adverse effects, both as pre- and post-treatment, including reproductive organ weight, semen parameters, oxidant-antioxidant balance, sperm DNA integrity, testicular apoptosis, and histological structure. Our findings clearly suggest that the beneficial effects of the extract are associated with countering oxidative stress, lipid peroxidation in particular.

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The aim of this study was to investigate oxidative stress induced by perfluorooctanoic acid (PFOA) in the brain and liver tissues of Balb/c mice as well as protective effects of taurine and coenzyme Q10 (CoQ10) in both organs. For this purpose, animals were treated with PFOA (15 and 30 mg/kg) orally and their lipid peroxidation, total glutathione levels (GSH), and antioxidant enzyme activities measured and both tissues analysed for histopathological changes. Our results showed a dose-dependent decrease in body weight and increase in relative brain and liver weights, PFOA-induced lipid peroxidation and reduced glutathione peroxidase (GPx) activity in the brain tissue, and changes in GSH levels, GPx, superoxide dismutase (Cu-Zn SOD), and catalase (CAT) activities in the liver tissue. Pre-treatment with taurine or CoQ10 provided protection against PFOA-induced Cu-Zn SOD reduction in the liver tissue. Our findings evidence the depleting effect of PFOA on antioxidative systems and confirm that PFOA exerts its (neuro)toxicity through oxidative stress, but further research is needed to identify the exact toxicity mechanisms, especially in the brain.