Abstract:Pesticides are a mixture of chemical substances used to kill pests. Apart from their toxicity to pests, thy affect nontarget organisms. They also generate free radicals producing reactive oxygen species (ROS) which can disturb cellular pathways by inhibiting various enzymes or receptors. Pesticides also induce oxidative DNA damage, DNA adducts, and single or double strand DNA breaks. Various mechanisms of DNA repair deal with such damages and help to maintain cell integrity. Alteration in DNA repair genes modu… Show more
“…Flubendiamide does not have genotoxic effects on bone marrow cells [1][2][3][4][5][6]. But there are reports that exposure to certain xenobiotics, either individually or in combination, may result in gene mutation, chromosomal aberrations and DNA damage [7][8][9].…”
Background: Living organisms are frequently exposed to more than one xenobiotic at a time either by ingestion of contaminated food/fodder or due to household practices, occupational hazards or through environment. These xenobiotics interact individually or in combination with biological systems and act as carcinogen or produce other toxic effects including reproductive and degenerative diseases. Present study was aimed to investigate the cyto-genotoxic effects of flubendiamide and copper and ameliorative potential of certain natural phyotconstituent antioxidants. Method: In vitro cytogenotoxic effects were evaluated by employing battery of assays including Propidium iodide staining, Tunel assay, Micronuclei, DNA fragmentation and Comet assay on isolated splenocytes and their prevention by resveratrol (5 and 10 μM), catechin (10 and 20 μM), curcumin (5 and 10 μM) and α-tocopherol (5, 10 and 20 μM). In vivo study was also undertaken daily oral administration of flubendiamide (200 mg/kg) or copper (33 mg/kg) and both these in combination, and also all these concurrently with of α-tocopherol to Wistar rats for 90 days. Results: Flubendiamide and copper produced concentration-dependent cytotoxic effects on splenocytes and at median lethal concentrations, flubendiamide (40 μM) and copper (40 μM) respectively produced 71 and 81% nonviable cells, higher number of Tunel+ve apoptotic cells, 7.86 and 9.16% micronucleus and 22.90 and 29.59 comets/100 cells and DNA fragmentation. In vivo study revealed significant (P < 0.05) increase in level of lipid peroxidation (LPO) and decrease in glutathione peroxidase (GPx), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in groups exposed to flubendiamide or copper alone or both these in combination. Histopathological examination of rat spleens revealed depletion of lymphoid tissue, separation of splenocytes and rarification in splenic parenchyma of xenobiotic(s) treated groups.
“…Flubendiamide does not have genotoxic effects on bone marrow cells [1][2][3][4][5][6]. But there are reports that exposure to certain xenobiotics, either individually or in combination, may result in gene mutation, chromosomal aberrations and DNA damage [7][8][9].…”
Background: Living organisms are frequently exposed to more than one xenobiotic at a time either by ingestion of contaminated food/fodder or due to household practices, occupational hazards or through environment. These xenobiotics interact individually or in combination with biological systems and act as carcinogen or produce other toxic effects including reproductive and degenerative diseases. Present study was aimed to investigate the cyto-genotoxic effects of flubendiamide and copper and ameliorative potential of certain natural phyotconstituent antioxidants. Method: In vitro cytogenotoxic effects were evaluated by employing battery of assays including Propidium iodide staining, Tunel assay, Micronuclei, DNA fragmentation and Comet assay on isolated splenocytes and their prevention by resveratrol (5 and 10 μM), catechin (10 and 20 μM), curcumin (5 and 10 μM) and α-tocopherol (5, 10 and 20 μM). In vivo study was also undertaken daily oral administration of flubendiamide (200 mg/kg) or copper (33 mg/kg) and both these in combination, and also all these concurrently with of α-tocopherol to Wistar rats for 90 days. Results: Flubendiamide and copper produced concentration-dependent cytotoxic effects on splenocytes and at median lethal concentrations, flubendiamide (40 μM) and copper (40 μM) respectively produced 71 and 81% nonviable cells, higher number of Tunel+ve apoptotic cells, 7.86 and 9.16% micronucleus and 22.90 and 29.59 comets/100 cells and DNA fragmentation. In vivo study revealed significant (P < 0.05) increase in level of lipid peroxidation (LPO) and decrease in glutathione peroxidase (GPx), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in groups exposed to flubendiamide or copper alone or both these in combination. Histopathological examination of rat spleens revealed depletion of lymphoid tissue, separation of splenocytes and rarification in splenic parenchyma of xenobiotic(s) treated groups.
“…1 Exposure to pesticides is concerning because many studies have associated occupational exposure to these chemicals with an increased incidence of various diseases, including cancer, Parkinson's disease, Alzheimer's disease, reproductive disorders, and birth defects. 2 Exposure to pesticides can induce oxidative stress by increased production of free radicals, which accumulate in cells and can cause gene mutations and chromosomal aberrations. [3][4][5] In recent years, genotoxicity from exposure to pesticides has been extensively investigated in cell lines and animal models.…”
“…More recently, occupational exposure to a variety of pesticides including herbicides, insecticides, and fungicides were associated with the development of PD in France [3]. In addition to preferentially damaging dopaminergic neurons, these agents share several common mechanisms of action including increasing neuronal oxidating stress, damaging mitochondrial complex I, and impairing the ubiquitin-proteasome system [4,5].…”
Background Multiple studies have suggested that various pesticides are associated with a higher risk of developing Parkinson’s disease (PD) and may influence the progression of the disease. This study examines whether pesticide exposure influences the risk of mortality among patients with PD in Southern Brazil, when accounting for socioeconomic status, nicotine exposure, and caffeine exposure. Methods 150 patients with idiopathic PD were enrolled from 2008-2013 and followed until 2019. In addition to undergoing a detailed neurologic evaluation, patients completed surveys regarding socioeconomic status and environmental exposures. Results Twenty patients (13.3%) reported a history of occupational pesticide exposure with a median duration of exposure of 10 years (mean = 13.1, SD = 11.2). Patients with a history of occupational pesticide exposure had higher UPDRS-III scores, though there were no significant differences in regards to age, sex, disease duration, Charlson Comorbidity Index, and age at symptom onset. Patients with occupational pesticide exposure were more than twice as likely to die than their unexposed PD counterparts (HR = 2.32, 95% CI [1.15, 4.66], p = 0.22). Occupational pesticide exposure was also a significant predictor of death in a cox-proportional hazards model which included smoking and caffeine intake history and another which included several measures of socioeconomic status. Conclusion In this prospective cohort study, we found an increased all-cause mortality risk in PD patients with occupational exposure to pesticides. More studies are needed to further analyze this topic with longer follow-up periods, more detailed exposure information, and more specific causes of mortality.
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