Alteration of membrane integrity and respiratory function of brain mitochondria in the rats chronically exposed to a low dose of acetamiprid (original) (raw)
Related papers
Impact of Imidacloprid on the Mitochondrial Function of Wistar Rats' Nervous System
Journal of chemical health risks, 2024
Pesticides are chemicals used to struggle against harmful pests; they could affect any compartment after getting into nature. Most pesticides are made up of only a selective molecule. When compared to bulk materials like powders, plates, and sheets, pesticides have a relatively large specter-to-volume ratio because of their extremely potent chemical makeup. Because of this characteristic, pesticides might have unexpected chemical and physical characteristics because they interact with the molecules in the environment and compartment. The present assessment aims to test the neurotoxicity induced by a pesticide of Imidacloprid at 1.252 mM kg-1 per day in the Wistar rat's brain. After gavage to the rats for 3 months in laboratory conditions of the groups (light/dark; humidity), tests on nervous system enzymes figured that pesticide caused a significant enhancement of inter-mitochondrial metabolites amount (proteins, fats, and carbohydrates) and mitochondrial enzyme activity (GST and SOD); decreased amount of mitochondrial GSH; an enhancement of mit-CAT and mit-GPx activity; a rise in MDA level. Mitochondrial functions of the treated Rat's brains showed a notable rise in mitochondrial swelling and permeability. Rather, there was a statistically significant drop in the amount of oxygen consumed by mitochondrial respiration. All results confirm that the pesticide caused a dose-dependent response.
Ecotoxicology and Environmental Safety, 2012
Organophosphate pesticides are among the most widely used synthetic chemicals for controlling domestic and agricultural pests. Present study was aimed to evaluate the potential of chlorpyrifos, parathion and malathion, to disturb glutathione homeostasis in rat tissues and to find out whether the pre-feeding of antioxidant vitamins has some ameliorating effect on the pesticide-induced alterations. The results showed that these pesticides, alone or in combination, caused decrease in the levels of GSH and the corresponding increase in the levels of GSSG, decreasing the GSH/GSSG ratio. The results also showed NADPH/NADP þ and NADH/NAD þ ratios were also decreased in the rat tissues on pesticide exposure. These pesticides, alone or in combination, caused increase in the activities of glutathione reductase and glucose-6-phosphate dehydrogenase in all the rat tissues studied. The findings show that these pesticides generate oxidative stress and prior feeding of mixture of antioxidant vitamins tend to reduce the toxicities of these pesticides.
Environmental Sciences and Pollution Research, 2024
Imidacloprid (IMI), a neonicotinoid pesticide, has been widely used due to its high efficiency against insect pests. However, its prolonged exposure may pose significant risks to non-target organisms, including mammals. Recent studies have raised concerns about its potential neurotoxicity, yet the underlying mechanisms remain poorly understood. This study aimed to assess the neurotoxic effects of chronic Imidacloprid exposure in Wistar rats, focusing on oxidative stress, mitochondrial dysfunction, and lysosomal disruption. Wistar rats were orally administered two doses of Imidacloprid (5 mg/kg and 50 mg/ kg body weight) for three months. Neurotoxic effects were assessed by measuring key biochemical markers such as the enzymatic activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione S-transferase (GST). Non-enzymatic markers, including glutathione (GSH) levels and malondialdehyde (MDA) index, were also evaluated. Mitochondrial function was assessed by analyzing oxygen consumption, swelling, and membrane permeability and histopathological changes. Lysosomal stability was examined using the Neutral Red Retention Time (NRRT) assay. Neutral red is a dye that accumulates in the acidic environment of lysosomes. Healthy lysosomes retain the dye, while compromised lysosomes lose it, indicating destabilization. By measuring the amount of neutral red retained in lysosomes, the NRRT assay assesses lysosomal integrity. Lysosomal pH variations were also monitored to evaluate functional changes. Microscopic analysis provided insight into structural changes in lysosomes and other cell components. Lysosomal destabilization was further confirmed by morphological alterations observed through light microscopy, revealing a progressive, time-dependent Responsible Editor: Lotfi Aleya Extended author information available on the last page of the article Content courtesy of Springer Nature, terms of use apply. Rights reserved. Environmental Science and Pollution Research degeneration of lysosomal structures, including lysosomal expansion, neutral red dye leakage, and cell rounding. These changes reflected a temporal evolution of lysosomal damage, progressing from minor structural disruptions to more severe alterations as exposure continued, observable at the microscopic level. During the study, clinical observations of intoxicated rats included symptoms such as lethargy, reduced activity levels, and impaired motor coordination. High-dose Imidacloprid exposure led to noticeable behavioral changes, including decreased exploratory behavior and altered grooming patterns. Additionally, signs of neurotoxic effects, such as tremors or ataxia, were observed in the rats exposed to the higher dose, reflecting the systemic impact of chronic pesticide exposure. The results revealed a significant decrease in the enzymatic activities of CAT, GPx, and SOD, accompanied by an increase in GST activity. A notable reduction in glutathione levels and a rise in MDA index were observed, indicating enhanced oxidative stress in the brain. Mitochondrial impairment was evidenced by disturbances in oxygen consumption, increased swelling, and altered membrane permeability. Lysosomal destabilization was confirmed by reduced retention of neutral red dye, structural changes in lysosomes, and a significant rise in lysosomal pH in the IMI-exposed groups. In addition, the histopathological features indicate that imidacloprid at the given dose and exposure duration may have caused notable neurotoxic effects in Wistar rat brain tissue. Chronic exposure to Imidacloprid induces oxidative stress, mitochondrial dysfunction, lysosomal disruption and histopathological alterations in the central nervous system of Wistar rats. These findings provide valuable insights into the neurotoxic mechanisms of neonicotinoid pesticides, highlighting the need for further research to understand the long-term effects of Imidacloprid exposure on mammalian health.
Oxidative Medicine and Cellular Longevity, 2022
Pesticides are important chemicals or biological agents that deter or kill pests. The use of pesticides has continued to increase as it is still considered the most effective method to reduce pests and increase crop growth. However, pesticides have other consequences, including potential toxicity to humans and wildlife. Pesticides have been associated with increased risk of cardiovascular disease, cancer, and birth defects. Labels on pesticides also suggest limiting exposure to these hazardous chemicals. Based on experimental evidence, various types of pesticides all seem to have a common effect, the induction of oxidative stress in different cell types and animal models. Pesticide-induced oxidative stress is caused by both reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are associated with several diseases including cancer, inflammation, and cardiovascular and neurodegenerative diseases. ROS and RNS can activate at least five independent signaling pathways including mitochondrial-induced apoptosis. Limited in vitro studies also suggest that exogenous antioxidants can reduce or prevent the deleterious effects of pesticides.
Pesticides-induced oxidative damage: Possible in vitro protection by antioxidants
This study was designed to investigate the effect of selenium (Se) and a combination of vitamin E (VE) vitamin C (VC) on pesticides induced biochemical alterations in rat erythrocytes and hepatocytes in vitro. Vitamin E and C and selenium are potential antioxidants, known to be able to protect cells against oxidative damage. In vitro changes in antioxidant systems and protective role of selenium and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes and hepatocytes induced by atrazine (AT), dimethoate (DM), or endosulfan (ES) at three different levels of 10, 20, and 30 mM for each in rat were investigated. Levels of lipid peroxidation (nmoles MDA/mg protein), glutathione content (µmole GSH/mg protein) and glutathione peroxidase level (µmoles NADPH/min/mg protein) were determined in erythrocytes and hepatocytes following treatment. In comparison with the control, pesticides stimulated thiobarbituric acid reactive substances (TBARS) activity and glutathione p...
PLoS ONE, 2012
Many pesticides are used increasingly in combinations during crop protection and their stability ensures the presence of such combinations in foodstuffs. The effects of three fungicides, pyrimethanil, cyprodinil and fludioxonil, were investigated together and separately on U251 and SH-SY5Y cells, which can be representative of human CNS glial and neuronal cells respectively. Over 48h, all three agents showed significant reductions in cellular ATP, at concentrations that were more than tenfold lower than those which significantly impaired cellular viability. The effects on energy metabolism were reflected in their marked toxic effects on mitochondrial membrane potential. In addition, evidence of oxidative stress was seen in terms of a fall in cellular thiols coupled with increases in the expression of enzymes associated with reactive species formation, such as GSH peroxidase and superoxide dismutase. The glial cell line showed significant responsiveness to the toxin challenge in terms of changes in antioxidant gene expression, although the neuronal SH-SY5Y line exhibited greater vulnerability to toxicity, which was reflected in significant increases in caspase-3 expression, which is indicative of the initiation of apoptosis. Cyprodinil was the most toxic agent individually, although oxidative stress-related enzyme gene expression increases appeared to demonstrate some degree of synergy in the presence of the combination of agents. This report suggests that the impact of some pesticides, both individually and in combinations, merits further study in terms of their impact on human cellular health.
European Journal of Molecular & Clinical Medicine, 2021
Neurodegenerative diseases are associated with oxidative stress. By using SH-SY5Y human neuroblastoma cells as a model, we assessed that pesticide containing carbamates as an active group targets mitochondria and responsible for oxidative cell death. Our results showed that when SH-SY5Y cells were exposed in time dependant manner with carbamates compound, cell death and mitochondrial SOD enzyme level were increased. However, there was no change in the level of cytosolic SOD1 enzyme was observed in time dependant manner in SH-SY5Y cells. These findings revealed that the cytotoxicity and oxidative stress in SH-SY5Y is linked with mitochondrial SOD2 induced by carbamates pesticide. These data also indicate that mitochondria are important early targets of carbamate-induced oxidative neurotoxicity.
Oxidative stress in the blood of farm workers following intensive pesticide exposure.
The aim of this study was to evaluate oxidative stress in workers who formulate organophosphate, synthetic pyrethroid and carbamate pesticides. In this survey, blood erythrocytes from a group of 94 pesticide-formulating workers (at least 5-years experience in pest-control in apple and cherry production) and 45 control subjects were examined for oxidative stress parameters. The control group was composed of 45 healthy people living in the same region with no exposure to pesticides. Lipid peroxidation level, catalase, superoxide dismutase and glutathione peroxidase activities in erythrocytes were analysed as biomarkers of oxidative stress. In addition, the acetylcholinesterase activity was measured as a biomarker of toxicity. Results indicated that chronic exposure to organophosphate, synthetic pyrethroid and carbamate pesticides were associated with increased activities of catalase, SOD and lipid peroxidation in erythrocytes (p < 0.05). Acetylcholinester-ase activity did not show any significant differences between the two groups (p > 0.05). It is concluded that human chronic exposure to pesticides may result in stimulated antioxidant enzymes.