Potential protective effects of red grape seed extract in a rat model of malathion-induced neurotoxicity (original) (raw)
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Journal of nanoscience and nanotechnology, 2018
The aim of this study was to investigate the effect of treatment with grape seed extract (GSE) on the neurotoxic and genotoxic effects of acute malathion exposure. Rats received malathion (150 mg/kg by i.p. injection) for two successive days alone or combined with GSE at doses of 150 or 300 mg/kg, orally or with GSE at 300 mg/kg and atropine at a dose of 2 mg/kg, i.p. Malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide, paraoxonase (PON1) were determined in cortex, striatum, and rest of brain tissue (subcortex). Interleukin-1β (IL-1β), and butyrylcholinesterase (BChE) activities were determined in brain regions. Cytogenetic analyses for chromosomal aberrations in somatic and germ cells, micronucleus test, Comet assay, DNA fragmentation of liver cells and histopathological examination of brain and liver sections were also performed. Malathion resulted in an increase in MDA, nitric oxide; a decrease in GSH and PON1 activity in different brain regions. IL-1β increased, while...
Basic & Clinical Pharmacology & Toxicology, 2008
The wide use of the organophosphate insecticide malathion is accompanied by the risk of human exposure, especially in developing countries, which underlines the need of basic studies in this area. Some reports have shown that low doses of malathion, in a repeated treatment regimen, are unable to reduce acetylcholinesterase (AChE) activity in the rat brain, in contrast to the inhibitory effect in acute treatment. In order to investigate if AChE activity is affected by repeated low-level malathion administration, female Wistar rats were exposed to malathion (50 and 100 mg/kg, intraperitoneally) for 3 consecutive days. Exposure to malathion 50 mg/kg did not affect AChE activity, as previously observed. Contrary to expectation, 100 mg/kg malathion produced a significant increase in AChE activity in both cerebral cortex and hippocampus. Besides AChE inhibition, malathion may act as a pro-oxidative agent by interfering with antioxidant defences, as shown by a decrease of glutathione peroxidase and glutathione reductase activity in the cerebral cortex (100 mg/kg malathion). These effects are in contrast to response in the hippocampus where the increase in AChE activity correlates positively with the antioxidant defences, while the opposite was found in the cerebral cortex. These data indicate that, with low doses, and after a short period of exposure, malathion induces an up-regulation of AChE activity, a pattern similar to that found in the hippocampus for the antioxidant defences studied. The cerebral cortex was more vulnerable to malathion, as reflected in a decrease of two antioxidant enzymes. This study indicates that (i) alternatively to AChE inhibition, interference with the antioxidant defence system may be another important target for malathion toxicity; (ii) hippocampal and cortical AChE activity in rats can be increased after repeated low-dose malathion exposure. This response suggests the occurrence of a pathophysiological response in order to maintain the homeostasis of the cholinergic system in these cerebral structures.
Neurotoxic Effects of Chronic Malathion Exposure in BALB/c Mice
Mansoura Journal of Forensic Medicine and Clinical Toxicology
Malathion is one of the commonly used organophosphates pesticides (OPs) in Egypt. Chronic exposure to some OPs has been linked to many neurological disorders such as cognitive deficits, Parkinson's disease and mood disturbances. It is suggested that neuroinflammation has an important role in mediating such diseases. The present research aims to investigate the neurotoxic effects of chronic malathion exposure in BALB/c mice and to clarify the possible role of inflammation. This study included 48 adult mice that were randomly divided into four groups (12 mice each) as follows: control group: mice did not receive any treatment and three test groups which were given malathion dissolved in distilled water once daily by gastric gavage for two months at 50, 100 and 200 mg / kg respectively. Neurotoxic effects were assessed through two behavioral tests then histopathological examination of the brains was done. The results revealed that malathion-exposed mice developed locomotor impairment in the form of increased foot slips and decreased efficient path in parallel rod floor test in addition to impaired performance of open field test. The neurobehavioral deficits were associated with histopathological changes e.g., decreased corpus striatum fiber density, increased dopaminergic neurodegeneration in substantianigra and increased microglial activation. The present findings suggest a potential role of neuro-inflammation in malathioninduced neurotoxicity.
Neuroprotection of Grape Seed Extract and Pyridoxine against Triton-Induced Neurotoxicity
Triton WR-1339 administration causes neurotoxicity. Natural products and herbal extracts can attenuate cerebral injury. In the present study, we investigated the neuroprotective role of grape seed extract and/or vitamin B6 against triton-induced neurotoxicity. Thirty-five adult male albino rats of the Sprague-Dawley strain, weighing 140-145 g, were divided into five groups: control, triton, grape seed extract + triton, grape seed extract + triton + vitamin B6, and vitamin B6 + triton. The hematological and biochemical analyses were carried out. Alteration in iNOS mRNA gene expression was determined using reverse-transcriptase PCR analysis. In addition, qualitative DNA fragmentation was examined using agarose gel electrophoresis. Triton-treatment caused significant disturbances in the hematological parameters, the neurological functions, and the antioxidant profile. Also, triton significantly increased the iNOS mRNA expression and DNA damage. Our results showed that grape seed extract and/or vitamin B6 could attenuate all the examined parameters. These natural substances could exhibit protective effects against triton-induced neurological damage because of their antioxidative and antiapoptotic capacities.
Malathion-induced Oxidative Stress in Rat Brain Regions
Neurochemical Research, 2006
Malathion is a pesticide with high potential for human exposure. However, it is possible that during the malathion metabolism, there is generation of reactive oxygen species (ROS) and malathion may produce oxidative stress in intoxicated rats. The present study was therefore undertaken to determine malathion-induced lipid peroxidation (LPO), protein carbonylation and to determine whether malathion intoxication alters the antioxidant system in brain rats. Malathion was administered intraperitoneally in the acute and chronic protocols in the doses of 25, 50, 100 and 150 mg malathion/kg. The results showed that LPO in brain increased in both protocols. The increased oxidative stress resulted in an increased in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), observed in cortex, striatum in the acute malathion protocol and hippocampus in the chronic malathion protocol. Our results demonstrated that malathion induced oxidative stress and modulated SOD and CAT activity in selective brain regions.
International Journal of Advanced Research in Biological Sciences (IJARBS)
Aim: Pesticide residues contamination in exported grapes has been monitored in this study, then the obtained results of this survey were used to create laboratory simulations of mixtures that would be encountered by a consumption of contaminated grapes. Experiment: Malathion, lambada-cyhalothrin and diniconazole were the highest frequented pesticides in grapes. It has been detected in 45 (75%) samples out of 60 grapes samples were analyzed. The impact of those pesticides residues were applied in mixtures typical of what real exposure would experience has been studied. Rats have been treated with two different concentrations the higher and lower concentration which detected in grapes. Results: Our results reported that the exposure to pesticide mixture induced dose dependent effect in experimental animals expressed by significant inhibition of AChE, hyperglycemia that it is a mechanism of oxidative stress induced degeneration in liver and pancreas tissues. Conclusion: results indicated that low-level, widespread exposures to pesticide mixtures could impair biological activities in rats. It also shows that traditional approaches to assessing the pesticide toxicity effects one pesticide at a time completely miss understand the health impact of pesticides residues exposure. Further studies to examine the molecular changes of pesticides mixtures exposure are recommended.
Nutritional Neuroscience, 2012
One of the main concerns regarding organophosphate pesticides (OP) is their possible toxic effects. Doses that do not produce acute toxicity are capable of altering the structure and biochemistry of different tissues and organs by production of reactive oxygen species (ROS). Curcumin (CUR) is the main substance in Curcuma longa (Zingiberacea) rhizome that has strong antioxidant activity. However, the neuroprotective properties of curcumin against oxidative stress induced by prolonged exposure to parathion (PAR) is not clear. Objective: The present work evaluated the protective effect of curcumin against the oxidative damage induced in the rat hippocampus by the OP PAR. Methods: Forty female Wistar rats were distributed in four groups as follows: exposed to PAR by inhalation (PAR group); pre-treated with CUR and then exposed to PAR by inhalation, (CUR + PAR group); exposed to environmental air and treated with CUR in the food (CUR group); and exposed to environmental air (the control group). At the end of the handling process, the concentration of erythrocyte cholinesterase was monitored, as indicator of PAR intoxication and lipoperoxidation, immunohistochemistry for astrocytes, and activated microglia and apoptosis was determined in the hippocampus. Results: In the present study, we show that the administration of CUR (200 mg/kg body weight) significantly diminished the oxidative damage in the hippocampus of rats exposed to the OP PAR. Discussion: These data suggest that CUR may be an alternative to prevent neurodegenerative damage after pesticide exposure.
Journal of Drug Delivery and Therapeutics
Background: Parastar is an agricultural insecticide formulation composed of two active ingredients; a pyrethroid lambda-cyhalothrin and a neonicotinoid imidachloprid used in Cameroon for vegetable protection. Previous studies showed reprotoxicity and neurotoxicity of this pesticide formulation. Momordica foetida Schumach. Et Thonn is a medicinal plant with potent antioxidant properties used traditionally in Cameroon for the treatment of several aliments. As farmers are currently exposed to Parastar pesticide formulation, this study was designed to evaluate the protective effect of M. foetida on behavioral impairment, motor incoordination and brain oxidative stress induced by subchronic administration of Parastar. Methods: The study was carried out using 40 Wistar male rats, divided into 5 groups of 8 rats each. The groups received a vehicle (distilled water; 10 mL/kg), Parastar alone (6.23 mg/kg), or concomitantly with M. foetida methanol extract (50, 100 and 200 mg/kg) for 60 days....
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.