2009
DOI: 10.1016/j.pestbp.2009.02.003
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Neurotoxic effects of subacute exposure of dichlorvos and methyl parathion at sublethal dosages in rats

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Cited by 18 publications
(10 citation statements)
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“…This is consistent with the study of Celik and Isik (2009). They reported that in animals intoxicated with methyl parathione and dichlorvos at sub lethal concentrations, AChE and butyl cholinesterase (BChE) activities are Newairy and Abdou 5239 inhibited.…”
Section: Chlorpyrifossupporting
confidence: 89%
“…This is consistent with the study of Celik and Isik (2009). They reported that in animals intoxicated with methyl parathione and dichlorvos at sub lethal concentrations, AChE and butyl cholinesterase (BChE) activities are Newairy and Abdou 5239 inhibited.…”
Section: Chlorpyrifossupporting
confidence: 89%
“…Neurotoxicity of OP compounds has been mainly explained by accumulation of acetylcholine, due to the inhibition of AChE and BChE activities, that produces cholinergic effects (Lotti, 2001;Darvesh et al, 2003;Celik and Isik, 2009;Sekar Babu et al, 2010;Li et al, 2011). Other pathways, including changes of the lipid profile of the nervous tissue as well as induction of apoptosis and necrosis of the nervous cells seem also to be involved (Brocardo et al, 2005;Üner et al, 2006;Kaur et al, 2007;El-Demerdash, 2011;Li et al, 2011;Solati et al, in press); however, up to now the non-cholinergic (non-cholinesterases-related) mechanisms have not been appropriately evaluated.…”
Section: Discussionmentioning
confidence: 99%
“…The impact of OP compounds on the nervous system was a subject of numerous studies (Lotti, 2001;Sekar Babu et al, 2010;Kaur et al, 2007;Celik and Isik, 2009;Li et al, 2011;Solati et al, in press); however, still there is a lack of investigations focused on the effect of low oral exposure, being the main route of human intoxication with these compounds during the lifetime, on the non-cholinergic pathway. The measurements performed in the present study draw attention to the involvement in the OP pesticides-induced CNS damage of the non-related to cholinesterases inhibition pathways such as destroying the brain lipid profile and reduction of the living brain cells due to their enhanced apoptosis and necrosis.…”
Section: Variablementioning
confidence: 99%
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