Effect of permethrin insecticide on rat polymorphonuclear neutrophils

Gabbianelli, Rosita; Falcioni, Maria Letizia; Nasuti, Cinzia; Cantalamessa, Franco; Imada, Isuke; Inoue, Masayasu

doi:10.1016/j.cbi.2009.09.006

Cited by 43 publications

(28 citation statements)

References 41 publications

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“…Because, increases in TOS levels and decreases in TAC levels were determined in PM alone treated cultures as compared to control group. In accordance with our findings, recent investigations clearly indicated that PM-induced oxidative stress leads to biochemical and functional changes in organisms (Hu et al, 2010;Nasuti et al, 2007;Gabbianelli et al, 2009;Issam et al, 2011).…”

Section: Discussionsupporting

confidence: 93%

Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes

Türkez

Toğar

2011

J. Toxicol. Sci.

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-The aim of this study was to investigate the protective effects of olive leaf extract (OLE) on genotoxicity and oxidative damage in cultured human blood cells treated with permethrin (PM) in the presence of a rat liver S9 mix containing cytochrome P 450 enzymes. Anti-genotoxic activities of OLE were studied using sister chromatid exchange (SCE) and chromosome aberration (CA) tests and furthermore total antioxidant capacity (TAC) and total oxidative status (TOS) were examined to determine the oxidative damage. Our results clearly revealed that treatment with PM (200 mg/l) alone increased SCE and CA rates and TOS level, decreased TAC level in cultured human blood cells. The OLE alone at the all tested doses did not induce any significant changes in the genotoxicity endpoint. However OLE leads to increases of plasma TAC level in vitro. OLE starts showing this positive effect at 100 mg/l. The combined treatment showed significant improvements in cytogenetic and biochemical parameters tested. Moreover, this improvement was more pronounced in the group received the high dose of the OLE. It could be concluded that the ethanol extract of OLE induced its genoprotective effect via the increase in the antioxidant capacity, inhibition of oxidative stress and scavenging of free radicals.

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Section: Discussionsupporting

confidence: 93%

Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes

Türkez

Toğar

2011

J. Toxicol. Sci.

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“…Because, the PM administration (group C) caused increases of TOS level and decrease of TAC level as compared to control group (group A). In accordance with our findings, recent investigations clearly indicated that PM-induced oxidative stress leads to biochemical and functional changes in organisms (Nasuti et al 2007;Gabbianelli et al 2009;Issam et al 2011). The present study also demonstrated that the reduction of PM induced oxidative and DNA damages was caused by the protective effect of OLE.…”

Section: Discussionsupporting

confidence: 93%

Olive leaf extract modulates permethrin induced genetic and oxidative damage in rats

2012

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Permethrin is a common synthetic chemical, widely used as an insecticide in agriculture and other domestic applications. The previous reports indicated that permethrin is a highly toxic synthetic pyrethroid pesticide to human and environmental health. Therefore, the present experiment was undertaken to determine the effectiveness of olive leaf extract in modulating the permethrin induced genotoxic and oxidative damage in rats. The animals used were broadly divided into four (A, B, C and D) experimental groups. Group A rats served as control animals and received distilled water intraperitoneally (n = 5). Groups B and C rats received intraperitoneal injections of permethrin (60 mg kg -1 b.w) and olive leaf extract (500 mg kg -1 b.w), respectively. Group D rats received permethrin (60 mg kg -1 b.w) plus olive leaf extract (500 mg kg -1 b.w). Rats were orally administered their respective feed daily for 21 days. At the end of the experiment rats were anesthetized and serum and bone marrow cell samples were obtained. Genotoxic damage was assessed by micronucleus and chromosomal aberration assays. Total antioxidant capacity and total oxidant status were also measured in serum samples to assess oxidative status. Treatment of Group B with permethrin resulted in genotoxic damage and increased total oxidant status levels. Permethrin treatment also significantly decreased (P \ 0.05) total antioxidant capacity level when compared to Group A rats. Group C rats showed significant increases (P \ 0.05) in total antioxidant capacity level and no alterations in cytogenetic parameters. Moreover, simultaneous treatments with olive leaf extract significantly modulated the toxic effects of permethrin in Group D rats. It can be concluded that olive leaf extract has beneficial influences and could be able to antagonize permethrin toxicity. As a result, this investigation clearly revealed the protective role of olive leaf extract against the genetic and oxidative damage by permethrin in vivo for the first time.

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“…The role of sensitization in modulating this permethrin effect in the heart is not clear; however, pyrethroid insecticides have been shown to disrupt normal cardiac conduction by interrupting sodium channel activation (41). Permethrin has also been shown to be immunotoxic (42); however, permethrin did not cause an inflammatory response in the BAL fluid or blood. Thus, permethrin, at the doses we used, does not appear to have deleterious effects on lung function and inflammation in either nonsensitized or sensitized guinea pigs; however, it may affect cardiac function in sensitized animals.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Sensitization on Mechanisms of Organophosphorus Pesticide–Induced Airway Hyperreactivity

Proskocil

Bruun

Garg

et al. 2015

Am J Respir Cell Mol Biol

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We previously demonstrated that antigen sensitization increases vulnerability to airway hyperreactivity induced by the organophosphorus pesticide (OP) parathion. Sensitization also changes the mechanism of parathion-induced airway hyperreactivity to one that is dependent on IL-5. To determine whether this effect can be generalized to other OPs, and to other classes of pesticides, we measured airway responsiveness to vagal stimulation or intravenous acetylcholine in nonsensitized and ovalbumin-sensitized guinea pigs 24 hours after a single subcutaneous injection of the OPs diazinon or chlorpyrifos, or the pyrethroid permethrin. Sensitization exacerbated the effects of chlorpyrifos on bronchoconstriction in response to vagal stimulation or intravenous acetylcholine. Pretreatment with function-blocking IL-5 antibody prevented chlorpyrifos-induced airway hyperreactivity in sensitized, but not in nonsensitized, guinea pigs. In sensitized guinea pigs, blocking IL-5 decreased eosinophil activation, as measured by decreased eosinophil major basic protein in the trachea. In contrast, sensitization did not alter diazinon-induced airway hyperreactivity, and permethrin did not cause airway hyperreactivity in either nonsensitized or sensitized guinea pigs. None of the pesticides affected inflammatory cells in the bronchoalveolar lavage fluid or blood. We have previously shown that three different OPs cause airway hyperreactivity via loss of neuronal M2 muscarinic receptor function. Similar to parathion, but unlike diazinon, the mechanism of chlorpyrifos-induced airway hyperreactivity is changed by sensitization. Thus, OP-induced airway hyperreactivity is dependent on sensitization status and on the OP used, which may influence therapeutic approaches.Keywords: airway hyperreactivity; eosinophils; organophosphorus pesticides; permethrin; sensitization Clinical RelevanceA low subcutaneous dose of an organophosphorus pesticide (OP) causes airway hyperreactivity that is dependent on the specific OP and on atopic phenotype. Understanding the mechanism(s) of OP toxicity in different populations will be critical to predicting the physiological response to OP exposure and to designing better therapeutic interventions.The canonical mechanism of acute neurotoxicity after organophosphorus pesticide (OP) exposure is the irreversible inhibition of acetylcholinesterase (AChE), which is the enzyme that hydrolyzes the neurotransmitter, acetylcholine (ACh). ACh plays an integral role in controlling respiration via both the central (1) and peripheral nervous systems. OP poisoning can cause respiratory failure through central cholinergic disruption and acute bronchoconstriction and mucus

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Effect of permethrin insecticide on rat polymorphonuclear neutrophils

Cited by 43 publications

References 41 publications

Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes

Olive (Olea europaea L.) leaf extract counteracts genotoxicity and oxidative stress of permethrin in human lymphocytes

Olive leaf extract modulates permethrin induced genetic and oxidative damage in rats

The Influence of Sensitization on Mechanisms of Organophosphorus Pesticide–Induced Airway Hyperreactivity

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