Activation and modulation of human α4β2 nicotinic acetylcholine receptors by the neonicotinoids clothianidin and imidacloprid

Li, Ping; Ann, Jason; Akk, Gustav

doi:10.1002/jnr.22644

Cited by 78 publications

(62 citation statements)

References 28 publications

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“…It has been reported (Bray et al, 2005) that sperm nAChRs play a central role in the control of motility associated with calcium influx mechanisms, and mice deficient in the nAChR subunit, a7, produce impaired sperm motility. Li et al (2011) have also reported that imidacloprid, but not CTD, strongly inhibits the a4 and b2 subunits of nAChRs activated by acetylcholine in human embryonic kidney cells. Therefore, any drug-affected nicotinic system may cause disturbed function of testicular tissue and sperm.…”

Section: Discussionmentioning

confidence: 92%

Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

Bal¹,

Türk²,

Tuzcu³

et al. 2013

Drug and Chemical Toxicology

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Clothianidin (CTD) is a novel, broad-spectrum insecticide. In the current study, it was aimed to study the effect of subchronic exposure to low doses of CTD (2, 8 and 24 mg/kg body weight/day) on the reproductive system in adult rats. CTD treatment did not significantly change serum testosterone level or sperm parameters (e.g. concentration, motility and morphology), but caused significant decreases in weights of epididymis, right cauda epididymis and seminal vesicles. CTD treatment did not cause sperm DNA fragmentation and did not change the apoptotic index in the seminiferous tubules and levels of α-tocopherol and glutathione, but increased the level of thiobarbituric acid-reactive substances and cholesterol levels significantly at all doses. CTD exposure caused significant elevations in palmitic, linoleic and arachidonic acids in testis in all CTD-exposed groups. There was a drop in 20:4/18:2 (arachidonic acid/linoleic acid) ratio and an increase in 18:1n-9/18:0 (oleic acid/stearic acid) ratios in all CTD groups, in comparison to the control group. In conclusion, CTD had little detectable detrimental effects on the reproductive system of male rats over the measured parameters.

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Section: Discussionmentioning

confidence: 92%

Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

Bal¹,

Türk²,

Tuzcu³

et al. 2013

Drug and Chemical Toxicology

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show abstract

“…It has been reported (Bray et al 2005) that sperm nAChRs play a central role in the control of motility associated with the calcium influx mechanisms, and mice deficient in nAChR subunit α7 produce impaired sperm motility. Li et al (2011) have also reported that although neonicotinoids imidacloprid but not CTD strongly inhibits the α4 and β2 subunits of nAChR activated by acetylcholine in human embryonic kidney cells. Therefore, any drug affected nicotinic system may cause disturbed function of the testicular tissue and sperm.…”

Section: Discussionmentioning

confidence: 93%

Effects of clothianidin exposure on sperm quality, testicular apoptosis and fatty acid composition in developing male rats

et al. 2012

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Clothianidin (CTD) is one of the latest members of the synthetic organic insecticides, the neonicotinoids. In the present study, it was aimed to investigate if daily oral administration of CTD at low doses for 90 days has any deleterious effects on reproductive functions of developing male rats. Animals were randomly divided into four groups of six rats each, assigned as control rats, or rats treated with 2 (CTD-2), 8 (CTD-8) or 32 (CTD-32) mg CTD/kg body weight by oral gavage. The significant decreases of the absolute weights of right cauda epididymis and seminal vesicles, and body weight were detected in the animals exposed to CTD administration at 32 mg/kgBW/day. Epididymal sperm concentration decreased significantly in CTD-32 group and the abnormal sperm rates increased in CTD-8 and CTD-32 groups when compared to control group. The testosterone level was significantly decreased in CTD-32 group when compared to control group. The administration of all CTD doses resulted in a significant decrease in the level of GSH. The number of TUNEL-positive cells significantly increased in the germinal epithelium of testis of rats exposed to CTD at 32 mg/kgBW/day. In groups CTD-8 and CTD-32, only docosapentaenoic, arachidonic, palmitic and palmitoleic acids were significantly elevated when compared to control. The ratios of 20:4/18:2 and 18:1n-9/18:0 were decreased when rats exposed to CTD. Sperm DNA fragmentation was observed in CTD-32 group, but not CTD-2 and CTD-8. It is concluded that low doses of CTD exposure during critical stages of sexual maturation had moderate detrimental effects on reproductive organ system and more severe effects are likely to be observed at higher dose levels. In addition, the reproductive system may be more sensitive to exposure of CTD even earlier in development (prenatal and early postnatal), and therefore it could be expected that more severe effects could also be observed at the NOAEL dose levels, if dosing had occurred in utero or early postnatal.

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“…Neonicotinoids are not only used for agricultural crop protecNeonicotinoids are broad-spectrum insecticides, acting on nicotinic acetylcholine receptors providing a selecnicotinic acetylcholine receptors compared to the vertebrate equivalents (Matsuda et al, 2001;Bal et al, 2010;Li et al, 2011). Previously the correlation between nicand improved insulin sensitivity was reported (Xu et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Imidacloprid, a neonicotinoid insecticide, induces insulin resistance

Kim

Park

Yoon³

et al. 2013

J. Toxicol. Sci.

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exposures, which includes insecticides, and development of type 2 diabetes. However, there is limited -betes. Thus, the purpose of the study was to determine effects of imidacloprid, a neonicotinoid insecticide, on glucose metabolism. Three different cell models were used; adipocytes (3T3-L1), hepatocytes 4-6 days followed by treatment with insulin for 15 min to determine responses. Insulin stimulated glucose uptake was reduced by imidacloprid in all three cell culture models. Treatment with imidacloprid reduced phosphorylation of protein kinase B (AKT), one of the major regulators of insulin signaling, without changing overall AKT expression. Subsequently, imidacloprid reduced phosphorylation of ribosomal S6 kinase (S6K), which is a downstream target of AKT and also a feed-back inhibitor of insulin signaling. These results suggest that imidacloprid could induce insulin resistance by affecting the insulin signaling cascade, particularly up-stream of AKT, in adipocytes, liver, and muscle.

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Activation and modulation of human α4β2 nicotinic acetylcholine receptors by the neonicotinoids clothianidin and imidacloprid

Cited by 78 publications

References 28 publications

Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

Effects of clothianidin exposure on sperm quality, testicular apoptosis and fatty acid composition in developing male rats

Imidacloprid, a neonicotinoid insecticide, induces insulin resistance

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