Toxicity of parathion, systox, octamethyl pyrophosphoramide, and methyl parathion in man

Rider, J. Alfred; Moêller, H.; Puletti, Ernesto J.; Swader, Joyce I.

doi:10.1016/0041-008x(69)90019-2

Cited by 47 publications

(16 citation statements)

References 10 publications

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“…Plasma butyrylcholinesterase (BuChE) activity, which is used to monitor occupational exposure to organophosphorus compounds (Rider et al 1969), was recorded throughout the exposure period. Results are presented in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The neurotoxicity of organophosphorus compounds is generally attributed to their inhibition of acetylcholinesterase (AChE); the resulting rise in synaptic acetylcholine concentration over-stimulates and can desensitize cholinergic receptors (Rider et al 1969;Aoshima et al 1981;Cio and El-Fakahany 1986;Tang et al 1999;Liu et al 1999;Moser and Padilla 1998;Bushnell et al 1993Bushnell et al , 1994Nostrandt et al 1997;Zheng et al 2000). Acute over-stimulation of muscarinic cholinergic receptors in the airways results in hypersecretion that complicates breathing, while desensitization of nicotinic cholinergic receptors produces ataxia and respiratory paralysis (Abou-Donia 1992).…”

Section: Introductionmentioning

confidence: 99%

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Effects of sub-chronic in vivo chlorpyrifos exposure on muscarinic receptors and adenylate cyclase of rat striatum

Huff

Abu-Qare

Abou‐Donia

2001

Archives of Toxicology

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In this study dosing regimens were designed such that cholinesterase inhibition following exposure to chlorpyrifos was produced in one treatment group, but was absent in the other. The higher dosing regimen inhibited plasma and brain cholinesterase activities by 51 and 70%, respectively, and resulted in decreased [3H]cis-methyldioxolane ([3H]CD) binding, which was attributable to a decrease in Bmax. No concomitant loss of [3H]quinuclidinyl benzilate ([3H]QNB) binding sites was observed, indicating that the M2 muscarinic receptor subtype to which [3H]CD binds is particularly susceptible to alterations induced by chlorpyrifos treatment. As the M2 receptor subtype is surmised to be the muscarinic autoreceptor, decreases in this receptor may exacerbate poisoning by organophosphorus agents as a result of decreased ability to terminate synaptic acetylcholine release. The ability of carbachol to inhibit striatal adenylate cyclase, which is an effector molecule associated with the M2 receptor, was unaltered in chlorpyrifos-treated rats. Decreases in M2 receptors occurred with the higher dosing regimen, in the absence of any clinical manifestations. Thus, in the absence of overt clinical signs, perturbations of the muscarinic receptor system did occur as a result of sub-chronic chlorpyrifos exposure. Such alterations may contribute to neurological impairments that develop following chronic organophosphorus exposure.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of sub-chronic in vivo chlorpyrifos exposure on muscarinic receptors and adenylate cyclase of rat striatum

Huff

Abu-Qare

Abou‐Donia

2001

Archives of Toxicology

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“…Hartwell et al (1964) estimated that respiratory exposure was conservatively 10 fold as toxic as the dermal route. Rider et al ( 1969) studied the effect of parathion, systox, octamethyl pyrophosphoramide, and methyl parathion in human volunteers. Rider et al (1969) defined minimal toxicity as 20o/~r25% RBC AChE or plasma BChE depression.…”

Section: Selected Studies In Humans and Small Animalsmentioning

confidence: 99%

“…Rider et al ( 1969) studied the effect of parathion, systox, octamethyl pyrophosphoramide, and methyl parathion in human volunteers. Rider et al (1969) defined minimal toxicity as 20o/~r25% RBC AChE or plasma BChE depression. Volunteers were dosed orally over 30 d. The doses per day to reach 20o/o-25% plasma or RBC enzyme depression were parathion, 7.5 mg; systox, 6.75-7.125 mg; OMPA, 1.5 mg; and methyl parathion, >19.0 mg.…”

Section: Selected Studies In Humans and Small Animalsmentioning

confidence: 99%

Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Nigg

Knaak

2000

Reviews of Environmental Contamination and Toxicology

100

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“…BuChE is generally more sensitive to OP inhibitors compared to red blood cell AChE (Carter and Maddux, 1974;Grob, 1950;Grob and Harvey, 1949;Grob et al, 1950;Rider et al, 1969). a-Chaconine and other potato alkaloids also produce OP-type, cholinergic-type symptoms in humans (Hellenas et al, 1992a).…”

mentioning

confidence: 99%

Inhibition of Human Plasma and Serum Butyrylcholinesterase (EC 3.1.1.8) by α-Chaconine and α-Solanine

et al. 1996

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The purpose of these experiments was to determine the reversibility of a-chaconine and a-solanine inhibition of human plasma butyrylcholinesterase (BuChE). For the substrate a-naphthylacetate, optimal assay conditions were 0.50 M sodium phosphate buffer and a substrate concentration of 3-5 X 10~4 M. Dibucaine (1 X 10~5 M) indicated the usual phenotype for all subjects; achaconine and a-solanine at 2.88 X 10~6 M inhibited BuChE about 70 and 50%, respectively. One-and 24-hr incubations at 1 X 10~! M with a-chaconine, a-solanine, paraoxon, eserine, and ethanol yielded reversible inhibition with dilution except for paraoxon. Twenty-four-hour dialyses of incubations showed no inhibition except for paraoxon. PAGE enzyme activity gels of 1-and 24-hr incubations also showed no inhibition except for paraoxon. aChaconine and a-solanine are reversible inhibitors of human butyrylcholinesterase. At estimated tissue levels, a-chaconine, a-solanine, and solanidine inhibited BuChE 10-86%. In assays which combined a-chaconine, a-solanine, and solanidine, inhibition of BuChE was less than additive. No inhibition of albumin a-naphthylacetate esterase (an arylesterase) was noted with any inhibitor. The importance of these data to adverse toxicological effects of potato alkaloids is diSCUSSed. C 1996 SodMy of Toxicology.Potatoes, consumed by humans for at least 2000 years (Spoerke, 1994;Ugent, 1970), contain the steroidal alkaloids, a-chaconine, a-solanine, and solanidine. The toxicology of these known butyryl-and acetylcholinesterase inhibitors (Harris and Whittaker, 1962;Orgell, 1963) has been reviewed

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Toxicity of parathion, systox, octamethyl pyrophosphoramide, and methyl parathion in man

Cited by 47 publications

References 10 publications

Effects of sub-chronic in vivo chlorpyrifos exposure on muscarinic receptors and adenylate cyclase of rat striatum

Effects of sub-chronic in vivo chlorpyrifos exposure on muscarinic receptors and adenylate cyclase of rat striatum

Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Inhibition of Human Plasma and Serum Butyrylcholinesterase (EC 3.1.1.8) by α-Chaconine and α-Solanine

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