Organophosphorus Ester-Induced Delayed Neurotoxicity

Abou‐Donia, Mohamed B.

doi:10.1146/annurev.pa.21.040181.002455

Cited by 395 publications

(104 citation statements)

References 97 publications

(156 reference statements)

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“…Similar result was obtained by Buhalla et al (2007) who found a significant increase in LPO level in brain tissue after Li treatment. Peroxidation of polyunsaturated fatty acids leads to degradation of phospholipids and cellular deterioration (Abou-Donia, 1981). The present result showed that Zn, VE and their interaction countered the LPO produced by Li.…”

Section: Discussionmentioning

confidence: 47%

The Protective Effects of Vitamin E and Zinc Supplementation Against Lithium-Induced Brain Toxicity of Male Albino Rats

Ibrahim¹,

Magdy²,

Ahmed³

et al. 2014

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Lithium (Li) therapy has widely used in the treatment of bipolar disorder. Consequently, consciousness of the side effects and pathogenesis of this metal is needed for such treatments. Recently, information on the interaction of Li with oxidative markers and organs toxicity attend the researchers over the world. In the present study we have tried to evaluate the influence of oral administration of LiCl for 4 weeks on the oxidative stress marker and histological structure of brain in male rats. Fifty adult male albino rats weighing 135±15 gm was categorized into 5 groups (10 rats each). Group I worked as negative control, group II administrated with LiCl (0.20 mg/kg bw) in drinking water, group III, IV and V were administrated with Zn (10 mg/kg bw), VE (100 mg/kg bw) and their combination twice a week besides the daily administration of LiCl for 4 weeks, respectively. Rats after anesthesia with ether killed for collocation of brain for histopathological and biochemical analysis. Data obtained showed a significant increase in LPO, NO, GSH and Li content and the activities of SOD, CAT and AChE with demylination of the nerve fibers and degeneration of neurons in brain of LiCl treated rats. Co-treatment of rats with Zn or VE results in a significant decrease in LPO, NO, GSH content in the activities of SOD, CAT and AChE with less or normal structure of the brain. However, co-treatment with combination of Zn and VE caused a significant increase in SOD, CAT and AChE activities with normal histological structure.In conclusion, the data from the present study show that Zn and VE and their interaction are effective in protection against Liinduced brain toxicity in rat with priority for the combination.

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Section: Discussionmentioning

confidence: 47%

The Protective Effects of Vitamin E and Zinc Supplementation Against Lithium-Induced Brain Toxicity of Male Albino Rats

Ibrahim¹,

Magdy²,

Ahmed³

et al. 2014

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“…Pathogenesis is independent of inhibition of acetylcholinesterase (AChE) and can be induced by OP compounds with low acute toxicity (Johnson, 1982;Makhaeva et al, 1987). Although OPIDN has occurred in epidemic proportions throughout the world, accidental episodes are currently rare (Abou-Donia, 1981;Richardson, 1998). Nevertheless, the high human susceptibility to OPIDN (Cole et al, 1998;Lotti, 1987), its insidious onset, and the usually permanent debilitating effects suggest the possibility of neuropathic OP compounds being used as agents for chemical terrorism.…”

Section: And Between Brain and Blood (R = 997) The Results Suggest mentioning

confidence: 99%

Biosensor Detection of Neuropathy Target Esterase in Whole Blood as a Biomarker of Exposure to Neuropathic Organophosphorus Compounds

Махаева¹,

Sigolaeva²,

Zhuravleva³

et al. 2003

Journal of Toxicology and Environmental Health, Part A

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Public Reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. 44379.1-LSNeuropathy target esterase (NTE) is the target for neuropathic organophosphorus compounds (OPs) that produce delayed neurotoxicity (OPIDN). Inhibition/aging of brain NTE predicts the potential for OPIDN in animal models. Lymphocyte NTE has also found use as a biomarker of human exposure to neuropathic OPs. Recently, a sensitive NTE biosensor was developed using a tyrosinase carbon-paste electrode for amperometric (Amp) detection of phenol produced by hydrolysis of the substrate, phenyl valerate. The I50 (20 min at 37 °C) for N,N'-di-2 propylphosphorodiamidofluoridate (mipafox) against hen lymphocyte NTE was 6.94 ± 0.28 •uM (Amp) and 6.02 ± 0.71 uM colorimetrically (Col). For O,O-di-1-propyl O-2,2-dichlorvinyl phosphate (PrDChVP), the I50 against hen brain NTE was 39 ± 8 nM (Amp) and 42 ± 2 nM (Col). I50 values (Amp) for PrDChVP against hen and human blood NTE were 66 ± 3 and 70 ± 14 nM, respectively. NTE activities in brain, lymphocytes, and blood were measured 24 h after dosing hens with PrDChVP. NTE inhibition was highly correlated between brain and lymphocyte (r = 0.994) and brain and blood (r = 0.997). Biosensor NTE assay for whole blood could serve as a biomarker of exposure to neuropathic OPs.12 (excluding cover forms) Biosensor, Delayed neurotoxicity, Mipafox, Organophosphorus compounds (OPs), Neuropathy target esterase (NTE).

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“…This possibility points to a common metabolic basis for many distal axonopathies, ie, that neurotoxic compounds deplete energy supplies in the axon by inhibiting nerve fiber enzymes required for the maintenance of energy synthesis and lead to a local blockade of energy-dependent axonal transport (68, tory step, ageing, must take place, leaving a negatively charged phosphorus group attached to the esterase, which is itself tightly bound to membranous material in the nervous system. Studies on the relationship between the chemical structure of organophosphorous esters and their neurotoxic potencies suggest that two hydrophobic areas may be present in the vicinity of the active site of the neurotoxic protein (1). Abou-Donia (1) postulated that delayed neurotoxic organophosphorus esters phosphorylate the active center of neurotoxic target proteins in the axon.…”

Section: Axonal Transport and Distal Axonopathymentioning

confidence: 99%

Occupational toxic neuropathies--an update.

He¹

1985

Scand J Work Environ Health

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Occupational toxic neuropathies--an update.by He F This article in PubMed: www.ncbi.nlm.nih.gov/pubmed/2999969 REVIEWS Scand j work environ health II (1985) [321][322][323][324][325][326][327][328][329][330] Occupational toxic neuropathies -An update by Fengsheng He, MD1 HE F. Occupational toxic neuropathies -An update. Scand J Work Environ Health II (1985) 321-330. Peripheral neuropathy is the commonest neurol ogical syndrome produced by indu strial and agricultural chemicals. A number of chemicals have been recently found to be neurotoxins; in addition some known occupational neurotoxic hazards more often produ ce subtle alterat ions in the peripher al nervous system. Ther e have been problem s of both evaluating neuroto xic effects and identifying toxic causes. This article reviews and discusses th e current research and progress covering neurophysiological, neuropathological, biochemical , and epidemiologic approaches in clinical and experimental neurotoxicology, as related to the assessment and path ogenesis of occupa tion al toxic neuropathies.Key terms: assessment , clinical neur ophysiological testing, distal axonopathy, epidemiologic investigation, identi fication, neuropathological approach, pathogenesis, toxic causes.Alon g with the development of various chemical industries there has been a growing list of indu strial chemicals which can cause damage to the peripheral nervous system . On the other hand, occupational exposure to low levels of known neurotoxins more oft en causes subtle alterations of peripheral nervous function. This occurrence raises problems in occupational health practice and stimulates research concerning the early diagnosi s and prevention of occupational toxic neuropathies. In the meantime , modern technique s of neurophysiology, neuropathology, and biochemistry have been introduced and utilized to explore the mechani sms of some neurotoxic effects . All these methods lead to a substantial amount of progress in evaluat ing and understanding occupational toxic neuropathies, which have been reviewed in this article. PROGRESS IN ASSESSMENT AND IDENTIFICATIONThe diagnosis of chemically-induced neuropathies can be reasonably made in those subj ects who have a verified history of exposure to neurotoxins and characteristic clinical evidence of neuropathy with exclusion of other causative factors. But there are some asymptomatic individuals under neurotoxicologic risk who may be suspected of having subclinical peripheral neuropathies and, on the other hand, a number of symptomatic patients having the presumptive diagnosis of polyneuropathy without a known etiology. In these cases, the question of either the existence or the etiology of the peripheral neuropathies remain s to be settled. Detection of neurotoxic effects on the peripheral nervous system

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Organophosphorus Ester-Induced Delayed Neurotoxicity

Cited by 395 publications

References 97 publications

The Protective Effects of Vitamin E and Zinc Supplementation Against Lithium-Induced Brain Toxicity of Male Albino Rats

The Protective Effects of Vitamin E and Zinc Supplementation Against Lithium-Induced Brain Toxicity of Male Albino Rats

Biosensor Detection of Neuropathy Target Esterase in Whole Blood as a Biomarker of Exposure to Neuropathic Organophosphorus Compounds

Occupational toxic neuropathies--an update.

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