Identification of the Dopaminergic Neurotoxin 1-Trichloromethyl-1,2,3,4-tetrahydro-β-carboline in Human Blood after Intake of the Hypnotic Chloral Hydrate

Bringmann, Gerhard; God, Ralf; Fähr, Silvia; Feineis, Doris; Fornadi, Katalin; Fornádi, Ferenc

doi:10.1006/abio.1999.4088

Cited by 28 publications

(6 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TCE is a major environmental contaminant in the air, the water system and soil, and there is, therefore, exposure at low levels to various groups in the population. It has been discovered that TCE can be converted to the β -carboline TaClo in man [198]. TaClo can cross the blood brain barrier following intraperitoneal injection in the rat [199].…”

Section: Neurotoxins That Link Mitochondrial Dysfunction and Pdmentioning

confidence: 99%

Mitochondrial Dysfunction in Parkinson's Disease

Keane

Kurzawa

Blain

et al. 2011

Parkinson's Disease

108

View full text Add to dashboard Cite

Parkinson's disease (PD) is a progressive, neurodegenerative condition that has increasingly been linked with mitochondrial dysfunction and inhibition of the electron transport chain. This inhibition leads to the generation of reactive oxygen species and depletion of cellular energy levels, which can consequently cause cellular damage and death mediated by oxidative stress and excitotoxicity. A number of genes that have been shown to have links with inherited forms of PD encode mitochondrial proteins or proteins implicated in mitochondrial dysfunction, supporting the central involvement of mitochondria in PD. This involvement is corroborated by reports that environmental toxins that inhibit the mitochondrial respiratory chain have been shown to be associated with PD. This paper aims to illustrate the considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta (SNpc) of PD patients and to highlight the important need for further research in this area.

show abstract

Section: Neurotoxins That Link Mitochondrial Dysfunction and Pdmentioning

confidence: 99%

Mitochondrial Dysfunction in Parkinson's Disease

Keane

Kurzawa

Blain

et al. 2011

Parkinson's Disease

108

View full text Add to dashboard Cite

show abstract

“…There have been links between chronic exposure to TCE and parkinsonian symptoms [[4], [5], [6], [7]], and treatment of rats or mice with TCE causes SNpc DA neurone degeneration [8,9]. TCE can be converted, via chloral, to a potential neurotoxin, 1-trichloromethyl-1,2,3,4-tetrahydro-β-carboline (TaClo) in man [10], which can cross the blood brain barrier [11]. TaClo can cause up to 50% cell death in primary DA neurones cultures [12], as well as in vivo exposure, leading to a reduction in DA metabolism [13] and altered locomotor activity [[14], [15], [16]].…”

Section: Introductionmentioning

confidence: 99%

Trichloroethylene and its metabolite TaClo lead to degeneration of substantia nigra dopaminergic neurones: Effects in wild type and human A30P mutant α-synuclein mice

Keane

Hanson

Patterson

et al. 2019

Neuroscience Letters

View full text Add to dashboard Cite

show abstract

“…Chloral hydrate can form 2,3, in vivo, a molecule with structural similarities to MPTP, a toxin known to cause parkinsonism (Akundi et al 2004). TaClo has been detected in human subjects receiving treatment with chloral hydrate (Bringmann et al 1999).…”

Section: Anaesthesiamentioning

confidence: 99%

Environmental Risk Factors for Parkinson’s Disease

Gorell¹,

Ford²,

Rybicki³

2003

Handbook of Parkinson's Disease

View full text Add to dashboard Cite

Parkinson's disease (PD) is a progressive, degenerative, neurological disease. The progressive disability associated with PD results in substantial burdens for those with the condition, their families and society in terms of increased health resource use, earnings loss of affected individuals and family caregivers, poorer quality of life, caregiver burden, disrupted family relationships, decreased social and leisure activities, and deteriorating emotional well-being. Currently, no cure is available and the efficacy of available treatments, such as medication and surgical interventions, decreases with longer duration of the disease. Whilst the cause of PD is unknown, genetic and environmental factors are believed to contribute to its aetiology. Descriptive and analytical epidemiological studies have been conducted in a number of countries in an effort to elucidate the cause, or causes, of PD. Rural residency, farming, well water consumption, pesticide exposure, metals and solvents have been implicated as potential risk factors for PD in some previous epidemiological studies. However, there is substantial disagreement between the results of existing studies. Therefore, the role of environmental exposures in the aetiology of PD remains unclear.The main component of this thesis consists of a case-control study that assessed the contribution of environmental exposures to the risk of developing PD. An existing, previously unanalysed, dataset from a local case-control study was analysed to inform the design of the new case-control study. The analysis results suggested that regular exposure to pesticides and head injury were important risk factors for PD. However, due to the substantial limitations of this existing study, further confirmation of these results was desirable with a more robustly designed epidemiological study. A new exposure measurement instrument (a structured interviewer-delivered questionnaire) was developed for the new case-control study to obtain data on demographic, lifestyle, environmental and medical factors. Prior to its use in the case-control study, the questionnaire was assessed for test-retest repeatability in a series of 32 PD cases and 29 healthy sex-, age-and residential suburb-matched electoral roll controls. High repeatability was demonstrated for lifestyle exposures, such as smoking and coffee/tea Title .

show abstract

Identification of the Dopaminergic Neurotoxin 1-Trichloromethyl-1,2,3,4-tetrahydro-β-carboline in Human Blood after Intake of the Hypnotic Chloral Hydrate

Cited by 28 publications

References 12 publications

Mitochondrial Dysfunction in Parkinson's Disease

Mitochondrial Dysfunction in Parkinson's Disease

Trichloroethylene and its metabolite TaClo lead to degeneration of substantia nigra dopaminergic neurones: Effects in wild type and human A30P mutant α-synuclein mice

Environmental Risk Factors for Parkinson’s Disease

Contact Info

Product

Resources

About