Abstract |
The causative interrelationship between long-term, low level exposure to chlorinated volatile organic solvents (VOSs) and neurodegenerative diseases ( polyneuropathy, encephalopathy) are still an issue of controversial debate. Endogeneously formed chlorinated tetrahydro- beta-carbolines found by Bringmann 1995 (TaClo hypothesis) may contribute, in particular, to the development of ( idiopathic) Parkinson's disease (PD) in the presence of the sufficient amount of trichloroacetaldehyde, an intermediate in metabolism of trichloroethylene (TRI). Long-term storage of specific VOSs over years, evident frrom exhalation pattern during the postexposure period, may serve as a promoting factor to form continuously TaClo non-enzymatically from tryptamine and trichloroacetaldehyde. Thus, the induction of TaClo-mediated neurotoxic processes extends over years. The onset of Parkinson's disease in three chronic TRI-exposed individuals during the postexposure period could be associated with the presence of TaClo in ng-range. Consequently, determination of TaClo and its derivatives in blood of humans exposed to chlorinated VOSs may serve as a marker of risk indicating either causative or supportive processes of neurodegeneration that may lead to manifestation of PD after many years.
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Authors | Walter Kochen, Dirk Kohlmüller, Peter De Biasi, Ray Ramsay |
Journal | Advances in experimental medicine and biology
(Adv Exp Med Biol)
Vol. 527
Pg. 253-63
( 2003)
ISSN: 0065-2598 [Print] United States |
PMID | 15206739
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- Carbolines
- Neurotoxins
- 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline
- Trichloroethylene
- Serotonin
- Dopamine
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Topics |
- Aged
- Animals
- Behavior, Animal
(drug effects)
- Carbolines
(metabolism, toxicity)
- Cells, Cultured
- Dopamine
(metabolism)
- Humans
- Male
- Mitochondria
(drug effects, metabolism)
- Neuroglia
(drug effects, metabolism)
- Neurons
(drug effects, metabolism)
- Neurotoxins
(metabolism, toxicity)
- Parkinson Disease
(etiology, metabolism)
- Parkinsonian Disorders
(etiology, metabolism)
- Rats
- Serotonin
(metabolism)
- Trichloroethylene
(metabolism, toxicity)
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