An endogenous dopaminergic neurotoxin: Implication for Parkinson's disease

Mattammal, Michael B.; Haring, John H.; Chung, Haung D; Raghu, Girija; Strong, Randy

doi:10.1016/1055-8330(95)90016-0

Cited by 104 publications

(111 citation statements)

References 25 publications

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“…Some aldehyde metabolites are neurotoxic and their intraneuronal accumulation has been regarded as one mechanism that might be involved in cell death associated with neurodegenerative conditions, i ncluding Parkinson's disease and Alzheimer's disease (Mattammal et al 1995;Burke et al 2003). Thus, through inhibiting aldehyde dehydrogenases, MC-LR treatment could cause an accumulation of aldehyde, which results in oxidative stress (Wang et al 2010).…”

Section: Oxidative Stressmentioning

confidence: 99%

A review of neurotoxicity of microcystins

Chen

Fan

et al. 2016

Environ Sci Pollut Res

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Cyanobacterial blooms-produced microcystins are secondary metabolites which can accumulate in the food chain and contaminate water, thus posing a potential threat to the health of aquatic animals and even humans. Microcystin toxicity affects not only the liver but also the other organs, i.e., the brain. The serious neurotoxicity effects caused by microcystins then lead to various symptoms. This review focuses on the neurotoxicity of microcystins. Microcystins can cross bloodbrain barrier with the transport of Oatps/OATPs, causing neurostructural, functional, and behavioral changes. In this review, potential uptake mechanisms and neurotoxicity mechanisms are summarized, including neurotransmissions, neurochannels, signal transduction, oxidative stress, and cytoskeleton disruption. However, further researches are needed for detailed studies on signaling pathways and the downstream pathways of neurotoxicity of microcystins.

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Section: Oxidative Stressmentioning

confidence: 99%

A review of neurotoxicity of microcystins

Chen

Fan

et al. 2016

Environ Sci Pollut Res

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“…4-1): (a) Oxidation of DA produces a toxic semiquinone. The electron-deficient semiquinone reacts readily with nucleophilic compounds such as sulfhydryl (-SH) groups (Scheulen, et al, 1975;Graham et al, 1978;Ito, 1988 (Mattammal et al, 1993;Mattammal et al, 1995).…”

Section: Chapter 4 General Discussionmentioning

confidence: 99%

Glutathione protects PC12 cells from ascorbate- and dopamine-induced apoptosis

Si¹,

Ross

Shin³

1998

Experimental Brain Research

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“…DOPAL is taken up by rat neostriatal synaptosomes, and studies using mazindol, a selective dopamine uptake inhibitor, have suggested that the aldehyde reenters dopaminergic nerve terminals via the dopamine transporter (DAT) (Mattammal et al, 1995). The DAT is expressed in presynaptic terminals of SN neurons where it primarily mediates the reuptake of neuronally released dopamine (Reith et al, 1997;Jones et al, 1998).…”

Section: B Transport Mechanismsmentioning

confidence: 99%

“…Dopamine is deaminated to 3,4-dihydroxyphenylacetaldehyde (DOPAL), and both norepinephrine and epinephrine are deaminated to form 3,4-dihydroxyphenylglycolaldehyde (DOPEGAL). Increasing evidence suggests that these catecholamine-derived aldehydes may in fact be neurotoxins, and their intraneuronal accumulation has been theorized as one mechanism that may be involved in cell death associated with neurodegenerative conditions, including Parkinson's disease (PD) and Alzheimer's disease (AD) (Mattammal et al, 1995;Burke et al, 2003). Aldehydes, including DOPAL and DOPEGAL, are detoxified by various enzyme systems including aldehyde dehydrogenase (ALDH), which is exclusively responsible for their oxidative metabolism ( Fig.…”

Section: Introductionmentioning

confidence: 99%