Neurochemical perspectives to the function of monoamine oxidase

Riederer, Peter; Konradi, Christine; Hebenstreit, G.; Youdim, Moussa B. H.

doi:10.1111/j.1600-0404.1989.tb01781.x

Cited by 60 publications

(21 citation statements)

References 16 publications

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“…Excessive iron accumulation in the brain is really a potential risk to neuronal damage and may contribute to the aetiology of PD. Furthermore, while there is no history of contamination by exogenous or endogenous MPTP or MPTP-like toxins in most cases of PD, the brain iron content, MAO-B activity and neuromelanin in SNc are known to be increased with aging (Hallgren and Sourander, 1958;Riederer et al, 1989b;Hirsch et al, 1988). Thus, in the elderly, a "natural" tendenr for free radical damage in dopaminergic neurons may be established.…”

Section: Discussionmentioning

confidence: 94%

Excessive iron accumulation in the brain: A possible potential risk of neurodegeneration in Parkinson's disease

Lan

Jiang

1997

J. Neural Transmission

100

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In this study a chronic cerebral iron-loaded model was established by feeding mice with high iron diet. Data indicated that brain iron concentrations were significantly increased in iron-fed mice compared with those of controls. A significant increase in oxidized glutathione (GSSG), decrease in total glutathione (oxidized and reduced glutathione, GSSG + GSH), and therefore increase in the GSSG/(GSSG + GSH) ratios were observed in iron-loaded mice. Hydroxyl radical (.OH) levels in striatum and brainstem were also significantly increased. Excessive iron alone did not change either dopamine (DA) or lipid peroxidation (LPO) concentrations in striatum. However, a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg, i.p.) into the iron-loaded mice caused a great enhancement in all these biochemical abnormalities. These findings suggest that iron does induce oxidative stress, but not severely injury neurons per sc. Excessive iron accumulation in the brain, however, is a potential risk for neuronal damage, which may promote by triggering factor(s). This supports the hypothesis that excessive cerebral iron may contribute to the aetiology of Parkinson's disease (PD).

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Section: Discussionmentioning

confidence: 94%

Excessive iron accumulation in the brain: A possible potential risk of neurodegeneration in Parkinson's disease

Lan

Jiang

1997

J. Neural Transmission

100

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“…In the human brain, MAO-A preferentially deaminates serotonin and norepinephrine and is concentrated in catecholaminergic neurons including the locus ceruleus and substantia nigra (Westtund, 1988;Konradi et al, 1988Konradi et al, , 1989. MAO-B preferentially deaminates phenylethylamine and is concentrated in serotonergic cell bodies including the raphe nuclei (Konradi et al, 1988;Riederer et al, 1989) and area postrema (Westlund et al, 1988). Dopamine is deaminated by either MAO-A or MAO-B both in humans and lower animals.…”

Section: Trials Of Nonselective Irreversible Mao Inhibitors In Patiementioning

confidence: 96%

In vivo comparison of the effects of inhibition of MAO-A versus MAO-B on striatal L-DOPA and dopamine metabolism

Brannan

Prikhojan

Martinez-Tica

et al. 1995

J Neural Transm Gen Sect

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Utilizing the cerebral microdialysis technique, we have compared in vivo the effects of selective MAO-A, MAO-B, and nonselective MAO inhibitors on striatal extracellular levels of dopamine (DA) and DA metabolites (DOPAC and HVA). The measurements were made in rats both under basal conditions and following L-DOPA administration. Extracellular levels of dopamine were enhanced and DA metabolite levels strongly inhibited both under basal conditions and following L-DOPA administration by pretreatment with the nonselective MAO inhibitor pargyline and the MAO-A selective inhibitors clorgyline and Ro 41-1049. The MAO-B inhibitor deprenyl had no effect on basal DA, HVA, or DOPAC levels. Nevertheless, deprenyl significantly increased DA and decreased DOPAC levels following exogenous L-DOPA administration, a finding compatible with a significant glial metabolism of DA formed from exogenous L-DOPA. We conclude that DA metabolism under basal conditions is primarily mediated by MAO-A. In contrast, both MAO-A and MAO-B mediate DA formation when L-DOPA is administered exogenously. The efficacy of newer, reversible agents which lack the "cheese effect" such as Ro 41-1049 are comparable to the irreversible MAO-A inhibitor clorgyline. The possible relevance of these findings for the treatment of Parkinson's disease is discussed.

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“…Components of cigarette smoke may afford neuroprotection by reducing enzymatic activity of type B monoamine oxidase (MAO-B) in the brain (18). MAO-B catabolizes dopamine (19) and may activate neurotoxicants similar to the established experimental PD-inducing chemical 1-methyl-4-phenyl-1,2,3,6-tetrahdropyridine (MPTP) (20). Recently, a MAO-B-inhibiting compound in tobacco, 2,3,6-trimethyl-1,4-naphthoquinone, was found to attenuate the dopaminergic system toxicity of MPTP in experiments on mice (21).…”

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confidence: 99%

Parkinson's Disease Risks Associated with Cigarette Smoking, Alcohol Consumption, and Caffeine Intake

Checkoway

Powers

Smith‐Weller

et al. 2002

American Journal of Epidemiology

346

248

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A reduced risk for Parkinson's disease (PD) among cigarette smokers has been observed consistently during the past 30 years. Recent evidence suggests that caffeine may also be protective. Findings are presented regarding associations of PD with smoking, caffeine intake, and alcohol consumption from a case-control study conducted in western Washington State in 1992-2000. Incident PD cases (n = 210) and controls (n = 347), frequency matched on gender and age were identified from enrollees of the Group Health Cooperative health maintenance organization. Exposure data were obtained by in-person questionnaires. Ever having smoked cigarettes was associated with a reduced risk of PD (odds ratio (OR) = 0.5, 95% confidence interval (CI): 0.4, 0.8). A stronger relation was found among current smokers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was an inverse gradient with pack-years smoked (trend p < 0.001). No associations were detected for coffee consumption or total caffeine intake or for alcohol consumption. However, reduced risks were observed for consumption of 2 cups/day or more of tea (OR = 0.4, 95% CI: 0.2, 0.9) and two or more cola drinks/day (OR = 0.6, 95% CI: 0.3, 1.4). The associations for tea and cola drinks were not confounded by smoking or coffee consumption. Am J Epidemiol 2002;155:732-8.

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Neurochemical perspectives to the function of monoamine oxidase

Cited by 60 publications

References 16 publications

Excessive iron accumulation in the brain: A possible potential risk of neurodegeneration in Parkinson's disease

Excessive iron accumulation in the brain: A possible potential risk of neurodegeneration in Parkinson's disease

In vivo comparison of the effects of inhibition of MAO-A versus MAO-B on striatal L-DOPA and dopamine metabolism

Parkinson's Disease Risks Associated with Cigarette Smoking, Alcohol Consumption, and Caffeine Intake

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