Atrial Myxoma With Multiple Myeloma

Graham, S.; Sellers, Alvin L.

doi:10.1001/archinte.1979.03630380092032

Cited by 9 publications

(6 citation statements)

References 9 publications

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“…37) This imbalance results in apoptosis of neurons and auto-oxidation of dopamine. 38) Our studies show a decrease in the activities of SOD and GSH-PX in the MPTP group. However, the decrease of antioxidant enzyme activities caused by MPTP was markedly restored by pre-treatment with kaempferol.…”

Section: Discussionmentioning

confidence: 46%

Neuroprotective Effect of Kaempferol against a 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease

Shen

2011

Biological & Pharmaceutical Bulletin

137

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Parkinson's disease (PD) is a progressive, age-related, neurodegenerative disorder characterized by bradykinesia, rigidity, resting tremor and gait disturbance 1) ; it occurs in 1-2% of the population over the age of 60 years.2) Typical neuropathologic features of the disease are dopaminergic neuron degeneration in the substantia nigra and the presence of eosinophilic intracytoplasmic inclusions (Lewy bodies) in the residual dopaminergic neurons. The most widely used mouse model of PD is produced by systemically administering the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).3) MPTP is converted by monoamine oxidase B (MAO-B) to 1-methyl-4-phenylpyridinium (MPP ϩ ), which is a neurotoxic metabolite and could block cellular respiration, promote reactive oxygen species (ROS) formation, and cause neuronal death. 4,5) Oxidative stress has been implicated either as the cause or as a consequence of the pathogenetic mechanisms responsible for neurodegenerative disease, including PD. Indeed, the brain is prone to producing ROS and oxidative stress, due to its high metabolic rate, combined with the high content of oxidizable molecules, such as dopamine and neuromelanin, whose metabolism generates ROS. [6][7][8] Superoxide dismutase (SOD) is one of the key enzymes that provide the first line of defense against pro-oxidants. Glutathione peroxidase (GSH-PX) is thought to play an important role in protecting membranes from damage due to lipid peroxidation. The major detoxification function of GSH-PX is the termination of radical chain propagation by quick reduction to yield further radicals.9) The levels of SOD and GSH-PX activity reflect the ability of organism to eliminate free radicals. Malondialdehyde (MDA) is the end product of lipid peroxidation, and its level could indirectly reflect the metabolic degree of oxygen radicals, thus serving as an index of oxidative damage. 10)Kaempferol is a prototype member of the flavonol subclass of flavonoids, which is widely found in tea, broccoli, grapefruit, brussel sprouts and apple and is claimed to have strong antioxidant and anti-inflammatory properties. 11)Kaempferol, can be given orally, is absorbed well and the bioavailability is proportionate to its dose.12) Kaempferol had earlier been shown to afford efficient neuroprotection against several apoptosis and necrosis-inducing insults, such as oxidized low-density lipoproteins 13,14) and L-glutamate. 15,16)Ishige et al. 15) demonstrated that kaempferol efficiently blocked the increase in ROS associated with the oxidative stress caused by glutamate in the mouse hippocampal cell line demonstrated that kaempferol exerted a strong and prolonged protective effect against rotenone toxicity, which was a classical toxin inducing PD. Striatal glutamatergic response of rat brain slices was also preserved by kaempferol, posing a more general protection of kaempferol in PD.Preliminary studies in our laboratory have shown that kaempferol derivatives prevent oxidative stress-induced cell death in a DJ-1-dependent manner in...

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Section: Discussionmentioning

confidence: 46%

Neuroprotective Effect of Kaempferol against a 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease

Shen

2011

Biological & Pharmaceutical Bulletin

137

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“…2. The reaction was first carried out in H 2 O without buffer, as described in a previous study (18). Upon addition of NaIO 4 , the absorption at ϭ 280 nm decreases, indicating the disappearance of dopamine.…”

Section: Resultsmentioning

confidence: 99%

“…NM is a dark polymer present in the brain of humans and, to a lesser amount, of some other primates. It is primarily distributed in the dopaminergic neurons of the substantia nigra and the noradrenergic neurons of the locus coeruleus (18). No physiological function has been defined for NM, although the hypothesis of a protective role has been suggested in the literature.…”

mentioning

confidence: 99%

Kinetic and Structural Analysis of the Early Oxidation Products of Dopamine

Bisaglia

Mammi

Bubacco

2007

Journal of Biological Chemistry

271

257

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Oxidative stress appears to be directly involved in the pathogenesis of several neurodegenerative disorders, including Alzheimer and Parkinson diseases. Nigral dopaminergic neurons are particularly exposed to oxidative stress because a pathological accumulation of cytosolic dopamine gives rise to various toxic molecules, including free radicals and reactive quinones. These latter species can react with proteins preventing them from exerting their physiological functions. Among the possible targets of quinones, ␣-synuclein is of primary interest because of its direct involvement in dopamine metabolism. Contrary to the neurotoxic processes, neuromelanin synthesis seems to play a protective role by its ability to sequester a variety of potentially damaging substances. In this study, we carried out a kinetic and structural analysis of the early oxidation products of dopamine. Specifically, considering the potential high toxicity of aminochrome for both cells and mitochondria, we focused our attention on its rearrangement to 5,6-dihydroxyindole. After the spectroscopic characterization of the products derived from the oxidation of dopamine, the structural information obtained was used to analyze the reactivity of quinones toward ␣-synuclein. Our results suggest that indole-5,6-quinone, rather than dopamine-o-quinone or aminochrome, is the reactive species. We propose that the observed reactivity could represent a general reaction pathway whenever cysteinyl residues are absent in proteins or if they are sterically protected.Parkinson disease, the second most common neurodegenerative disorder, is a chronic and progressive disease characterized by degeneration of dopaminergic neuromelanin-containing neurons in the substantia nigra pars compacta (1) and by the presence of cytoplasmic inclusions that are mainly composed of fibrillar ␣-synuclein (␣syn) 2 (2). Postmortem studies support the involvement of oxidative stress and the production of reactive oxygen species in Parkinson disease (3, 4). A possible source of oxidative stress is the redox reactions that specifically involve dopamine (DA). A critical aspect is the amount of DA present in the cytoplasm, outside the synaptic vesicles where the neurotransmitter is confined under physiological conditions. Spontaneous oxidation of DA in the presence of molecular oxygen leads to the formation of several cytotoxic molecules, including superoxide anions (O 2 . ), hydroxyl radicals (OH ⅐ ), and reactive quinones (DAQs) (5). Reactive oxygen species derived from the oxidation of DA can damage cellular components such as lipids, proteins, and DNA (6). The electrondeficient quinones can also react with cellular nucleophiles, leading to further cytotoxicity. DAQs have been shown to bind covalently to cysteinyl residues of proteins both in vitro and in vivo (7-12). Because these residues are often located at the active site of a protein, it has been proposed that covalent modifications result in an impairment of protein function with potentially deleterious effects on the cell (10...

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“…Furthermore, it was shown that there was a correlation between deregulated IL-6 production and polyclonal plasmacytosis in patients with cardiac myxoma (3) and Castleman's disease (5). Moreover, several cases of rheumatoid arthritis, cardiac myxoma, and Castleman's disease were reported to result in the generation of myeloma and/or plasmacytoma (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

IgG1 plasmacytosis in interleukin 6 transgenic mice.

Suematsu

Matsuda

Aozasa

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

552

305

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Interleukin 6 (IL-6) has been suggested to be involved in the pathogenesis of polyclonal and monoclonal plasma cell abnormalities. To address this possibility, transgenic mice carrying the human IL-6 genomic gene fused with a human immunoglobulin heavy chain enhancer were generated. High concentrations of human IL-6 and polyclonal increase in IgGi (120-to 400-fold) in sera of all transgenic mice were observed.

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Atrial Myxoma With Multiple Myeloma

Cited by 9 publications

References 9 publications

Neuroprotective Effect of Kaempferol against a 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease

Neuroprotective Effect of Kaempferol against a 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease

Kinetic and Structural Analysis of the Early Oxidation Products of Dopamine

IgG1 plasmacytosis in interleukin 6 transgenic mice.

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