lathyrus aureus/atrofi

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Role of glutamate and nitric oxide in onset of motor neuron degeneration in neurolathyrism.

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Neurolathyrism is associated with a complex pattern of alterations in the glutamatergic system of the cortical motor region of brain. It is a neurological disorder consorted with excessive consumption of Lathyrus sativus (Grass pea), comprising large amounts of the neurotoxin,

Differential effect of beta-N-oxalylamino-L-alanine, the Lathyrus sativus neurotoxin, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate on the excitatory amino acid and taurine levels in the brain of freely moving rats.

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We studied the effect of beta-oxalylamino-L-alanine, a glutamate analog present in Lathyrus sativus seeds and implicated in the etiopathogenesis of neurolathyrism, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate on the extracellular levels of aspartate, glutamate and taurine in the

Lathyrus hirsutus (Caley Pea) intoxication in a herd of horses.

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BACKGROUND Caley Pea (Lathyrus hirsutus) is potentially toxic to horses, but large case series are not reported. OBJECTIVE To describe the clinical signs of horses intoxicated with Lathyrus hirsutus and speculate on the neuroanatomical lesion localization and pathogenesis based upon the observed

An Improved HILIC HPLC-MS/MS Method for the Determination of β-ODAP and Its α Isomer in Lathyrus sativus.

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β-N-Oxalyl-l-α,β-diaminopropionic acid (β-ODAP) is a non-protein amino acid present in Lathyrus sativus (grass pea) and other Lathyrus species, in parallel with its nontoxic isomer, α-ODAP. When consuming grass pea for several months as staple food, β-ODAP may cause

Differential induction of oxidative impairments in brain regions of male mice following subchronic consumption of Khesari dhal (Lathyrus sativus) and detoxified Khesari dhal.

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Neurolathyrism is a neurodegenerative disease caused by the chronic consumption of Khesari dhal (Lathyrus sativus L). It is generally accepted that beta-N-oxalylamino-l-alanine (b-ODAP), a non-protein amino acid present in the seeds is the primary causative agent. Based on in vitro studies with

Sulfur amino acids deficiency caused by grass pea diet plays an important role in the toxicity of L-β-ODAP by increasing the oxidative stress: studies on a motor neuron cell line.

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Neurolathyrism is a motor neuron disease caused by the overconsumption of grass pea (Lathyrus sativus L.) containing L-β-ODAP. The precise mechanism to cause motor neuron degeneration has yet to be elucidated, but should agree with the epidemiological backgrounds. Considering the amino acid content

The central nervous system in a case of neurolathyrism.

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We examined the central nervous system of a 67-year-old man who showed symptoms of lathyrism after being imprisoned at age 35 and fed on a diet of chick peas, Lathyrus sativus. The most obvious changes were loss of axons and myelin in the pyramidal tract in the lumbar spinal cord. These alterations

Human neurolathyrism, a follow-up study of 200 patients. Part I: Clinical investigation.

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Two hundred patients with chronic neurolathyrism were clinically examined, 25 to 35 years after exposure to the lathyrus sativus pea. All the patients were prisoners in a labour camp under similar nutritional and physical conditions at the outbreak of the syndome. The main symptoms were spastic

A rat model of neurolathyrism: repeated injection of L: -beta-ODAP induces the paraparesis of the hind legs.

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Neurolathyrisim is a motor neuron disease characterized by spastic paraparesis in the hind legs, and is caused by grass pea, Lathyrus sativus, which contains the excitotoxic amino acid, 3-N-oxalyl-L: -2,3-diaminopropanoic acid (L: -beta-ODAP), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic

Food toxins, ampa receptors, and motor neuron diseases.

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Environmental chemicals involved in the etiology of human neurodegenerative disorders are challenging to identify. Described here is research designed to determine the etiology and molecular pathogenesis of nerve cell degeneration in two little known corticomotoneuronal diseases with established

Apoptosis induced by beta-N-oxalylamino-L-alanine on a motoneuron hybrid cell line.

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It has been suggested that beta-N-oxalylamino-L-alanine, a non-protein amino acid present in the Lathyrus Sativus seeds, may play a role in the etiopathogenesis of neurolathyrism, a toxic form of motor neuron disease clinically characterized by a severe spastic paraparesis. In order to investigate

Clinical aspects of neurolathyrism in Unnao, India.

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To study the clinical picture of lathyrism in Unnao, India and compare it with that reported from other endemic areas, 41 patients from Unnao were studied. Their mean age was 42.9 years (range 22-85) and the mean duration of the illness was 17.1 years (range 2-30). They had been regularly consuming

Unraveling the mechanism of β-N-oxalyl-α,β-diaminopropionic acid (β-ODAP) induced excitotoxicity and oxidative stress, relevance for neurolathyrism prevention.

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β-N-Oxalyl-α,β-diaminopropionic acid (β-ODAP) is a plant metabolite present in Lathyrus sativus (L. Sativus) seeds that is proposed to be responsible for the neurodegenerative disease neurolathyrism. This excitatory amino acid binds to α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)

Effect of beta-N-oxalylamino-L-alanine on cerebellar cGMP level in vivo.

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Beta-N-oxalylamino-L-alanine (BOAA), a non-protein amino acid present in the seeds of Lathyrus Sativus (LS), is one of several neuroactive glutamate analogs reported to stimulate excitatory receptors and, in high concentrations, cause neuronal degeneration. In the present study, the in vivo acute

Specific antagonism of behavioral action of "uncommon" amino acids linked to motor-system diseases.

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Beta-N-methylamino-L-alanine (BMAA) and beta-N-oxalylamino-L-alanine (BOAA) are chemically related amino acids present in the seeds of Cycas circinalis and Lathyrus sativus, respectively. Consumption of these seeds has been linked to Guam amyotrophic lateral sclerosis (BMAA) and lathyrism (BOAA; a

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