Explore chapters and articles related to this topic
Antibodies to Glutathione: Production, Characterization, and Immunocytochemical Application to the Central Nervous System
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
Ole P. Hjelle, E. Rinvik, D. Huster, W. Reichelt, Ole P. Ottersen
The structural dissimilarity between oxidized and reduced glutathione should be sufficient to make them immunologically distinguishable. In support of this view it should be noted that the present immunization procedure was previously used to raise antibodies that distinguished between two stereoisomers of the same amino acid (Zhang, Storm-Mathisen, and Ottersen 1993; Gundersen et al. 1993) and between such closely related amino acids as glutamate and glutamine (Ottersen et al. 1992; see also Fig. 4 B) or homocysteic acid and glutamate (Zhang and Ottersen 1992). It is likely, therefore, that our failure to produce antibodies specific for the oxidized or reduced forms of glutathione reflects the instability of the conjugate used for immunization. Specifically, part of the reduced glutathione in the immunogen may spontaneously oxidize before or after inoculation, while oxidized glutathione may be subject to the converse process. According to this line of reasoning the addition of an antioxidant to the immunogen should favor the formation of antibodies with higher selectivities for the reduced form of glutathione. This appears to be borne out by the available experimental data (Pow and Crook 1995; Hjelle et al., unpublished).
100 MCQs from Dr. Guy Molyneaux and Colleagues
Published in David Browne, Selena Morgan Pillay, Guy Molyneaux, Brenda Wright, Bangaru Raju, Ijaz Hussein, Mohamed Ali Ahmed, Michael Reilly, MCQs for the New MRCPsych Paper A, 2017
Dr Pauline Devitt, Dr Angela Noonan, Dr Klaus Oliver Schubert, Prof Finian O’Brien
The excitatory amino acids that cause depolarisation of neurons include glutamic acid, aspartic acid, cysteic acid and homocysteic acid. The inhibitory amino acids include GABA and glycine, and they cause hyperpolarisation in neurones. NMDA (N-methyl-d-aspartic acid) receptors are a form of glutamic acid receptors. Memantine is an NMDA receptor antagonist used in the management of moderate to severe Alzheimer’s dementia. GABA has been found to be reduced in the brains of patients with Huntington’s disease and Alzheimer’s disease. (1, pp 117–8)
Excitatory Amino Acids in Epilepsy
Published in Elling Kvamme, Glutamine and Glutamate in Mammals, 1988
Henry F. Bradford, Dale W. Peterson
Other attempts to demonstrate the involvement of A2 receptors in the mediation of epileptic seizures have used the A2 agonist homocysteic acid together with glutamate diethyl ester (GDEE), a nonselective A2 antagonist. Homocysteic acid-induced seizures were blocked by a dose of GDEE which had no effect on pentylenetetrazole seizures.73 The recently synthesized kainate analogue, ß kainic acid, could be expected to be a selective A3 (kainate) receptor antagonist. While ß kainic acid does have anticonvulsant activity against audiogenic seizures,74 this action may not be due to activity on A3 receptors.75 Stone and Collins76 were unable to demonstrate any antagonist action of ß kainic acid at the electrophysiological level in cortical or hippocampal slices, but have shown a weak agonist action, which they suggest may mediate anticonvulsant activity by a presynaptic mechanism.
Extensive intracranial arterial dolichoectasia involving distal branches of intracranial arteries: two cases report and review of the literature
Published in International Journal of Neuroscience, 2021
Bo Li, Bing Zhou, Ming-zhao Zhang, Rong-qing Qin, Yang He
We prescribed a Magnetic Resonance (MR) examination for her and made a careful film reading. Both T1WI and T2WI showed a “flow voids” signal in the region of the left lateral fissure, without obvious mass effect. Lacunar infarcts were found in the regions of the right thalamus and left external capsule as the typical imaging manifestations of long T1WI and T2WI signal. Enhanced MRI showed tortuous vascular images in the left lateral fissure cistern, which was more apparent in the sagittal plane image (Figure 2 (a,b)). To make a final diagnosis, we performed cerebral angiography on her. The DSA showed obvious enlargement and tortuosity of M2 and M3 segments of the left MCA, with contrast medium stagnation in the abnormal arteries and visualization delay of distal arteries. Enlarged and tortuous vessels were also shown in A3 and A4 segments of the left ACA, M4 of bilateral MCA, P3 of the right PCA, and P4 of bilateral PCA, which were not as severe as the M2 segment of the left MCA (Figure 2 (c–f)). Surprisingly, the vertebrobasilar arteries(VBA)and bilateral ICA were not involved. The related vascular risk factors such as hypertension, diabetes, hyperlipoidemia, high level of homocysteic acid, were also excluded. Although the diagnostic criteria for branching arteries IADE haven’t been established, the case could still be finally diagnosed by the definition of IADE.
Homocysteine, chronotype and clinical course in bipolar disorder patients
Published in Nordic Journal of Psychiatry, 2020
Meral Gunes Ozdogan, Esat Fahri Aydin, Mehmet Fatih Ustundag, Hacer Akgul Ceyhun, Elif Oral, Ebubekir Bakan
Our results were in line with a previous study showing elevated blood Hcy levels in alcohol use disorder patients with mixed episodes [28]. However, in 2013, Permoda-Osip et al. published a study of 112 BD patients with depressive episodes, which showed that high levels of Hcy were found more frequently during depressive episodes [29]. A recent meta-analysis showed that Hcy levels were elevated in BD patients during mania and euthymia when compared to healthy controls [30]. In our results, the number of mixed episodes was significantly associated with HHcy. Patients who experience mixed episodes tend to have a more severe form of BD with a poorer prognosis that is more commonly associated with a risk of suicide, substance abuse, comorbid conditions and poorer treatment outcomes than those who experience other types of episode [31–33]. Both Hcy and its oxidative metabolite, homocysteic acid, are NMDA receptor agonists, and the long-term activation of NMDA receptors due to HHcy would result in an increased calcium ion influx that exerts neurotoxic effects. This relationship connects Hcy to the known role of dysregulated glutamatergic activity in the pathology of BD [6,27]. Neurotoxic effects of Hcy may cause affective instability, and this could be a possible explanation of the relationship between HHcy and the number of mixed episodes.
Oxidative stress in epilepsy
Published in Expert Review of Neurotherapeutics, 2018
Ursula Geronzi, Federica Lotti, Salvatore Grosso
Further evidence of an OS intervention in epilepsy pathogenesis comes from studies on transgenic animals: transgenic mice overexpressing mitochondrial SOD (the enzyme that dismutates O2−) are resistant to seizure-induced neurodegeneration, whereas mice with partial SOD deficiency (SOD-/+) show increased seizure susceptibility and neurodegeneration [17]. On that basis, it can be stated that O2− may play a key role in seizure-induced brain changes. Although catalase levels are physiologically lower in brain tissue than in other organs, it is able to metabolize great amounts of H2O2 very rapidly. A significant increase in catalase levels has been found in acute [18] and chronic [19] models of epilepsy. According to Barros et al., the increased catalase activity may be the consequence of an enzymatic antioxidant response to increased basal free radical production, which may potentially lead to a damage of neural tissue, and free radical scavenging may take part in controlling seizure-induced damage [18]. However, it has been recently observed that in the immature rats brain with seizures induced by dl-homocysteic acid, catalase activity was decreased when compared to the control groups, suggesting limited antioxidant defense [20].