The brain tissue extracts from chronically alcoholized (15% ethanol intake for more than 18 months) rats were studied by mass spectrometry. The mass spectra for the striatum of control and alcohol-consuming rats were identical, while those for the hippocampus showed a significant difference: a great increase in the intensity of peaks typical of mass spectra for quinolinic acid.

Download full-text PDF

Source

Publication Analysis

Top Keywords

quinolinic acid
8
mass spectra
8
[the presence
4
presence quinolinic
4
acid structures
4
structures rat
4
rat brain]
4
brain] brain
4
brain tissue
4
tissue extracts
4

Similar Publications

Background And Objectives: Despite the absence of acute lesion activity in multiple sclerosis (MS), chronic neurodegeneration continues to progress, and a potential underlying mechanism could be the kynurenine pathway (KP). Prolonged activation of the KP from chronic inflammation is known to exacerbate the progression of neurodegenerative diseases through the production of neurotoxic metabolites. Among the 8 KP metabolites, six of them, namely kynurenine (KYN), 3-hydroxylkynurenine (3HK), anthranilic acid (AA), kynurenic acid (KYNA), and quinolinic acid (QUIN), have been associated with neurodegeneration.

View Article and Find Full Text PDF

Constitutive loss of kynurenine-3-monooxygenase changes circulating kynurenine metabolites without affecting systemic energy metabolism.

Am J Physiol Endocrinol Metab

January 2025

Molecular and Cellular Exercise Physiology, Department of physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Kynurenic acid (KYNA) and quinolinic acid (QUIN) are metabolites of the kynurenine pathway of tryptophan degradation with opposing biological activities in the central nervous system. In the periphery, KYNA is known to positively affect metabolic health, whereas the effects of QUIN remain less explored. Interestingly, metabolic stressors, including exercise and obesity, differentially change the balance between circulating KYNA and QUIN.

View Article and Find Full Text PDF

Colorectal cancer (CRC) is a prevalent and deadly disease, necessitating the exploration of novel therapeutic strategies. Traditional chemotherapy often encounters drug resistance and adverse side effects, highlighting the need for alternative approaches. , a plant rich in phytochemical constituents, was investigated for its potential as an anticancer agent against colorectal cancer (CRC).

View Article and Find Full Text PDF
Article Synopsis
  • This study investigates how metabolic profiles change in patients with patent foramen ovale (PFO) and migraines before and after surgery, using metabolomics techniques.
  • Significant differences in metabolites like linoleic acid and quinolinic acid were observed after surgery, indicating potential diagnostic markers for these patients.
  • The research highlights the importance of metabolic pathways related to inflammation and oxidative stress in understanding migraines associated with PFO.
View Article and Find Full Text PDF

Indoleamine 2, 3-dioxygenase 1 inhibition mediates the therapeutic effects in Parkinson's disease mice by modulating inflammation and neurogenesis in a gut microbiota dependent manner.

Exp Neurol

January 2025

Laboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi, School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China. Electronic address:

Abnormal tryptophan metabolism is closely linked with neurological disorders. Research has shown that indoleamine 2,3-dioxygenase 1 (IDO-1), the first rate-limiting enzyme in tryptophan degradation, is upregulated in Parkinson's disease (PD). However, the precise role of IDO-1 in PD pathogenesis remains elusive.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!