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A study on the spectroscopic, energy band, and optoelectronic properties of α,ω-dihexylsexithiophene/tris(8-hydroxyquinolinate) gallium blends; DH6T/Gaq3 composite system

Muhammad FF, Yahya MY, Ketuly KA, Muhammad AJ, Sulaiman K

Spectrochim Acta A Mol Biomol Spectrosc, 2016 Dec 05;169:144-51.
PMID: 27372510 DOI: 10.1016/j.saa.2016.06.031

In this work the optical response, spectroscopic behaviour, and optoelectronic properties of solution and solid state composite systems based on α,ω-dihexylsexithiophene/tris(8-hydroxyquinolinate) gallium (DH6T/Gaq3) are studied upon the incorporation of different molar percentages of Gaq3. UV-vis, PL, FTIR spectrophotometers and SEM technique were utilized to perform the investigations. The results showed a reduced energy band (Eg) (from 2.33eV to 1.83eV) and a broadened absorption spectrum for the blend system when 29.8% molar of Gaq3 was incorporated. These were attributed to the enhanced intermolecular interactions that are brought about by the increased strength of π-π overlap between the molecular moieties. A mathematical formula was developed to interpret the non-monotonic change occurred in Eg, while numerical calculations have been made to assign the type and nature of the electronic transitions governing the spectroscopic behaviour of the system. The results were elaborated and comprehensively discussed in terms of the exciton generation, energy band theory, molecular interactions, and spatial geometry.

Matched MeSH terms: Quinolinic Acid
Fulltext Altered Tryptophan-Kynurenine Pathway in Delirium: A Review of the Current Literature

Phing AH, Makpol S, Nasaruddin ML, Wan Zaidi WA, Ahmad NS, Embong H

Int J Mol Sci, 2023 Mar 15;24(6).
PMID: 36982655 DOI: 10.3390/ijms24065580

Delirium, a common form of acute brain dysfunction, is associated with increased morbidity and mortality, especially in older patients. The underlying pathophysiology of delirium is not clearly understood, but acute systemic inflammation is known to drive delirium in cases of acute illnesses, such as sepsis, trauma, and surgery. Based on psychomotor presentations, delirium has three main subtypes, such as hypoactive, hyperactive, and mixed subtype. There are similarities in the initial presentation of delirium with depression and dementia, especially in the hypoactive subtype. Hence, patients with hypoactive delirium are frequently misdiagnosed. The altered kynurenine pathway (KP) is a promising molecular pathway implicated in the pathogenesis of delirium. The KP is highly regulated in the immune system and influences neurological functions. The activation of indoleamine 2,3-dioxygenase, and specific KP neuroactive metabolites, such as quinolinic acid and kynurenic acid, could play a role in the event of delirium. Here, we collectively describe the roles of the KP and speculate on its relevance in delirium.

Matched MeSH terms: Quinolinic Acid/metabolism
Tuning the optical band gap of DH6T by Alq3 dopant

Fahmi Fariq Muhammad, Khaulah Sulaiman

Sains Malaysiana, 2011;40.

Dihexyl-sexithiophene (DH6T) was doped with tris (8-hydroxyquinolinate) aluminum (Alq3) to prepare blends of DH6T/ Alq3 by dissolving the mixture in the chloroform/hexane co-solvent. Solid films with different thickness deposited on quartz substrates were obtained from the blends via casting process. Optical absorption spectroscopy has been performed to measure the optical band gap of pure and doped DH6T as well as variations in the band gap with dopant concentration (weight %). This variation in optical band gap with dopant concentration was determined quantitatively with fitted and extrapolated techniques and observed qualitatively from the red shift appeared along the optical absorption spectra. The results showed that within a specific dopant content, the optical energy gap, Eg of DH6T decreases from 2.69 eV to 1.8 eV with increasing dopant concentration to 23.1%.

Matched MeSH terms: Quinolinic Acid
Fulltext Activation of the kynurenine pathway and increased production of the excitotoxin quinolinic acid following traumatic brain injury in humans

Yan EB, Frugier T, Lim CK, Heng B, Sundaram G, Tan M, et al.

J Neuroinflammation, 2015 May 30;12:110.
PMID: 26025142 DOI: 10.1186/s12974-015-0328-2

During inflammation, the kynurenine pathway (KP) metabolises the essential amino acid tryptophan (TRP) potentially contributing to excitotoxicity via the release of quinolinic acid (QUIN) and 3-hydroxykynurenine (3HK). Despite the importance of excitotoxicity in the development of secondary brain damage, investigations on the KP in TBI are scarce. In this study, we comprehensively characterised changes in KP activation by measuring numerous metabolites in cerebrospinal fluid (CSF) from TBI patients and assessing the expression of key KP enzymes in brain tissue from TBI victims. Acute QUIN levels were further correlated with outcome scores to explore its prognostic value in TBI recovery.
METHODS: Twenty-eight patients with severe TBI (GCS ≤ 8, three patients had initial GCS = 9-10, but rapidly deteriorated to ≤8) were recruited. CSF was collected from admission to day 5 post-injury. TRP, kynurenine (KYN), kynurenic acid (KYNA), QUIN, anthranilic acid (AA) and 3-hydroxyanthranilic acid (3HAA) were measured in CSF. The Glasgow Outcome Scale Extended (GOSE) score was assessed at 6 months post-TBI. Post-mortem brains were obtained from the Australian Neurotrauma Tissue and Fluid Bank and used in qPCR for quantitating expression of KP enzymes (indoleamine 2,3-dioxygenase-1 (IDO1), kynurenase (KYNase), kynurenine amino transferase-II (KAT-II), kynurenine 3-monooxygenase (KMO), 3-hydroxyanthranilic acid oxygenase (3HAO) and quinolinic acid phosphoribosyl transferase (QPRTase) and IDO1 immunohistochemistry.
RESULTS: In CSF, KYN, KYNA and QUIN were elevated whereas TRP, AA and 3HAA remained unchanged. The ratios of QUIN:KYN, QUIN:KYNA, KYNA:KYN and 3HAA:AA revealed that QUIN levels were significantly higher than KYN and KYNA, supporting increased neurotoxicity. Amplified IDO1 and KYNase mRNA expression was demonstrated on post-mortem brains, and enhanced IDO1 protein coincided with overt tissue damage. QUIN levels in CSF were significantly higher in patients with unfavourable outcome and inversely correlated with GOSE scores.
CONCLUSION: TBI induced a striking activation of the KP pathway with sustained increase of QUIN. The exceeding production of QUIN together with increased IDO1 activation and mRNA expression in brain-injured areas suggests that TBI selectively induces a robust stimulation of the neurotoxic branch of the KP pathway. QUIN's detrimental roles are supported by its association to adverse outcome potentially becoming an early prognostic factor post-TBI.

Matched MeSH terms: Quinolinic Acid/cerebrospinal fluid*