1.Protective effects of l-glutamine against toxicity of deltamethrin in the cerebral tissue.
Varol S1, Özdemir HH1, Çevik MU1, Altun Y1, Ibiloğlu I1, Ekinci A1, Ibiloğlu AO1, Balduz M1, Arslan D1, Tekin R1, Aktar F1, Aluçlu MU1. Neuropsychiatr Dis Treat. 2016 Apr 21;12:1005-11. doi: 10.2147/NDT.S104011. eCollection 2016.
BACKGROUND: Deltamethrin (DLM) is a broad-spectrum synthetic dibromo-pyrethroid pesticide that is widely used for agricultural and veterinary purposes. However, human exposure to the pesticide leads to neurotoxicity. Glutamine is one of the principal, free intracellular amino acids and may also be an antioxidant. This study was undertaken in order to examine the neuroprotective and antioxidant potential of l-glutamine against DLM toxicity in female Wistar albino rats.
2.Elevated basal glutamate and unchanged glutamine and gaba in refractory epilepsy.
Çavuş I1,2, Romanyshyn JC2, Kennard JT2, Farooque P3, Williamson A2, Eid T2,4, Spencer SS3, Duckrow R3, Dziura J5, Spencer DD2. Ann Neurol. 2016 Apr 30. doi: 10.1002/ana.24673. [Epub ahead of print]
OBJECTIVE: Aberrant glutamate and γ-aminobutyric acid (GABA) neurotransmission contribute to seizure generation and the epileptic state. However, whether levels of these neurochemicals are abnormal in epileptic patients is unknown. Here, we report interictal levels of glutamate, glutamine and GABA in epilepsy patients at seizure onset and non-epileptic sites, cortical lesions, and from patients with poorly localized neocortical epilepsies.
3.TXNIP Suppresses Expression of Glutamine Synthetase by Inducing Oxidative Stress in Retinal Muller Glia Under Diabetic Conditions.
Zhou J1, Shen X2, Lu Q1, Zhang M1. Med Sci Monit. 2016 May 1;22:1460-6.
BACKGROUND Diabetic retinopathy (DR) is a progressive neurodegenerative disease with early-stage symptoms such as dysfunction of Muller cells, which leads to ganglion cell death. Its pathogenesis is probably associated with oxidative stress and a recently discovered protein, thioredoxin-interacting protein (TXNIP). MATERIAL AND METHODS To explore the role of TXNIP in DR, we cultured Muller cells under diabetic conditions, and then used immunohistochemistry, Western blot, and RT-PCR to detect the expression level of TXNIP under diabetic conditions. We demonstrated the expression level of glutamine synthetase (GS) when TXNIP was inhibited. To explore the potential pathway of TXNIP-induced cell damage in DR, we confirmed the role of IL-1β under diabetic conditions. RESULTS Diabetes induces TXNIP expressions at mRNA levels, but shows the opposite effect on GS. IL-1β plays an important role in this pathway. Azaserine effectively increased the expression of GS via attenuating the expression of TXNIP.
4.RhoC is a Potent Regulator of Glutamine Metabolism and N-acetylaspartate Production in Inflammatory Breast Cancer Cells.
Wynn ML1, Yates JA1, Evans CR1, Van Wassenhove L2, Wu ZF1, Bridges S1, Bao L1, Fournier C1, Ashrafzadeh S1, Merrins MJ3, Satin LS1, Schnell S1, Burant CF1, Merajver SD4. J Biol Chem. 2016 Apr 25. pii: jbc.M115.703959. [Epub ahead of print]
Inflammatory breast cancer (IBC) is an extremely lethal cancer that rapidly metastasizes. While the molecular attributes of IBC have been described, little is known about the underlying metabolic features of the disease. Using a variety of metabolic assays including 13C tracer experiments, we found that SUM149 cells, the primary in vitro model of IBC, exhibit metabolic abnormalities that distinguish them from other breast cancer cells, including elevated levels of N-acetylaspartate (NAA), a metabolite primarily associated with neuronal disorders and gliomas. Here we provide the first evidence of NAA in breast cancer. We also report that the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well-known role in cytoskeletal rearrangement.