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Molecular Radiation Biology
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
β-Aminoisobutyric acid, a metabolite of thymidine, markedly increases in the urine of irradiated individuals.15 There is a rise in the level of taurine and β-aminoisobutyric acid (BAIBA) in the urine of accidentally irradiated humans.3 The urine levels of several amino acids, cysteic acid, valine, leucine, hydroxyproline, phenylalanine, arginine, aspartic acid, proline, threonine, and tryptophan markedly increase in irradiated (37–410 R) individuals.12,20 In patients who were accidentally exposed at Lockport, the increase in urine levels of amino acids was 20- to 30-fold. In some individuals, no change in the urine amino acid level has been observed following radiation therapy treatment.
Brain exosomes as minuscule information hub for Autism Spectrum Disorder
Published in Expert Review of Molecular Diagnostics, 2021
Deepika Delsa Dean, Sarita Agarwal, Srinivasan Muthuswamy, Ambreen Asim
The blood plasma metabolite profiling identified differential levels of homocitrulline aspartate, glutamate, DHEAS, citric acid, succinic acid, methylhexa-, tetra- and heptadecanoic acids, isoleucine, glutaric acid, 3-aminoisobutyric acid and creatinine between ASD children (4 to 6 years) and age-matched healthy children with high diagnostic accuracy [44]. Furthermore, an investigation of plasma mitochondrial biomarkers of oxidative stress and apoptosis depicted that pyruvate, CK, ETC Complex 1, GSH, GST, and Caspase 7 levels could differentiate ASD children and healthy children. Caspase 7 was the most discriminating marker, and only the most severe ASD children showed abnormalities in the ETC Complex 1 activity and Glutathione S-Transferase levels [45].
Tao-Hong-Si-Wu decoction improves depressive symptoms in model rats via amelioration of BDNF-CREB-arginase I axis disorders
Published in Pharmaceutical Biology, 2022
Xiaoping Zhang, Zeng Li, Chuanpu Shen, Jinzhi He, Longfei Wang, Lei Di, Bin Rui, Ning Li, Zhicheng Liu
However, unexpectedly, few metabolic differences were present for the model rats fed different dosages of TSD. Clear discrimination of metabolome was otherwise confirmed between the rats with CUMS and overall TSD-treated rats using another OPLS-DA (R2X = 0.075, R2Y = 0.811, Q2Y = 0.588, Figure 2(d)). Differential metabolites (p< 0.05 calculated by non-parametric tests), associated with CUMS modelling and with the effect of TSD intervention are shown in Table 1. The features that contributed to the separation of B versus M and M versus overall TSD-treated rats are listed in the Venn diagram (Figure 3(a)). Fifteen common discriminants were observed for the separation of blank versus model and the separation of model versus TSD-treated groups. Among these key metabolites, the levels of urea and ornithine (f) significantly increased in the model group compared with the control group but significantly decreased in the TSD treatment group. Other primary discriminants comprised four amino acids (AAs), phosphate, citrate acid, lactate, pseudouridine, myo-inositol and 3-aminoisobutyric acid (3-AIB). The levels of these components decreased in the model group but were restored in the treatment groups, as shown in Figure 3(d–p). An enrichment of primarily varied metabolic pathways was performed along with the determination of metabolic features between the groups. As shown in Figure 3(q,r), various metabolic pathways associated with depression (comparison between the M and S groups) were similar to those associated with the effect of TSD on depression (comparison between the M and integrated groups of rats treated with TSD). Notably, arginine-related pathways were determined as primary characteristics in both pathway analyses.