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Microbiological, West Nile Virus, and Lyme Disease
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Persistent immune stimulation of the brain is associated with changes in tryptophan catabolism that include an increase of the enzyme indoleamine 2,3-dioxygenase. This enzyme reduces the conversion of tryptophan into serotonin, melatonin, and kynurenic acid (a neuroprotective N-methyl-D-aspartate [NMDA] antagonist) and instead converts tryptophan into kynurenine, which results in an increase in the production of quinolinic acid, an excitotoxin and NMDA agonist that can cause excitotoxicity and contribute to the cognitive, mood, and behavioral symptoms seen in many LYD/TBD patients.64,77
Serum and urine toxicometabolomics following gentamicin-induced nephrotoxicity in male Sprague-Dawley rats
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Sung Ha Ryu, Ji Won Kim, Dahye Yoon, Suhkmann Kim, Kyu-Bong Kim
Previously, MS- or NMR-based metabolomics was used to assess GM-induced kidney injury. Sieber et al. (2009) investigated MS- and NMR-based metabolomics in GM-induced nephrotoxicity in rats and found that urinary citrate, hippurate, trigonelline, 2-oxoglutarate, phenyllactic acid, and 3-indoxylsulfate levels were decreased, whereas lactate, glucose, creatine, N,N-dimethylglycine, and 5-oxoproline concentrations were elevated. Hanna et al. (2013) studied NMR-based metabolomics in GM-mediated nephrotoxicity in rats and noted that GM interrupted tryptophan metabolism pathway, such that urinary tryptophan was significantly increased and kynurenic acid for tryptophan metabolite was markedly lowered. However, these metabolites alterations initiated by GM in the kidney are not always consistent. Therefore, it was of interest to carry out additional studies in search of biomarkers that might more reliably predict GM-induced kidney injury.