Systemic dl-Kynurenine and probenecid pretreatment attenuates quinolinic acid-induced neurotoxicity in rats
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Cited by (53)
Deficiency of kynurenine 3-monooxygenase exacerbates impairment of prepulse inhibition induced by phencyclidine
2022, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Administration of KYN significantly increased 3-HK, but not KA, levels in the PFC and HIP of mice (Fig. 4D). When KYN was co-administered with probenecid, which increases endogenous KA by inhibiting the efflux of KA [23,24], the attenuative effect of KYN on PPI impairment was diminished (Fig. 4J). The present doses of KYN metabolites i.c.v. induce seizures in rodents [35].
Kynurenine induces T cell fat catabolism and has limited suppressive effects in vivo
2021, EBioMedicineCitation Excerpt :D-kynurenine contributes to kynurenine derivatives independent of kynureninase such as kynurenic acid, but these are not associated with toxicity. In fact, kynurenic acid even has neuroprotective properties [15,18], and kynureninase inhibition is a neuroprotective treatment strategy to shunt kynurenine metabolites away from quinolinic acid to kynurenic acid [19,20]. Under these assumptions, D-kynurenine could potentially be a therapeutically interesting immunosuppressive metabolite.
Altered hippocampal plasticity by prenatal kynurenine administration, kynurenine-3-monoxygenase (KMO) deletion or galantamine
2015, NeuroscienceCitation Excerpt :The increase in kynurenic acid is associated with an inhibition of CNS function, such as the suppression of allodynia and chronic pain (Pineda-Farias et al., 2013), seizures (Nemeth et al., 2004) and reduced abilities in learning and other cognitive tasks (Alexander et al., 2013; Chess et al., 2007, 2009; Pershing et al., 2015; Pocivavsek et al., 2012, 2014; Shepard et al., 2003; Nilsson et al., 2006). In several studies, increased kynurenic acid has been shown to be protective against damage induced by ischemia (Sas et al., 2008; Robotka et al., 2008) or toxins such as 6-hydroxydopamine (Silva-Adaya et al., 2011), amyloid-β (Carrillo-Mora et al., 2010) and quinolinic acid (Santamaria et al., 1996; Harris et al., 1998). The concentrations that can be achieved by either kynurenine administration or KMO inhibition are 10–100 times greater than those measured in normal mammalian tissue but are likely to be relevant in pathological conditions where CNS involvement occurs and where behavioral aberrations are problematic, especially when KMO activity is itself compromised.
Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity
2013, Journal of Nutritional Biochemistry