Abstract Title:

Subchronic-acetylcysteine Treatment Decreases Brain Kynurenic Acid Levels and Improves Cognitive Performance in Mice.

Abstract Source:

Antioxidants (Basel). 2021 Jan 20 ;10(2). Epub 2021 Jan 20. PMID: 33498402

Abstract Author(s):

Tonali Blanco Blanco Ayala, Daniela Ramírez Ramírez Ortega, Paulina Ovalle Ovalle Rodríguez, Benjamín Pineda, Gonzalo Pérez de la Pérez de la Cruz, Dinora González González Esquivel, Robert Schwarcz, Korrapati V Sathyasaikumar, Anabel Jiménez Jiménez Anguiano, Verónica Pérez de la Pérez de la Cruz

Article Affiliation:

Tonali Blanco Blanco Ayala


The tryptophan (Trp) metabolite kynurenic acid (KYNA) is anα7-nicotinic and-methyl-d-aspartate receptor antagonist. Elevated brain KYNA levels are commonly seen in psychiatric disorders and neurodegenerative diseases and may be related to cognitive impairments. Recently, we showed that-acetylcysteine (NAC) inhibits kynurenine aminotransferase II (KAT II), KYNA's key biosynthetic enzyme, and reduces KYNA neosynthesis in rats. In this study, we examined if repeated systemic administration of NAC influences brain KYNA and cognitive performance in mice. Animals received NAC (100 mg/kg, i.p.) daily for 7 days. Redox markers, KYNA levels, and KAT II activity were determined in the brain. We also assessed the effect of repeated NAC treatment on Trp catabolism using brain tissue slices. Finally, learning and memory was evaluated with and without an acute challenge with KYNA's bioprecursor L-kynurenine (Kyn; 100 mg/kg). Subchronic NAC administration protected against an acute pro-oxidant challenge, decreased KYNA levels, and lowered KAT II activity and improved memory both under basal conditions and after acute Kyn treatment. In tissue slices from these mice, KYNA neosynthesis from Trp or Kyn was reduced. Together, our data indicate that prolonged treatment with NAC may enhance memory at least in part by reducing brain KYNA levels.

Study Type : Animal Study

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