Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Oct 6;13:979719. doi: 10.3389/fmicb.2022.979719

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2022 Labarrere and Kassab.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection alters metabolism and redox function of cellular glutathione (GSH). SARS-CoV-2 markedly decreases GSH levels [1], that could be explained by lower intake of the GSH precursor cysteine (Cys) [2] and increased efflux of cellular thiols [3]. Increased levels of oxidized glutathione (GSSG) and protein glutathionylation [4] along with upregulation of endoplasmic reticulum stress marker protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) [5] are also observed. Antivirals activate the Kelch-like ECH-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor2 (Nrf2)-antioxidant response element (ARE) redox regulator pathway, releasing Nrf2 [6] to regulate the expression of genes that control antioxidant, inflammatory and immune system responses (including the cystine (cys-cys)/glutamate transporter xCT and the membrane transporter multidrug resistance protein [MRP], which are decreased and markedly upregulated, respectively, during infection); restoring GSH levels in the infected cells and facilitating GSH synthesis [7] and activity. Abbreviations: γ-GT: γ-glutamyl transferase; ASCT: alanine-serine-cysteine transporter; LAT: L-type amino acid transporter; PSSG: S-glutathionylated Proteins; GST: glutathione-S-transferase; γ-GCL: γ-glutamate cysteine ligase; γ-glutamyl cysteine; GST: glutathione-S-transferase; GPx: glutathione peroxidase; GR: glutathione reductase; NADPH: reduced NADP+; NADP+: Nicotinamide adenine dinucleotide phosphate; GS: glutathione synthetase; xCT (SLC7A11)/SLC3A2: cystine/glutamate transporter light (xCT [SLC7A11]) and heavy (SLC3A2) chains. Modified from Bartolini et al. (2021).