Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency

• Main Authors: Vitor Teixeira (Author), Ibrahim Mohamed (Author), Jean-Claude Lavoie (Author)
• Format: Book
• Published: MDPI AG, 2023-06-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

In premature infants receiving parenteral nutrition, oxidative stress is a trigger for the development of bronchopulmonary dysplasia, which is an important factor in the development of adult lung diseases. Neonatal vitamin C and glutathione deficiency is suspected to induce permanent modification of redox metabolism favoring the development of neonatal and adult lung diseases. A total of 64 3-day-old guinea pigs were fed an oral diet that was either complete or deficient in vitamin C (VCD), cysteine (CD) (glutathione-limiting substrate) or both (DD) for 4 days. At 1 week of age, half of the animals were sacrificed while the other started a complete diet until 12 weeks of age. At 1 week, the decrease in lung GSH in all deficient groups was partially explained by the oxidation of liver methionine-adenosyltransferase. mRNA levels of kelch-like ECH-associated protein 1 (<i>Keap1</i>), glutathione-reductase (<i>Gsr</i>) and glutaredoxin-1 (<i>Glrx</i>) were significantly lower only in CD but not in DD. At 12 weeks, glutathione levels were increased in VCD and CD. <i>Keap1</i>, <i>Gsr</i> and <i>Glrx</i> mRNA were increased, while glutathione-reductase and glutaredoxin proteins were lower in CD, favoring a higher glutathionylation status. Both neonatal deficiencies result in a long-term change in glutathione metabolism that could contribute to lung diseases' development.

Item Description

10.3390/antiox12071361
2076-3921