Effects of cancer-induced cachexia and administration of l-glutathione on the intestinal mucosa in rat

Walker-256 tumor is an experimental model known to promote cachexia syndrome, oxidative stress, and systemic inflammation. This study evaluated the duodenal mucosa of rats with Walker-256 tumor administered with 1% l -glutathione, intending to evaluate the damage caused by cancer-associated cachexia...

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Veröffentlicht in:Amino acids 2024-04, Vol.56 (1), p.30-14, Article 30
Hauptverfasser: Sestak, Sabrina Silva, da Motta Lima, Fabiana Galvão, de Oliveira, Ana Paula, Barateiro, Letícia Ganem Rillo Paz, Vieira-Frez, Flávia Cristina, de Souza, Sara Raquel Garcia, Guarnier, Flávia Alessandra, Perles, Juliana Vanessa Colombo Martins, Zanoni, Jacqueline Nelisis
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Sprache:eng
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Zusammenfassung:Walker-256 tumor is an experimental model known to promote cachexia syndrome, oxidative stress, and systemic inflammation. This study evaluated the duodenal mucosa of rats with Walker-256 tumor administered with 1% l -glutathione, intending to evaluate the damage caused by cancer-associated cachexia in the gastrointestinal tract and the effects of antioxidant administration on mucosal protection. Twenty-four 55-day-old male Wistar rats were distributed into four groups: control (C); control administered with 1% l -glutathione (C-GSH); Walker-256 tumor (W) and Walker-256 tumor administered with 1% l -glutathione (W-GSH). After 14 days of treatment, the duodenum was harvested for morphometric analysis of the mucosa, proliferation, apoptosis, immunostaining of varicosities immunoreactive (IR) to vasoactive intestinal peptide (VIP) and 5-HT-IR cells, and quantification of mast cells and goblet cells. Walker-256 tumor-bearing rats showed cachexia syndrome, mucosal atrophy, reduced cell proliferation, reduced 5-HT-IR cells, and increased goblet cells and VIPergic varicosities, which were not reversed by l -glutathione. On the other hand, l -glutathione caused a reduction of cells in apoptosis and mast cell recruitment, demonstrating a partial recovery of the damage detected in the intestinal mucosa.
ISSN:1438-2199
0939-4451
1438-2199
DOI:10.1007/s00726-024-03391-9