Effects of Letrozole Treatment and Vitamin C Supplementation on Morphology, Endoplasmic Reticulum Stress, Programmed Cell Death, and Oxidative Stress in the Small Intestine of Adult Male Rats.
Anna PilutinSylwia RzeszotekAleksandra WilkKlaudia KlimaszewskaJulia ŁukasiewiczRufaro Lynnette MafutaThanushan NagendranRupia NdambaraBarbara WiszniewskaPublished in: Current issues in molecular biology (2024)
Estrogens are hormones that play an important role in the digestive tract, including in men. Letrozole is an inhibitor of cytochrome P450 aromatase, an enzyme converting androgens to estrogens. The use of letrozole may cause oxidative stress and endoplasmic reticulum stress in the cells. Factors modulating cellular stress may include vitamin C. The purpose of this study was to examine whether letrozole and/or vitamin C supplementation can affect the morphology of the small intestine, the parameters of endoplasmic reticulum stress, programmed cell death markers, and oxidative damage. Three-month-old male rats were divided into four groups and treated with the following: (I) CTRL-water; (II) CTRL+C-L-ascorbic acid; (III) LET-letrozole; and (IV) LET+C-letrozole + L-ascorbic acid. The morphometrical measurements included epithelial thickness, crypt and lumen area, crypt perimeter, nuclei number in the crypt, and the cell size of crypts. The expression levels of PERK, caspase-3, and catalase were determined. Significant differences in the morphometrical measurements and immunoexpression were observed. This may indicate that chronic treatment with letrozole can affect morphology and induce ER stress, oxidative stress, and programmed cell death in the epithelial cells of the small intestine of adult male rats. Vitamin C supplementation exerts an effect on some parameters of the molecular processes.
Keyphrases
- endoplasmic reticulum stress
- induced apoptosis
- polycystic ovary syndrome
- early breast cancer
- oxidative stress
- signaling pathway
- insulin resistance
- poor prognosis
- ischemia reperfusion injury
- stem cells
- adipose tissue
- combination therapy
- single cell
- metabolic syndrome
- long non coding rna
- replacement therapy
- mesenchymal stem cells
- cell proliferation
- cell death
- childhood cancer
- pi k akt
- diabetic rats