We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Chronic exposure to Zearalenone leads to endometrial hyperplasia in CD-1 mice by altering the inflammatory markers.
- Authors
Singh, Varsha; Mandal, Payal; Chauhan, Shweta Singh; Saifi, Ishrat Jahan; Marhaba; Sandeep, P V; Jagdale, Pankaj; Ayanur, Anjaneya; Ansari, Kausar Mahmood
- Abstract
Background Zearalenone (ZEA), a natural food contaminant, is reported to act as a mycoestrogen due to its estrogen-mimicking properties. According to studies, ZEA has a greater potential for estrogenic activity compared to any other naturally occurring non-steroidal estrogen. ZEA has been found in the endometrium of individuals with reproductive problems and the serum of children facing early puberty. These studies suggested a possible link between ZEA exposure and endometrial toxicity; nonetheless, no thorough research has been done. This study assessed the endometrium's response to chronic ZEA exposure. Methods Four groups of CD-1 female mice were exposed to control, estradiol (E2), and two different doses of ZEA for 90 days. At the end of treatment, blood and uterus were collected, and samples were used for inflammatory cytokines level, immunochemical, histopathological, and biophysical analysis. Results Our data indicated that the uterus showed a change in body/organ weight ratio, while other organs did not have any notable changes. Immunochemical and histological studies showed hyperplasia and a higher number of glands in the endometrium after ZEA and E2 exposure. Similarly, proliferation markers such as proliferative cell nuclear antigen (PCNA), Ki-67, and inflammatory cytokines such as interleukin 6 (IL-6), interleukin 8 (IL-8), and interferon-gamma (IFN-?) levels were found to be higher in the E2 and ZEA-exposed groups. Conclusion Our finding conclude that ZEA targets the uterus and cause inflammation due to increased levels of inflammatory cytokines and proliferation mediators, as well as systemic toxicity denoted by a strong binding affinity with serum proteins.
- Subjects
ENDOMETRIAL hyperplasia; INFLAMMATORY mediators; BLOOD proteins; ESTRADIOL; END of treatment; ENDOMETRIUM; MICE
- Publication
Toxicology Research, 2024, Vol 13, Issue 2, p1
- ISSN
2045-452X
- Publication type
Article
- DOI
10.1093/toxres/tfae055