Literature DB >> 35241514

Environmental Enrichment Increases Radiation-induced Apoptosis Not Spontaneous Apoptosis in Mouse Intestinal Crypt Cells.

Shinya Yokomizo1,2, Mayumi Nishimura1, Takamitsu Morioka3, Utako Enzaka1, Chizuru Tsuruoka1, Y I Shang1, Yukiko Nishimura1, Kazumasa Inoue2, Masahiro Fukushi2, Tatsuhiko Imaoka1,2, Shizuko Kakinuma1,2, Yoshiya Shimada3,4.   

Abstract

BACKGROUND/AIM: An enriched environment (EE) modifies apoptotic cell death and promotes cell proliferation in the central nervous system (CNS) in mice. However, few studies have examined the effects of an EE on apoptosis in non-CNS organs in model orgamisms. In addition, the intestinal tract is one of organs at high-risk of carcinogenesis after radiation exposure. Herein we evaluated the effects of an EE on spontaneous and radiation-induced apoptosis in intestinal crypt cells of mice.
MATERIALS AND METHODS: Juvenile (3-week-old) and adult (11-week-old) male B6C3F1 mice were housed in a standard environment or EE for 8 weeks and then were whole-body irradiated with 2 Gy X-rays. Apoptosis in the small intestine and colon was analyzed with antibody against cleaved caspase 3.
RESULTS: The EE significantly reduced body weight; adipose tissue weight; and serum levels of total cholesterol, triglyceride, leptin, and insulin. Although EE did not change the spontaneous apoptotic index without irradiation, it significantly increased the index after irradiation in the colonic crypt. The apoptotic index in the small intestinal crypt showed similar patterns.
CONCLUSION: An EE enhances radiation-induced apoptosis of stem/progenitor cells in the small intestine and colon without affecting spontaneous apoptosis. An EE may thus reduce the risk of cancer in the intestinal tract after radiation exposure such as radiotherapy.
Copyright © 2022, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Entities:  

Keywords:  Enriched environment; apoptosis; intestinal tract; radiation

Mesh:

Year:  2022        PMID: 35241514      PMCID: PMC8931893          DOI: 10.21873/invivo.12745

Source DB:  PubMed          Journal:  In Vivo        ISSN: 0258-851X            Impact factor:   2.155


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