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. 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.An enriched environment (EE) refers to an animal housing condition that provides physical, psychological, cognitive, and social stimulation (1). In this environment, animals are housed in much larger cages than conventional ones, and items of various shape, colour, size, and texture are used for sensory-motor and social stimulation (1, 2). As a result, an EE offers opportunities for animals to perform a repertoire of species-specific behaviors by integrating multiple sensory experiences (1). Thus, an EE is considered to be a 'eustress', which induces health-promoting or adaptive physiological responses in animals (3). It has been proposed that an EE significantly affects functions of the central nervous system (CNS) such as neurogenesis, plasticity, learning, and memory (4). Little is known, however, on the effects of an EE on other organs.Apoptosis is the process of programmed cell death and is an important mechanism for regulating the development and homeostasis of various organs and for eliminating damaged cells (5). One of the effects of an EE on the CNS is the inhibition of apoptosis. For example, an EE decreases spontaneous apoptosis in the granule cells of the hippocampus in male rats (6). In addition, an EE attenuates sevoflurane-and ketamine-induced neuronal apoptosis (7, 8). The inhibitory effects on neuronal apoptosis may contribute to improved learning and memory and disease prevention (9). Recently, Li et al. reported that an EE attenuates 618 This article is freely accessible online.