Colon cancer has been considered a leading cause of cancer-associated death. Folic acid is a vitamin necessary for cellular physiological functions and cell viability. However, the association between folic acid intake and colon cancer has been examined in several prospective cohort studies are controversial. This study investigated the effects of folate intake on colon carcinogenesis and oxidative stress in an azoxymethane (AOM)/dextran sodium sulfate (DSS) institute for cancer research (ICR) mouse model. Thirty male ICR mice (5 weeks old) were divided into the control group and the experimental group supplied 0.03% folic acid via drinking water (50 mL/week/mouse) for 6 weeks. To induce colonic pre-neoplastic lesions, the animals were subcutaneously injected three times weekly with AOM (10 mg/kg body weight), followed by 2% DSS in drinking water for a week. Folic acid supplementation significantly suppressed the total number of aberrant crypt foci and aberrant crypts. Histological image data showed that folic acid supplementation attenuated neoplastic change. In addition, we measured the thiobarbituric acid reactive substances concentration of dry feces samples to identify the effect of folic acid on reactive oxygen accumulation. The folic acid supplementation group had reduced reactive oxygen species levels in dry feces compared to the control group. In conclusion, these findings indicate that folic acid suppresses colon carcinogenesis and oxidative stress in an AOM/DSS mouse model.

Colon cancer is known as the third most widespread cancer in the world. The interaction of heme-iron and ascorbic acid (AA) in colon carcinogenesis is not evident. Hemin (ferric chloride heme) is an iron-containing porphyrin with chlorine that can be formed from a heme group. The purpose of this study was to investigate the protective effect of AA on the formation of pre-neoplastic lesions induced by azoxymethane (AOM)/dextran sodium sulfate (DSS) plus hemin in mice. Forty-five ICR male mice were divided into three experimental groups; AOM/ DSS treatment (control group), hemin (2 g hemin/kg of b.w.), hemin + AA (1.0% in drinking water). The mice had three s.c. injections (0–2nd weeks of the experiment) of AOM (10 mg/kg b.w.) weekly and 2% DSS as drinking water for the next one week and the animals fed on AIN-76A purified rodent diet for 6 weeks. The numbers of aberrant crypt foci (ACF) and aberrant crypts (ACs) in colonic mucosa were counted after methylene blue staining. Lipid peroxidation in feces was measured by the thiobarbituric acid-reactive substances (TBARS) assay. The numbers of ACF and ACs per colon significantly increased in Hemin group compared to the control group. However, the numbers of ACF and ACs per colon notably decreased in hemin + AA group compared to the control group or hemin group (p<0.05). In feces, the TBARS value of hemin group was higher than the control group (p<0.01). The TBARS value of hemin + AA group was slightly decreased compared to Hemin group. These results indicate that hemin can promote the experimental colon carcinogenesis in ICR mice. On the other hand, additional supplement of AA via drinking water has a protective effect against the colon carcinogenesis. The related mechanisms need to be illustrated by further studies in future.

Globally, colon cancer is increased gradually and known as one of the major causes of cancer death. Stevia, a substitute of sugar, is known to have many components including alpha-tocopherol and anthocyanin etc, as antioxidants. This study's purpose is to investigate whether stevia plant extract can have a protective effect against colon carcinogenesis induced by azoxymethane (AOM) and dextran sodium sulfate (DSS) in mice. Total 30 male ICR mice were divided into 2 groups; AOM/DSS treatment (control group), AOM/DSS + stevia extract (0.5%, in drinking water). After acclimation for 1 week, five weeks old mice received three intraperitoneal AOM (10 mg/kg b.w.) injections weekly for 3 weeks (0–2nd weeks of the experiment) and 2% DSS as drinking water for the next one week. AIN-76A purified rodent diet and 0.5% stevia extract water were supplied to the animals for 6 weeks. The colons of mice were collected and the number of aberrant crypt foci (ACF) and aberrant crypts (ACs) in colonic mucosa were counted after staining with methylene blue. Malondialdehyde (MDA) concentration in feces were determined. The numbers of ACF and ACs were significantly (p<0.01) decreased in stevia-treated group compared with the control group. The MDA concentration in feces was also significantly (p<0.01) decreased in stevia-treated group compared with the control group. In histopathology of colonic epithelium, hyperplasia of colonic epithelium was less observed in steviatreated group. These results indicate that stevia has a protective effect against colon carcinogenesis induced by AOM/DSS in mice and further study needs to illustrate the protective mechanisms.

Excessive intake of red meat has been associated with colon carcinogenesis. The effect of hemin and zinc on colon carcinogenesis was investigated in male ICR mice. After acclimation for 1 week, five-week-old mice received three s.c. injections (0-2nd weeks of the experiment) of azoxymethane (AOM; 10 mg/kg b.w.) weekly and were treated by 2% dextran sodium sulfate (DSS) in drinking water for the next 1 week to induce aberrant crypt foci (ACF). Mice were fed on AIN-76A purified rodent diet for 6 weeks. There were three experimental groups; control, hemin, and hemin + zinc groups. The daily oral doses of hemin and zinc were 534 mg/kg and 55 mg/kg b.w., respectively. After staining colonic mucosa with 0.2% methylene blue, the ACF, aberrant crypts (AC), and polyps were counted. Lipid peroxidation in liver was evaluated by thiobarbituric acid-reactive substances (TBARS) assay. The numbers of AC, ACF, large ACF (i.e., ≥4 AC/ACF), and polyps in the hemin group were higher than those in the control group. In hemin + zinc group, the numbers of AC, ACF, large ACF were significantly lower compared to the hemin or control groups (p < 0.05), and the number of polyps was also significantly lower compared to that in the hemin group (p < 0.05). The TBARS level in the livers of the hemin + zinc group was significantly lower than that of the hemin group (p < 0.05). These results suggest that hemin enhances colon carcinogenesis and that co-treatment with zinc can protect against the induction of colon carcinogenesis.

Colorectal cancer (CRC) is the third most prevalent cancer in the world, and heme iron is known to promote the CRC in an animal model. This study was conducted to investigate the effects of ascorbic acid in the presence of hemin on the formation of pre-neoplastic lesions induced by azoxymethane (AOM)/disodium sulfate (DSS) in mice. After acclimation for 1 week, five-week old mice received three s.c. injections (0-2 weeks of the experiment) of AOM [10 mg/kg body weight (BW)] weekly and were treated with 2% DSS in drinking water for the next week to induce aberrant crypt foci (ACF). All animals were fed the AIN-76A purified rodent diet for experimental period of 6 weeks. Experimental groups were then divided into three groups: carboxymethylcellulose (CMC) alone (control), CMC + Hemin, CMC + Hemin + ascorbic acid (AA). The CMC was used as a solvent for hemin. The daily doses were 534 mg/kg BW hemin and 246 mg/kg BW ascorbic acid administered orally. After the colonic mucosa were stained with methylene blue, aberrant crypt foci (ACF), aberrant crypt (AC) and polyps were counted. Lipid peroxidation in liver was evaluated by the thiobarbituric acid-reactive substances (TBARS) assay. The numbers of ACF, AC and large ACF (≥4 AC/ACF) per colon increased in the hemin group compared to the control group, while they decreased significantly in the hemin + ascorbic acid group compared to the control group or hemin group (p<0.01). The number of polyps/colon in the hemin + AA group was significantly decreased compared to the hemin group (p<0.05). In the liver, the TBARS value of the hemin group was significantly higher than that of the control group (p<0.01). Additionally, the TBARS value of the hemin + AA group decreased slightly compared to that of the hemin group. Taken together, these results suggest that hemin can promote colon carcinogenesis in a mouse model and that ascorbic acid has a protective effect against hemin-promoted colon carcinogenesis.

Excessive iron can promote the production of free radicals, thereby leading to harmful effects on cancer and aging. Ascorbic acid is not only an antioxidant but also a co-factor of iron absorption. The effect of iron-overload with ascorbic acid on experimental colon carcinogenesis was investigated in male ICR mice. Animals were treated weekly with azoxymethane (AOM, 10 mg/kg b.w.) at 0, 1, and 2 week and then drunk 2% dextran sodium sulfate (DSS)-containing water for the next 1 week. There were four experimental groups: carboxymethylcellulose (CMC) alone (control), CMC + ascorbic acid (AA), CMC + Fe, CMC + Fe + AA. The animals fed on AIN-76A purified rodent diet for six weeks. AA or Fe2O3 at the dose of 450 mg/kg b.w. were daily and orally treated for 6 weeks. The colonic mucosa was stained with methylene blue and then aberrant crypt foci (ACF) and polyps were counted. Thiobarbituric acid-reactive substances (TBARS) in serum and liver were determined. Iron concentration in liver was measured by inductively coupled plasma spectrophotometer. Fe-overload with AA strongly increased liver iron contents compared to control or Fe group (p<0.05). There were no significant differences in the number of ACF or polyps among all groups, although ironoverloaded groups had slightly higher numbers compared with the control or AA group. TBARS values in the liver were increased in the iron-overloaded groups compared to control and AA only group (p<0.05), but serum TBARS values were not changed. These results indicate that the excessive iron treatment did not affect the experimental colon carcinogenesis regardless of presence of AA in mice.

Colorectal cancer is one of the most common types of cancer in men and women who consume a Western diet. We investigated the inhibitory effect of selenium (sodium selenite, Na2SeO3) and selenium nanoparticles (nano-Se) on experimental colon carcinogenesis in ICR mice. After a 1-week acclimation, 6-week-old mice received three intraperitoneal (i.p.) injections (experimental week 0-2) of azoxymethane (AOM, 10 mg/kg body weight, b.w.), followed by 2% dextran sodium sulfate (DSS)-containing drinking water for the next 1 week. The three groups (10 mice/group) were orally administered either distilled water (control), selenium (1.7 ppm), or nano-Se (1.7 ppm) daily for 8 weeks. The numbers of aberrant crypt foci (ACF), aberrant crypt (AC), and tumorous lesions were measured in colonic mucosa. Se and nano-Se treatments significantly decreased the number of ACF, AC, and tumorous lesions compared with the control. However, there was no significant difference between the selenium and nano-Se groups. The glutathione peroxidase (GSH-Px) activity in the liver and 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity in serum, were high in the selenium and nano-Se groups, while thiobarbituric acid reactive substance (TBARS) level was low in both Se and nano-Se groups when compared with that in the control group. These findings indicate that selenium and nano-Se showed similar protective effects against colon carcinogenesis by inhibiting the development of ACF and tumorous lesions in mice.

Iron-overload can cause harmful effects such as cancer and aging via promoting the production of free radicals. The effect of orally administered nano-Fe overload with ascorbic acid on colon carcinogenesis was investigated in male ICR mice. After a 1-week acclimation, 5-week-old mice received three intraperitoneal injections (experimental week 0-2) of azoxymethane (AOM, 10 mg/kg body weight) weekly, followed by 2% dextran sodium sulfate (DSS) in drinking water for the next 1 week to induce aberrant crypt foci (ACF). Animals were divided into four groups; carboxymethylcellulose (CMC) alone (control), CMC + ascorbic acid (AA), CMC + nano-Fe (NFe), and CMC + NFe + AA groups. Animals were fed an AIN-76A purified rodent diet and daily administrated oral doses of 450 ppm each of nano-Fe and AA combination for 6 weeks. The colonic mucosa was stained with 0.5% methylene blue, and then the ACF and polyps were counted. Lipid peroxidation in the serum and liver was evaluated using the thiobarbituric acid-reactive substances (TBARS) assay. Iron concentration in the liver was measured using Inductively Coupled Plasma Optical Emission Spectrometer (ICP-OES). Iron concentration in the liver of the NFe-overloaded groups was higher than that of the control (p<0.05). AA treatment increased the iron concentration in the liver. The number of ACF was not significantly different among all the groups. The number of polyps in all the NFe-treated groups was slightly higher than that in the control group and AA only-treated group. The serum TBARS was not significantly different among all the groups, but that in the liver was higher in all the NFe-treated groups than it was in the control group (p<0.05). These results indicate that the additional NFe treatment did not affect the experimental colon carcinogenesis in mice regardless of the presence of ascorbic acid.

This study was conducted to evaluate the accumulation and distribution of hydrophobically modified glycol chitosan (HGC) as a degradable nanoparticle in the body. To determine the movement of degradable HGC nanoparticles in the body, 20 mg/kg of lutetium177-labeled HGC (Lu177-HGC) with the size ranging from 320 to 400 nm was injected intravenously into ICR mice, and the amount of radioactivity remaining in blood and several organs was measured at various time points during the period of 5 days. In the pharmacokinetics analysis using the Lu177 radioisotope, the free Lu177 was mainly distributed and accumulated in the order of kidney>liver>lung at 1 day after the injection of the radioisotope. However, the Lu177-HGC showed a high distribution of nanoparticles in the order of liver>spleen>kidney during the experimental period of 5 days. These results would provide a basic pharmacokinetics for the use of HGC as a drug carrier in drug delivery system.

The ultimate goal of this study is to assess the accumulation and distribution of hydrophobically modified glycol chitosan (HGC) as a degradable nanoparticle in the body. To understand the movement of degradable nanoparticle HGC in the body, we intravenously injected a dose of 20 mg/kg of Cy5.5-labeled HGC with size ranging from 320 to 400 nm into ICR mice, and measured the amount of fluorescence remaining in blood and several organs at various time intervals. In blood, the level of Cy5.5-labeled HGC was the highest at 15 min, then after 30 min it decreased rapidly and reached a plateau form 30 min to 28 days. In the tissue we confirmed the presence of nanoparticles at high levels in the order of kidney>liver>submandibular gland until 28 days after injection. However, we did not find the presence of the particles in the brain or testes. These results will provide basic information on HGC as a drug delivery agent.

Calcium exerts antiproliferative effects on cellular targets through the promotion of differentiation and apoptosis. We investigated the influence of calcium on the formation of colonic aberrant crypt foci (ACFs), which were induced by exposure to azoxymethane (AOM) followed by dextran sodium sulfate (DSS), in ICR mice. Six-week-old ICR mice received 3 (weeks 0–2) intraperitoneal injections of AOM (10 mg/kg BW), followed by treatment with 2% DSS via drinking water for a week to induce preneoplastic lesions. The mice were then divided into 3 groups: the control (AOM/DSS), AOM/DSS + 1.0% Ca, and AOM/DSS + 2.0% Ca groups. Calcium (1.0 or 2.0%) was administered via drinking water for 12 weeks. After sacrificing the mice, the total numbers of aberrant crypts (ACs) and ACFs were measured in the colonic mucosa after methylene blue staining. The control group displayed 11.58 ± 2.43 ACFs/colon, which were composed of a total of 30.42 ± 5.18 ACs/colon. The number of ACFs with more than 3 ACs, which are likely to progress to colon cancer, was 2.37 ± 0.68. Compared to the control, 1.0% or 2.0% calcium treatment significantly decreased the number of total ACFs and ACs in a concentration-dependent manner. The decrease in ACFs or ACs after calcium treatment was associated with decreases in cell proliferation and β-catenin expression and an increase in apoptosis in colonic mucosal cells. These results suggest that calcium may exert a protective effect against colon cancer by inhibiting the development of ACFs/ACs in ICR mice.

Copper is an essential micronutrient whose deficiency is often seen to occur in humans. Although many biomedical studies have focused on the use of nanoparticles, the nutritional effects of nano-sized copper oxide particles are not well known. This aim of this study was to investigate the nutritional bioavailability of nano- and micro-sized copper oxide (CuO) particles in copper-deficient (CuD) mice. Copper deficiency was induced in mice by feeding a CuD diet (0.93 mg Cu/kg diet) for 7 weeks. After the induction of copper deficiency, nano- or micro-sized copper oxide particles were administered orally at two different doses (0.8 and 4.0 mg CuO/kg body weight) to mice in the following groups: (1) normal control (NC), (2) CuD, (3) low dose micro-sized CuO, (4) high dose micro-sized CuO, (5) low dose nano-sized CuO, and (6) high dose nano-sized CuO. The hepatic copper concentration in the CuD group was significantly lower than that in the NC group. Compared to the NC group, the CuD group exhibited lower serum ceruloplasmin (CP) activity and CP level. The copper/zinc-superoxide dismutase activity in the CuD group was significantly lower than that in the NC group. Treatment with nano- or micro-sized copper oxide particles for 2 weeks restored the hepatic copper levels and serum CP activities to values similar to those observed in the NC group. The CP levels and copper/zinc-superoxide dismutase activities in all the copper oxide treatment groups also recovered to normal values after 3 weeks of copper oxide treatment. These results show that oral administration of either nano- or micro-sized copper oxide particles for 2–3 weeks restored the normal condition in previously CuD mice.

Iron is an essential trace element for normal functions of the body. Restriction of iron availability directly limits erythropoiesis. The objective of this experiment was to compare the bioavailability of iron nanoparticles (Fe-NPs) with iron-microparticles (Fe-MPs) in anemic mice. There were four experimental groups, including the normal control group, iron-deficiency anemia (IDA) group, Fe-NPs group, and Fe-MPs group. Animals in the normal group fed on an adequate iron-containing diet (45 ppm Fe). Meanwhile, animals in the other three groups fed on a low Fe diet (4.5 ppm Fe) for seven weeks. Double deionized water was supplied as drinking water ad libitum. After feeding for three weeks with the low Fe diet, animals in the Fe-NPs and Fe-MPs groups received oral administration of Fe-NPs or Fe-MPs at a daily dose of 40 mg/kg for four weeks. The IDA group showed markedly decreased red blood cell (RBC) count, hematocrit (Hct), and hemoglobin (Hb) values compared with the normal group throughout the experimental periods. Treatments with Fe-NPs or Fe-MPs for four weeks resulted in restoration of the decreased RBC count and hematological values similar to normal values. The Fe-NPs group showed faster restoration in values than Fe-MPs with passage of time. The iron contents of the upper small intestine in the Fe-NPs and Fe-MPs groups were higher than in the normal group at weeks 2 and 4. Treatment with Fe-NPs and Fe-MPs resulted in a significant increase in hepatic iron contents and lipid peroxidation, compared with the IDA group with passage of time. The iron contents in liver and ferritin deposits in spleen were identified in the Fe-NPs and Fe-MPs groups, similar to the normal group. These results indicate that oral administration of both Fe-NPs and Fe-MPs can result in recovery from anemia and Fe-NPs is more absorbable and available in the body than Fe-MPs.

Both iron-deficient and zinc-sufficient diets have been known to be associated with a decreased risk of colon cancer. We investigated that effect of dietary zinc on the formation of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM) followed by dextran sodium sulfate in iron-deficient mice. Five-week old ICR mice were acclimated for 1 week and fed on iron-deficient diet (4.50 ppm iron) with three different zinc levels (0.01, 0.1, and 1.0 ppm) for 12 weeks. The total number of aberrant crypt (AC) and ACF was measured in the colonic mucosa after methylene blue staining. The total ACF numbers of low Zn (LZn), medium Zn (MZn) and high Zn (HZn) diet groups were 10.00 ± 2.67, 8.78 ± 3.12, and 7.96 ± 2.44, respectively and there were no significant differences among the groups. However, the total AC numbers of HZn (27.07 ± 3.88) and MZn (26.39 ± 5.59) diet groups were significantly low compared to LZn (22.57 ± 5.09) diet group (p<0.01). Cytosolic SOD activity was the highest in LZn diet group. But thiobarbituric acid-reactive substances level in liver was also the highest in LZn diet group compared to other groups. There is no difference in cell proliferation in mucous membrane among the groups, while apoptotic positive cells were increased in the HZn diet group. The high zinc diet exhibited decreased β-catenin-stained areas on the mucous membrane of colon compared to the LZn or MZn diet group. These findings indicate that dietary zinc might exert a modulating effect on development of ACF/AC in the mice with iron-deficient status.

Iron nanoparticles (Fe-NPs) have recently been used for cancer diagnosis and therapy for imaging contrast and drug delivery. However, no study on nutritional bioavailability of Fe-NPs in the body has been reported. Ascorbic acid (AA) is known to aid in absorption of iron in the stomach by reducing Fe (III) to Fe (II). In this study, we investigated the bioavailability of Fe-NPs with AA in iron-deficiency-anemic mice in comparison with non-nano iron particles. Iron-deficient anemia was induced by feeding an iron-deficient diet (4.5 mg Fe/kg) and ocular bleeding from retro-orbital venous plexus for four weeks. Normal control mice were given a normal diet (45 mg Fe/ kg). After induction of anemia in mice, anemic mice received daily oral administration of Fe (40 mg/kg B.W.) + AA (5 g/kg B.W) and Fe-NPs (40 mg/kg B.W) + AA (5 g/kg B.W). After sacrifice, liver and spleen tissues were observed by haematoxylin & eosin stain. Amount of trace iron in liver and upper small intestine was investigated using an inductively coupled plasma-atomic emission spectrometer. Red blood cells (RBC), hematocrit (Hct), hemoglobin (Hb), and total iron binding capacity were also measured. The concentrations of iron in the Fe-NPs + AA group were significantly higher in liver and in upper small intestine than that in the Fe + AA group. The values of RBC, Hct, and Hb in the Fe-NPs + AA group were more rapidly increased to normal values compared with the Fe + AA group with increasing time. These results suggest that Fe-NPs in the presence of AA may be more bioavailable than non-nano Fe in Fe-deficient anemic mice.

The current study was conducted in order to investigate promotional effects of herbal extracts on hair growth in an animal model of mice. There were four experimental groups, including distilled water (DW) as a negative control (NC), 3% minoxidil (MXD) as a positive control (PC), 50% ethanol (EtOH) as a vehicle control (VC), and herbal extract (HE) as the experimental treatment (E). The HE was extracted with ethanol from plants, including Gardenia, Mentha arvensis, Rosemary, and Lavender. Six-week-old C57BL/6 male mice were shaved with an electric clipper and the test materials were topically treated with 0.2 ml per mouse daily for three weeks. Photographic evaluation of hair re-growth was performed weekly during a period of three weeks. The number of mast cells was counted on the dorsal skin section of mice. The enzymes, alkaline phosphatase (ALP) and γ-glutamyl transpeptidase (γ-GT), were determined using a biochemical autoanalyzer. No clinical signs were observed in any of the experimental groups. As a result of photometric analysis, topical application of HE to dorsal skin for two weeks resulted in significantly faster acceleration of hair regrowth, compared with that of the NC or VC group (P<0.05). The PC and E groups showed a significant decrease in mast cell population, compared to the NC group. Activities of ALP and γ-GT were significantly increased in the PC and E groups, compared to the NC or VC group (P<0.05). Taken together, these results suggest that the herbal extract may have hair-growth promoting activity equal to that of MXD.

To investigate the effect of carnosine on exhaustive exercise, swimming tests were conducted weekly with loads corresponding to 5% of body weight attached to the tails of mice, and the swimming time to exhaustion was measured. Eighty male ICR mice were divided into four groups, to which carnosine was administered at doses of 0 (control), 10, 50, and 250 mg/kg/day, respectively, for a period of four weeks. At the end of swimming exercise challenges, serum biochemistry, oxidative stress enzyme activity, and antioxidant enzyme activity in tissues were determined. Treatment with 250 mg/kg carnosine resulted in a significant increase in swimming times to exhaustion, compared to the control group in the first (P<0.01) and third week (P<0.05). Significantly lower serum lactate levels were observed after the swimming exercise in the carnosine-treated groups (10 and 250 mg/kg), compared with the control (P<0.01). Malondialdehyde levels in the liver (10 and 50 mg/kg carnosine treated groups) and skeletal muscle (250 mg/kg carnosine treated group) were significantly lower, compared with the control (P<0.05). Significantly lower protein carbonyl levels in skeletal muscle were observed in the 50 and 250 mg/kg carnosine treated groups, compared with the control (P<0.01). Superoxide dismutase and glutathione peroxidase activities in skeletal muscle did not differ significantly among the groups. These results indicate that carnosine may improve swimming exercise capacity by attenuating production of lactate and reducing oxidative stress in mice.

본 연구에서는 azoxymethane (AOM)과 dextran sodium sulfate (DSS)로 유도된 대장 발암과정에 대한 셀레늄의 방어 효과를 조사하였다. 셀레늄 결핍(0.02 ppm Se), 정상(0.1 ppm Se), 과다(0.5 ppm Se)사료를 12주간 식이로 급여하여 혈액검사와 대장암 발생의 초기단계인 aberrant crypt foci (ACF)수를 측정했으며, 암 발생율을 조사하였다. ICP-AES 를 사용하여 간의 셀레늄 농도를 측정하였으며, 또한 셀레늄포함 항산화효소인 glutathione peroxidase (GPx) 활성을 알아보았다. 또한 TUNEL assay와 PCNA, β-catenin에 대한 면역조직 염색을 수행하였다. ACF 수 및 종양 발생률에 있어서, 셀레늄과다사료를 급여한 군이 정상셀레늄사료를 급여한 군보다 낮았으며, 셀레늄결핍사료를 급여한 군은 오히려 ACF 수 및 종양 발생률이 높았다. GPx 활성은 셀레늄의 섭취가 과다한 군에서 높게 나타났으며, 이 때, TUNEL 에서 apoptotic positive cell이 증가하는 것을 확인했다. 또 한 셀레늄의 섭취가 과다한 군에서 PCNA와 β-catenin의 발현이 감소됨을 볼 수 있었다. 본 마우스 모델실험에서 셀레늄은 여러 기전에 의해 대장암 발생을 억제할 수 있을 것으로 사료된다.