This study investigated ethopabate (EPB) residues in edible tissues of broiler chickens given in drinking water and established the withdrawal time (WT) of EPB in poultry tissues. Twenty-four healthy Ross broiler chickens were orally administered with EPB at the concentration of 3.8 mg/L for 14 days (EPB-1, n=24) and 15.2 mg/L for 7 days (EPB-2, n=24) through drinking water, respectively. After the drug treatment, tissue samples were collected from six broiler chickens at 0, 1, 3, and 5 days, respectively. EPB residue concentrations in poultry tissues were determined using LC-MS/MS. Correlation coefficient values ranged from 0.9980 to 0.9998, and the limits of detection and quantification (LOQ) were 0.03~0.09 and 0.1~0.3 μg/kg, respectively. Mean recoveries in muscle, liver, kidney and skin/fat tissues were 95.9~109.8, 108.7~115.3, 89.9~96.6 and 86.7~96.8%, respectively, and coefficient of variations were less than 17.11%. At the end of the drug-administration period (0 day), EPB was detected at levels under the LOQ in all tissues from both the EPB-1 and EPB-2 groups. According to the results of EPB residue in Ross broiler tissues, withdrawal periods of both EPB-1 and EPB-2 in poultry tissues were established to 0 day. In conclusion, the developed analytical method is suitable for the detection of EPB in poultry tissues, and the estimated WT of EPB in poultry tissues will contribute to ensuring the safety of Ross broiler chickens.

From 2020, Korean Animal and Plant Quarantine Agency has reset the withdrawal time (WT) for veterinary drugs typically used in livestock in preparation for the introduction of positive list system (PLS) program in 2024. This study was conducted to reset the MRL for amprolium (APL) in broiler chickens as a part of PLS program introduction. Forty-eight healthy Ross broiler chickens were orally administered with APL at the concentration of 60 mg/L (APL-1, n=24) for 14 days and 240 mg/L (APL-2, n=24) for 7 days through drinking water, respectively. After the drug treatment, tissue samples were collected from six broiler chickens at 0, 1, 3 and 5 days, respectively. Residual APL concentrations in poultry tissues were determined using LC-MS/MS. Correlation coefficient (0.99 >), the limits quantification (LOQ, 0.3~5.0 μg/kg), recoveries (81.5~112.4%), and coefficient of variations (<15.5%) were satisfied the validation criteria of Korean Ministry of Food and Drug Safety. In APL-1, APL in all tissues except for kidney was detected less than LOQ at 3 days after drug treatment. In APL-2, APL in liver and kidney was detected more than LOQ at 5 days after treatment. According to the European Medicines Agency’s guideline on determination of withdrawal periods, withdrawal periods of APL-1 and APL-2 in poultry tissues were established to 3 and 2 days, respectively. In conclusion, the developed analytical method is sensitive and reliable for detecting APL in poultry tissues. The estimated WT of APL in poultry tissues is longer than the current WT recommendation of 2 days for APL in broiler chickens.

Colorectal cancer causes the most cancer-associated death worldwide, having a high cancer incidence. Pectin is a complex polysaccharide present in various fruits, emerging as an anti-carcinogenic candidate. Although pectin has a suppressive capacity for colon carcinogenesis, the effect of reactive oxygen species (ROS) generation and colonic aberrant foci formation in the colon carcinogenesis mouse model remains unclear. Therefore, this study investigates the regulatory effect of pectin supplementation on colon carcinogenesis induced by azoxymethane (AOM) and dextran sodium sulfate (DSS) in mice. In an animal experiment, thirty male institute for cancer research (ICR) mice were divided into two experimental groups; AOM/DSS (control group) and AOM/DSS + pectin (5% in drinking water). Furthermore, the number of aberrant crypt foci (ACF) and aberrant crypt (AC) on colonic mucosa were counted, and thiobarbituric acid-reactive substances (TBARS) assay was performed to estimate lipid peroxidation in feces. Pectin treatment significantly decreased the number of ACF and AC per colon compared with the control. Additionally, fecal TBARS level in the pectin group was significantly lower than those in the control group. Conclusively, these findings indicate that pectin-inhibited hyperplastic alteration and oxidative stress suppress colitis-associated colon carcinogenesis.

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.