Assessment of nitrous oxide production in eutrophicated rivers with inflow of treated wastewater based on investigation and statistical analysis.

Accurate estimation and control of greenhouse gas emissions have been recognized as imperative in recent years. Therefore, frequent investigations under uniform environmental conditions are required to better understand this concept. Thus, six sampling sites with characteristic concentrations of nitrogen and other water quality parameters were selected to investigate the behavior of water quality parameters throughout the year and to statistically examine the correlations among the parameters. Dissolved nitrous oxide (D-N2O) showed the highest positive correlation coefficient with NO2-N among nitrogen species. The results of the principal component analysis suggested that river water quality could be broadly classified based on photosynthesis and contamination from treated wastewater. Photosynthesis caused an increase in pH, with concomitant decrease in D-N2O concentration. Using the results of multiple regression analysis, D-N2O was accurately estimated based on nitrogen concentration, pH, and concentration of organic matter in various situations. The results of a detailed survey suggested that D-N2O was produced in the river from nitrogen sources released from the wastewater treatment plant. The main roles of the wastewater treatment plant for D-N2O behavior in the river were the supply of the nitrogen source that was the precursor of D-N2O, the supply of the nutrients that induced the photosynthesis, and the direct supply of D-N2O at a low water temperature. The models based on multiple regression analysis could efficiently predict the D-N2O concentration produced in rivers at sites downstream of the wastewater treatment plant, except for the direct supply of D-N2O as an effluent at low water temperature.

Operator-derived particles and falling bacteria in biosafety cabinets.

Introduction: To ensure the sterility of cell products that cannot undergo conventional sterilization processes, it is imperative to establish and maintain a clean room environment, regulated through environmental monitoring, including particle counts. Nevertheless, the impact of particles generated by operators as potential contaminants remains uncertain. Thus, in this study, we conducted an accelerated test to assess the correlation between particles generated by operators and airborne bacteria, utilizing biosafety cabinets within a typical laboratory setting. These biosafety cabinets create a controlled environment with air conditioning and high-efficiency particulate air (HEPA) filters, offering fundamental data relevant to cell production. Materials and methods: We conducted a simulation followed by real-time experiments involving human operations to explore the quantity of particles, particle sizes, and the percentage of bacteria within these particles. This investigation focused on conditions with heightened particle generation from operators within a biosafety cabinet. The experiment was conducted on operators wearing textile and non-woven dustless clothing within biosafety cabinets. It entailed tapping the upper arms for a duration of 2 min. Results: Observations under biosafety cabinet-off conditions revealed the presence of various particles and falling bacteria in textile clothing. In contrast, no particles or falling bacteria were detected in operators wearing dustless clothing within biosafety cabinets. Notably, a correlation between 5 µm particles and colony-forming units in textile clothing was identified through this analysis. The ratio of falling bacteria to the total number of particles within the biosafety cabinet was 0.8 ± 0.5 % for textile clothing, while it was significantly lower at 0.04 ± 0.2 % for dustless clothing. Conclusion: This study demonstrated that the number of particles and falling bacteria varied depending on the type of clothing and that quantitative data could be used to identify risks and provide basic data for operator education and evidence-based control methods in aseptic manufacturing areas. Although, this study aims to serve as an accelerated test operating under worst-case conditions, the results need to make sure the study range in general research.

Volatile organic compounds and ionic substances contamination in cell processing facilities during rest period; a preliminary assessment of exposure to cell processing operators.

Introduction: Cell processing operators (CPOs) use a variety of disinfectants that vaporize in the workspace environment. These disinfectants can induce allergic reactions in CPOs, due to their long working hours at cell processing facilities (CPFs). Ionic substances such as CH3COO- generated from peracetic acid, nitrogen oxides (NOx) and sulfur oxides (SOx) from outdoor environment are also known to pollute air. Therefore, our objective was to assess the air quality in CPFs and detect volatile organic compounds (VOCs) from disinfectants and building materials, and airborne ionic substances from outdoor air. Methods: Sampling was conducted at three CPFs: two located in medical institutions and one located at a different institution. Air samples were collected using a flow pump. Ion chromatographic analysis of the anionic and cationic compounds was performed. For VOC analysis, a thermal desorption analyzer coupled with capillary gas chromatograph and flame ionization detector was used. Results: Analysis of the ionic substances showed that Cl-, NOx, and SOx, which were detected in large amounts in the outdoor air, were relatively less in the CPFs. Ethanol was detected as the main component in the VOC analysis. Toluene was detected at all sampling points. As compared to the other environments, air in the incubator contained larger amounts of VOCs, that included siloxane, tetradecane, and aromatics. Conclusions: No VOCs or ionic substances of immediate concern to the health of the CPOs were detected during the non-operating period. However, new clinical trials of cell products are currently underway in Japan, and a variety of new cell products are expected to be approved. With an increase in cell processing, health risks to CPOs that have not been considered previously, may become apparent. We should continue to prepare for the future expansion of the industry using a scientific approach to collect various pieces of information and make it publicly available to build a database.

Oncostatin M's Involvement in the Pathogenesis of Chronic Rhinosinusitis: Focus on Type 1 and 2 Inflammation.

OBJECTIVES: The cytokine oncostatin M (OSM) elicits pathogenic effects involving disruption of the epithelial barrier function as a part of immunological response networks. It is unclear how these integrated cytokine signals influence inflammation and other physiological processes in the pathology of chronic rhinosinusitis (CRS). We investigated the expression and distribution of OSM and OSM receptor (OSMR) in CRS patients' sinonasal specimens, and we compared the results with a panel of inflammatory cytokine levels and clinical features. PATIENTS AND METHODS: We classified CRS patients as eosinophilic (ECRS, n = 36) or non-eosinophilic (non-ECRS, n = 35) based on the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis phenotypic criteria and compared their cases with those of 20 control subjects. We also examined OSM's stimulatory effects on cytokine receptor expression levels using the human bronchial epithelium cell line BEAS-2B. RESULTS: RT-PCR showed that the OSM mRNA levels were significantly increased in the CRS patients' ethmoid sinus mucosa. The OSM mRNA levels were positively correlated with those of TNF-α, IL-1ß, IL-13, and OSMR-ß. In BEAS-2B cells, OSM treatment induced significant increases in the OSMRß, IL-1R1, and IL-13Ra mRNA levels. CONCLUSIONS: OSM is involved in the pathogenesis of CRS in both type 1 and type 2 inflammation, suggesting the OSM signaling pathway as a potential therapeutic target for modulating epithelial stromal interactions.

Chemopreventive effect of mofezolac on beef tallow diet/azoxymethane-induced colon carcinogenesis in rats.

BACKGROUND/AIMS: We have previously shown that long-term consumption of 10% beef tallow diet promotes colon carcinogenesis in both saline- and azoxymethane (AOM)-treated rats. Here, we investigated the effects of mofezolac, a selective COX-1 inhibitor, on beef tallow-fed rats with saline- or AOM treatment. METHODOLOGY: Male SD rats were intraperitoneally injected with saline or AOM and fed 10% beef tallow diet with or without 1200 ppm mofezolac. At 12 weeks, aberrant crypt foci (ACF) were examined. At 44 weeks, tumors were counted, the proliferation and expression of COX-1 and 8-catenin on normal-appearing colonic mucosa was evaluated using the BrdU incorporation assay and Western blotting respectively. RESULTS: Mofezolac decreased the number of ACF at 12 weeks (p < 0.05) and reduced tumor multiplicity and incidence at 44 weeks in beef tallow-fed rats with AOM treatment (p < 0.05). At 44 weeks, reduction of the BrdU-positive cells (p < 0.05) and beneficial distribution changes of these cells within the colon crypts in both groups with mofezolac supplementation were observed. The expression of COX-1 and beta-catenin also reduced in mofezolac-added groups simultaneously (p < 0.05). CONCLUSIONS: This study suggested that mofezolac suppressed beef tallow-promoted colon carcinogenesis in rats, which probably was, appropriate for populations with high fat intake.

RANKL-induced DC-STAMP is essential for osteoclastogenesis.

Osteoclasts are bone-resorbing, multinucleated giant cells that are essential for bone remodeling and are formed through cell fusion of mononuclear precursor cells. Although receptor activator of nuclear factor-kappaB ligand (RANKL) has been demonstrated to be an important osteoclastogenic cytokine, the cell surface molecules involved in osteoclastogenesis are mostly unknown. Here, we report that the seven-transmembrane receptor-like molecule, dendritic cell-specific transmembrane protein (DC-STAMP) is involved in osteoclastogenesis. Expression of DC-STAMP is rapidly induced in osteoclast precursor cells by RANKL and other osteoclastogenic stimulations. Targeted inhibition of DC-STAMP by small interfering RNAs and specific antibody markedly suppressed the formation of multinucleated osteoclast-like cells. Overexpression of DC-STAMP enhanced osteoclastogenesis in the presence of RANKL. Furthermore, DC-STAMP directly induced the expression of the osteoclast marker tartrate-resistant acid phosphatase. These data demonstrate for the first time that DC-STAMP has an essential role in osteoclastogenesis.

Suppression of intestinal mucosal apoptosis by ghrelin in fasting rats.

Ghrelin is mainly produced in the stomach and has several physiologic functions. The aim of this study was to investigate whether ghrelin regulates apoptosis in the small intestinal mucosa of fasting rats. Intestinal mucosal apoptosis was evaluated as the percentage of fragmented DNA, villus height, and terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end-labeling (TUNEL) staining and by Western blot analysis of caspase-3 in 48-hr fasting rats. Crypt cell proliferation was evaluated by counting the number of 5-bromo-2-deoxyuridine (BrdU) positive cells. Ghrelin was administered intraperitoneally at dosages of 2.5, 25, and 250 microg/kg per 48 hrs by continuous infusion via an Alzet micro-osmotic pump or injections at 12-hr intervals. Ghrelin was also infused in rats that underwent truncal vagotomy. The lowest dosage of ghrelin (2.5 microg/kg per 48 hrs) was administered into the third cerebroventricle. Ghrelin treatment attenuated the percentage of fragmented DNA in the small intestinal mucosa in 48-hr fasting rats in a dose-dependent manner. Continuous infusion of ghrelin and injections of ghrelin at 12-hr intervals suppressed intestinal apoptosis almost equally. This effect on apoptosis was not attenuated by truncal vagotomy. Cerebroventricular infusion of ghrelin also attenuated intestinal apoptosis. The antiapoptotic effect of ghrelin was confirmed by decreased TUNEL staining, recovery of the villus height, and decreased expression of caspase-3. BrdU uptake indicated that ghrelin enhanced cell proliferation in the intestinal crypt. Taken together, these data indicate that ghrelin enhanced intestinal growth with the suppression of small intestinal mucosal apoptosis in 48-hr fasting rats, suggesting that ghrelin controls intestinal function through the regulation of intestinal apoptosis.

Indigestible material attenuated changes in apoptosis in the fasted rat jejunal mucosa.

We have previously demonstrated that fasting induced apoptosis and decreased cell proliferation in the rat intestinal mucosa. The aim was to investigate the effect of expanded polystyrene as indigestible material on apoptosis and cell proliferation in rat small intestinal mucosa during fasting. Male SD rats were divided into 3 groups. The first group was fed with chow and water ad libitum. The second group fasted for 72 hrs. The third group was fasted for 24 hrs and was fed expanded polystyrene. Intestinal apoptosis was evaluated by percent fragmented DNA assay, terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end-labeling (TUNEL) staining, and caspase-3 assay. Cell proliferation was analyzed by 5-bromo-2'-deoxyuridine (5-BrdU) uptake. Truncal vagotomy was performed to evaluate a role of the central nervous system. In the 72-hr fasted rat, mucosal height of the rat jejunum was decreased to 73% of that in rats fed ad libitum, and this decrease was partly restored to 90% in rats fed expanded polystyrene. The fragmented DNA was increased in fasted rats (28.0%) when compared with that in rats fed ad libitum (2.6%). The increase in fragmented DNA in fasted rats was recovered by feeding them expanded polystyrene (8.3%). TUNEL staining confirmed this result. The effect of polystyrene on apoptosis was decreased by truncal vagotomy. Expression of cleaved caspase-3 was increased in fasted rats, which was then decreased by feeding of expanded polystyrene. In contrast to apoptosis, feeding of expanded polystyrene had no reconstructive effect on 5-BrdU uptake in the intestinal epithelium, which was decreased by fasting to 60% of that in rats fed ad libitum. In conclusion, feeding of indigestible material partly restored the decrease in intestinal mucosal length in the fasted rats through the apoptotic pathway without any influence on BrdU uptake. Further exploration focused on the mechanism of this effect of indigestible material is required.

Antibiotic effect of amoxicillin on the feces composting process and reactivation of bacteria by intermittent feeding of feces.

The aim of this work was to investigate the single exposure effect of amoxicillin on the feces composting process and the possibility of its bacterial reactivation by intermittent feeding of feces. The respiratory activity of the bacteria during the process after receiving exposure to several dosages of amoxicillin indicated a decrement of treatment performance, which was caused by the reduction of the initial viable bacterial count and activity brought about by the amoxicillin dosage. The amount of remaining feces was proportional to the initial concentration of amoxicillin, and even though no amoxicillin was detected, no automatic reactivation was observed, either. An intermittent feces feeding test was conducted to reactivate the bacteria. For the 10 and 100microg-amoxicillin/g dry systems, reactivation was observed, but for the 1000microg/g dry, no reactivation was seen. Finally, an intermittent feces feeding test was conducted with sterilized sawdust and the result indicated that the feces acted as a substrate rather than as a bacterial carrier.

Factors affecting the degradation of amoxicillin in composting toilet.

The biological and non-biological factors that affect the degradation of amoxicillin in the composting process of feces have been investigated. The effect of living bacteria and the enzyme (beta-lactamase) on amoxicillin decay was examined, and our results indicated that the biological effects are likely to be negligible. Consequently, the effect of phosphate, ammonia and pH level as non-biological factors was investigated by monitoring the reduction rate of amoxicillin in phosphate and ammonia buffer solutions with several pH levels. Each reduction rate constant was integrated by a simulation model, and the each calculated amoxicillin reduction profile was compared to the reduction profiles of amoxicillin in the composting process of feces. The calculated results corresponded almost exactly to the experimental profiles. We therefore concluded that the degradation of amoxicillin in a toilet matrix was dependent on the concentration of ammonia, phosphate and hydroxyl ion.

Fetal Gene Therapy for Ornithine Transcarbamylase Deficiency by Intrahepatic Plasmid DNA-Micro-Bubble Injection Combined with Hepatic Ultrasound Insonation.

We evaluated the therapeutic efficacy of hepatic transfection of plasmid DNA using micro-bubbles and ultrasound insonation for fetal correction of ornithine transcarbamylase (OTC) deficiency in mice. Twenty-three sparse-fur heterozygous pregnant mice (day 16 of gestation) were divided into three groups: injection of plasmid-DNA micro-bubble mixture into fetal liver with ultrasound insonation (Tr, n = 11); control group 1 (C1), injection of plasmid-DNA micro-bubble mixture into fetal liver with no insonation (n = 5); and control group 2 (C2), injection of saline-micro-bubble mixture into fetal liver with ultrasound insonation (n = 7). Levels of blood ammonia and urinary orotic acid were significantly lower in the Tr group than in the C1 and C2 groups (p < 0.05, p < 0.01, respectively), whereas OTC activity was not different between groups. Therefore, ultrasound insonation with micro-bubbles enhanced plasmid DNA transfection into fetal mouse liver, leading to one of the therapeutic methods in ammonia metabolism. This might provide more time for OTC-deficient infants until liver transplantation.

Expression patterns of the tumor suppressor PDCD4 and correlation with ß-catenin expression in gastric cancers.

The expression patterns of PDCD4, a tumor suppressor, and ß-catenin were immunohistologically investigated in gastric carcinoma tissues. In normal gastric tissues, PDCD4 was strongly expressed in the cell nuclei, but weakly expressed in the cytoplasm. In gastric adenocarcinoma tissues, nuclear PDCD4 expression was decreased, while cytoplasmic PDCD4 expression was unchanged or somewhat increased. In gastric signet ring cell carcinoma tissues, PDCD4 expression patterns were different from the expression patterns of the adenocarcinoma tissues, and PDCD4 was localized in the nuclei of the carcinoma cells as a belt in the middle of the epithelial layer. The nuclear localization of PDCD4 in the adenocarcinoma tissues was correlated with the membrane localization of ß-catenin, the activation of which stimulates invasion of colon cancer cells. PDCD4 expression was correlated with ß-catenin expression in gastric carcinoma cell lines, but not with E-cadherin, as the binding partner in the cell membrane.

Conjugated linoleic acid suppresses colon carcinogenesis in azoxymethane-pretreated rats with long-term feeding of diet containing beef tallow.

BACKGROUND: We have indicated previously that long-term feeding of beef tallow increases colorectal cancer in rats. In this study, we investigated the effects of conjugated linoleic acid (CLA) on colon carcinogenesis in rats under long-term feeding of beef tallow diets, pretreated with azoxymethane (AOM). METHODS: Six-week-old male Sprague-Dawley rats were fed with 10% beef tallow diet only, 10% beef tallow with 1% CLA in triglyceride form (CLA-TG), or 10% beef tallow with 1% CLA in free fatty acid form (CLA-FFA). Colon carcinogenesis was induced by two intraperitoneal injections of AOM. Aberrant crypt foci (ACFs) were examined at 12 weeks. Cancer, cell proliferation, apoptosis, Wnt signaling, and the arachidonic acid cascade were examined at 44 weeks. RESULTS: At 12 weeks, CLA-TG and CLA-FFA attenuated the increase in ACFs induced by 10% beef tallow and AOM pretreatment. At 44 weeks, both forms of CLA attenuated multiple colon cancers, and CLA-FFA reduced the incidence of colon cancer to 50% of that seen with CLA-TG. CLA-TG and CLA-FFA decreased the number of 5-bromo-2'-deoxyuridine-positive cells in AOM-pretreated rats fed with 10% beef tallow. CLA-FFA increased the number of apoptotic cells and the activity of caspase-3 in the colon mucosa, and CLA-TG enhanced the activity of caspase-3. Both forms of CLA suppressed Wnt signaling and the arachidonic acid cascade in rats treated with beef tallow and AOM. CONCLUSION: These results suggested that CLA-TG and CLA-FFA suppressed colon carcinogenesis in rats with long-term feeding of a 10% beef tallow diet, through several mechanisms. The results of the present study with rats might be applicable to humans.

Long-term ingestion of reduced glutathione suppressed an accelerating effect of beef tallow diet on colon carcinogenesis in rats.

PURPOSE: We have shown previously that long-term feeding of beef tallow increases colorectal cancer in rats. This study investigated the effects of enzymic antioxidant, reduced glutathione (GSH), on colon carcinogenesis in rats fed with beef tallow. METHODS: Colon carcinogenesis was induced by intraperitoneal injection of azoxymethane (AOM) to rats. Rats were fed with 10% beef tallow supplemented with or without 1% GSH in drinking water. Aberrant crypt foci (ACF) and expression of beta-catenin in colonic mucosa were examined at 12 weeks. Cancers, related substances of oxidative stress and arachidonic acid cascade in plasma and normal colonic mucosa were determined at 44 weeks. RESULTS: GSH attenuated the number of ACF increased by beef tallow, but GSH had no influence on expression of beta-catenin increased by AOM. Incidence of colon cancer was no different with or without GSH, but GSH attenuated the number of colon cancers in each rat. GSH suppressed plasma malondialdehyde concentration. GSH increased GSH concentration and activities of catalase, glutathione peroxidase and superoxide dismutase in colonic mucosa, and decreased cyclooxygenase-2, prostaglandin E2 and thromboxane B2 levels. CONCLUSIONS: This study indicated that GSH suppressed the number of ACF, but the attenuation of colon carcinogenesis was limited to the number of colon cancers, although anti-oxidative effects and suppressive effects of arachidonic acid cascade were demonstrated by several indexes. These results suggested that colon carcinogenesis enhanced by beef tallow was partly caused by oxidative stress and arachidonic acid cascade, which were reduced by GSH.

Long-term feeding of various fat diets modulates azoxymethane-induced colon carcinogenesis through Wnt/beta-catenin signaling in rats.

The Wnt signaling pathway plays an essential role in carcinogenesis, and the amount of fat intake and composition of dietary fatty acids are crucial factors for colon carcinogenesis. We investigated whether various dietary fats affected the Wnt signaling pathway of colon tumorigenesis in azoxymethane (AOM)-treated rats. Male Sprague-Dawley rats were given intraperitoneal injections of AOM and supplemented with 10% corn, olive, beef, and fish oil for 44 wk. Aberrant crypt foci (ACF) and tumors were examined at 12 and 44 wk. Normal appearing colon mucosal proliferation and apoptosis were evaluated by 5-bromo-2'-deoxyuridine (BrdU) incorporation and percentages of fragmented DNA, respectively. Expressions of beta-catenin, cyclin D(1), Wnt2, Wnt3, and Wnt5a of normal appearing colon mucosa were analyzed by Western blot analysis. Long-term dietary corn oil and beef tallow increased ACF, tumor incidence, and tumor numbers in AOM-treated rats. In contrast, both olive and fish oil inhibited them. Dietary corn oil and beef tallow increased BrdU incorporation and the expression of cytosolic beta-catenin and cyclin D(1) and decreased apoptosis in the colon mucosa. Expressions of Wnt2 and Wnt3 in rats fed with beef tallow and Wnt5a in rats fed with corn oil increased with or without AOM-treatment. BrdU-incorporated cells were often observed at the tops of crypts in rats fed with beef tallow, whereas this was not observed in rats fed with the other diet. Long-term high intake of corn oil and beef tallow enhanced cell proliferation through Wnt signaling and modulated the distribution of proliferating cells, which might contribute to promoting effects in colon tumorigenesis.

Adipocytes and preadipocytes promote the proliferation of colon cancer cells in vitro.

Obesity, a risk factor for colon cancer, is associated with elevated serum levels of leptin, a protein produced by adipocytes. The aim of the present study was to clarify the effects of adipose tissue on colon cancer proliferation by using cultured cell lines. To achieve this, colon cancer cells (CACO-2, T84, and HT29) were cocultured with adipose tissue, isolated mature adipocytes, and isolated preadipocytes in a three-dimensional collagen gel culture system. The adipocytes and preadipocytes used were isolated from C57BL/6J and leptin-deficient ob/ob mice. Proliferation of the cancer cells was evaluated by nuclear bromodeoxyuridine uptake. The adipose tissue, mature adipocytes, and preadipocytes isolated from C57BL/6J mice significantly increased the proliferation of the colon cancer cells. This trophic effect of mature adipocytes on the cancer cell lines was observed only for cells from lean littermates and not for those from ob/ob mice. In contrast, the trophic effect of preadipocytes was not abolished in ob/ob mice, and this finding was supported by the result that leptin had a trophic effect on cancer cells. In conclusion, adipocytes were able to enhance the proliferation of colon cancer cells in vitro, partly via leptin, suggesting that adipose tissues, including mature adipocytes and preadipocytes, may promote the growth of colorectal cancer.

Differentiation of gastric surface mucous cells (GSM06) induced by air-liquid interface is regulated partly through mitogen-activated protein kinase pathway.

BACKGROUND AND AIM: The aim of the present study was to examine the role of mitogen-activated protein (MAP) kinase pathway on gastric surface epithelium using an established cell culture model in which differentiation is promoted in GSM06 cells by air-liquid interface. METHODS: A double-dish culture system of mouse gastric surface mucous cell line GSM06 in Ham's F12 medium supplemented with 10% fetal calf serum and 50 microg/mL gentamicin at 37 degrees C in a humidified atmosphere of 5% CO(2) in air was used for an air-liquid interface. Culture cells were examined on histology, cell proliferation was evaluated by bromodeoxy-uridine (BrdU) uptake, and western blot analysis of extracellular signal-regulated kinase (ERK)1/2 and phosphate ERK1/2. On day 3, U0126, an inhibitor of MAP kinase kinase (MEK), was added to medium of incubated cells. RESULTS: GSM06 cells were differentiated with an air-liquid interface for 3 weeks. Compared to immersion control culture, phosphorylated ERK 1/2 expression increased significantly. This increase was completely suppressed with U0126, and tall columnar cells developed by air-liquid interface in GSM06 were not observed in U0126-treated cells. Increase in BrdU uptake with air-liquid interface was suppressed by U0126. CONCLUSION: These results suggested that MAP kinase signaling, activated by air-liquid interface, was, at least in part, related to cell differentiation in GSM06 cells induced by air-liquid interface.

Apoptotic pathway in the rat small intestinal mucosa is different between fasting and ischemia-reperfusion.

We have previously demonstrated that fasting and ischemia-reperfusion (I/R) induced apoptosis in rat intestinal mucosa. It is widely accepted that apoptosis is induced through two main pathways. This study aimed to compare apoptotic pathways following fasting and I/R. Rats were divided into two groups: the I/R group involved occlusion of the superior mesenteric artery for 60 min, followed by 60-min reperfusion, whereas the fasting group involved fasting for 24 or 48 h. Intestinal apoptosis was assessed as percentage of fragmented DNA, by electrophoresis and by a terminal deoxynucleotidyl transferase mediated dUDP-biotin nick- end labeling (TUNEL) assay. Apoptotic proteins including death ligands/receptors and caspases were evaluated by Western blot analysis. Small intestinal mucosal height and mitochondrial dehydrogenase function were assessed. Fasting and I/R significantly induced intestinal apoptosis. Mucosal height was significantly decreased in fasting rats, and mitochondrial dysfunction was induced only by I/R. Expressions of Fas, Fas ligand, and TNF-alpha type 1 receptor were enhanced in fasting and I/R rats. After I/R, expressions of cytochrome c and cleaved caspase-9 were significantly increased. In contrast, expressions of cleaved caspase-8 and cleaved caspase-3 increased in fasting rats. Fasting promoted mucosal apoptosis via a receptor-mediated type I apoptotic pathway in the rat small intestine, and I/R induced apoptosis via a mitochondria-mediated type II pathway.