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This study evaluated the hypothesis that untreated and irradiated grapefruit as well as the isolated citrus compounds naringin and limonin would protect against azoxymethane (AOM)-induced aberrant crypt foci (ACF) by suppressing proliferation and elevating apoptosis through anti-inflammatory activities. Male Sprague-Dawley rats (n = 100) were provided one of five diets: control (without added grapefruit components), untreated or irradiated (300 Gy, 137Cs) grapefruit pulp powder (13.7 g/kg), naringin (200 mg/kg) or limonin (200 mg/kg). Rats were injected with saline or AOM (15 mg/kg) during the third and fourth week and colons were resected (6 weeks post second injection) for evaluation of ACF, proliferation, apoptosis, and cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein levels. Experimental diets had no effect on the variables measured in saline-injected rats. However, in AOM-injected rats, the experimental diets suppressed (P < or = 0.02) aberrant crypt and high multiplicity ACF (HMACF; P < or = 0.01) formation and the proliferative index (P < or = 0.02) compared with the control diet. Only untreated grapefruit and limonin suppressed (P < or = 0.04) HMACF/cm and expansion (P < or = 0.008) of the proliferative zone that occurred in the AOM-injected rats consuming the control diet. All diets elevated (P < or = 0.05) the apoptotic index in AOM-injected rats, compared with the control diet; however, the greatest enhancement was seen with untreated grapefruit and limonin. Untreated grapefruit and limonin diets suppressed elevation of both iNOS (P < or = 0.003) and COX-2 (P < or = 0.032) levels observed in AOM-injected rats consuming the control diet. Although irradiated grapefruit and naringin suppressed iNOS levels in AOM-injected rats, no effect was observed with respect to COX-2 levels. Thus, lower levels of iNOS and COX-2 are associated with suppression of proliferation and upregulation of apoptosis, which may have contributed to a decrease in the number of HMACF in rats provided with untreated grapefruit and limonin. These results suggest that consumption of grapefruit or limonin may help to suppress colon cancer development.

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org. . Wiley and Nordic Society Oikos are collaborating with JSTOR to digitize, preserve and extend access to Ornis Scandinavica. . 1992. Energy and nutrient use during moult by White-crowned Sparrows Zonotrichia leucophrys gambelii. -Ornis Scand. 23: 304-313.The apparent nutrient and energy costs of moult in Gambel's Sparrows estimated from the materials deposited in the integument are relatively mild compared with the maintenance requirements (5.3% of BMR, and 45% of the minimum maintenance requirement for protein (MMRP)) and with those of reproduction (34% BMR and 165% MMRP), except perhaps for cystine. Measures of the actual costs of moult indicate that processes in addition to plumage synthesis combine to create daily energy costs for peak moult equaling 58% BMR. These processes include (1) recrudescence of the integument, (2) a cyclic osteoporosis, and (3) a large diel cycling in body protein content (as much as 8%). The main adjustments in nutritional requirements during moult are greater needs for protein to supply substrate and for energy. Also, the needs for iron for erythrocyte production (item 1 above) and for calcium for bone formation (item 2 above) presumably increase. Analyses of several food groups reveal that the energy and essential amino acid (EAA) needs for moult can likely be met by a wide variety of food types. When the total daily EAA needs of moulting birds are taken together the profile of the EAA demands is realigned so that the disproportionately high demand for cystine for keratin synthesis is obscured. Consequently, dietary protein can be used more efficiently for whole-body protein synthesis.

We have shown that a combination of fish oil (high in n-3 fatty acids) with the butyrate-producing fiber pectin, upregulates apoptosis in colon cells exposed to the carcinogen azoxymethane, protecting against colon tumor development. We now hypothesize that n-3 fatty acids prime the colonocytes such that butyrate can initiate apoptosis. To test this, 30 Sprague-Dawley rats were provided with diets differing in the fatty acid composition (corn oil, fish oil or a purified fatty acid ethyl ester diet). Intact colon crypts were exposed ex vivo to butyrate, and analyzed for reactive oxygen species (ROS), mitochondrial membrane potential (MMP), translocation of cytochrome C to the cytosol, and caspase-3 activity (early events in apoptosis). The fatty acid composition of the three major mitochondrial phospholipids was also determined, and an unsaturation index calculated. The unsaturation index in cardiolipin was correlated with ROS levels (R = 0.99; P = 0.02). When colon crypts from fish oil and FAEE-fed rats were exposed to butyrate, MMP decreased (P = 0.041); and translocation of cytochrome C to the cytosol (P = 0.037) and caspase-3 activation increased (P = 0.032). The data suggest that fish oil may prime the colonocytes for butyrate-induced apoptosis by enhancing the unsaturation of mitochondrial phospholipids, especially cardiolipin, resulting in an increase in ROS and initiating apoptotic cascade.

It has often been alleged that avian molt can be interrupted or delayed by food deprivation or malnutrition. We examined this experimentally in captive White-crowned Sparrows (Zonotrichia leucophrys gambelii). Beginning either at the natural onset of postnuptial molt or 1 month before its onset, groups of birds were fed either inadequate amounts of a balanced diet (60 or 80% of the ad libitum intake of a control group) or unlimited amounts of a diet deficient only in cyst(e)ine and methionine. Except in the 60% premolt group, the malnourished birds did not postpone or interrupt molt in spite of losses ranging from 20 to 38% of initial body mass. Molt was significantly protracted in all except the 60% premolt group as a result of both increased shedding interval and decreased feather growth rates. Their new plumage weighed less than that of control birds, and their remiges were slightly shorter and often deformed or achromatic. The occurrence of fault bars corresponded to the times when the birds were handled, but was not correlated with other plumage defects. Surviving birds of the 60% premolt group did not molt until allowed to feed ad libitum, but then produced a normal plumage in about two-thirds of the time required by the controls. To summarize, molt is a very conservative aspect of self maintenance that is distorted only by planes of malnutrition that free-living sparrows either do not encounter during the summer or do not survive.

We have shown that dietary fish oil and pectin (FP) protects against radiation-enhanced colon cancer by upregulating apoptosis in colonic mucosa. To investigate the mechanism of action, we provided rats (n = 40) with diets containing the combination of FP or corn oil and cellulose (CC) prior to exposure to 1 Gy, 1 GeV/nucleon Fe-ion. All rats were injected with a colon-specific carcinogen, azoxymethane (AOM; 15 mg/kg), 10 and 17 days after irradiation. Levels of colonocyte apoptosis, prostaglandin E(2) (PGE(2)), PGE(3), microsomal prostaglandin E synthase-2 (mPGES-2), total beta-catenin, nuclear beta-catenin staining (%) and peroxisome proliferator-activated receptor delta (PPARdelta) expression were quantified 31 weeks after the last AOM injection. FP induced a higher (P < 0.01) apoptotic index in both treatment groups, which was associated with suppression (P < 0.05) of antiapoptotic mediators in the cyclooxygenase (COX) pathway (mPGES-2 and PGE(2)) and the Wnt/beta-catenin pathway [total beta-catenin and nuclear beta-catenin staining (%); P < 0.01] compared with the CC diet. Downregulation of COX and Wnt/beta-catenin pathways was associated with a concurrent suppression (P < 0.05) of PPARdelta levels in FP-fed rats. In addition, colonic mucosa from FP animals contained (P < 0.05) a proapoptotic, eicosapentaenoic acid-derived COX metabolite, PGE(3). These results indicate that FP enhances colonocyte apoptosis in AOM-alone and irradiated AOM rats, in part through the suppression of PPARdelta and PGE(2) and elevation of PGE(3). These data suggest that the dietary FP combination may be used as a possible countermeasure to colon carcinogenesis, as apoptosis is enhanced even when colonocytes are exposed to radiation and/or an alkylating agent.

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