Cholinesterase Activities in Uterus of Normal and Fenchlorphos Treated Blue Foxes (Alopex Lagopus) during Various Reproductive States

The uterine acetylcholinesterase and total cholinesterase (acetylcholinesterase plus butyrylcholinesterase) activities in normal and fenchlorphos treated blue fox vixens were determined during various reproductive states. AChE and Total-ChE of non-medicated vixens in oestrus were about one half of those in anoestrus. In pregnant uteri (luteal phase) the activities were 25 % and 30% compared to anoestrus. In vixens given 100 mg/kg fenchlorphos for 3 weeks during anoestrus, the remaining activity of AChE in uterus were in average 37%. Pregnant and non-pregnant vixens in the luteal phase medicated prior to mating and during time of implantation, displayed AChE activities which were only moderabely reduced (remaining activities 83% and 72% compared to medicated animals in anoestrus: remaining activity 37%). Plasma ChE-activity increased during pregnancy in the controls while enzyme activity was strongly reduced in animals given 100 mg/kg fenchlorphos daily through the whole pregnancy. It was concluded that the previous reported embryotoxic effect of fenchlorphos in the blue fox did not seem to be directed towards the moderate inhibition of the uterine cholinesterases.     

Ovarian and Testicular Function in the Blue Fox (Alopex Lagopus) after Oral Administration of Fenchlorphos During the Breeding Season

The possible effect of fenchlorphos, 0-0-dimethy1-0-(2.4.5-trichlorophenyl) phosphorothioate, upon the reproductive endocrinology in blue foxes (Alopex lagopus) was investigated. Five females were administered fenchlorphos orally at a dose of 100 mg/kg daily from 10 days before oestrus and up to the 21st day of gestation. This dose represents the therapeutic dose for the treatment of sarcoptic mange. Blood samples were collected for the analyses of progesterone, oestradiol-17β and luteinizing hormone (LH) in plasma. The vixens were ovario-hysterectomized on day 23, except 1 animal in the control group which was operated on day 17. Additionally, sperm quality and mating performance in 3 male blue foxes, which were administered 100 mg/kg fenchlorphos daily during the first 3 weeks of the mating season, were examined. Pregnancy was recorded in 2 medicated and 4 control animals. No pathological changes were observed in the uterus and the ovaries. The plasma concentrations of the hormones were similar to those obtained from the control group. No evidence of any disturbances concerning spermatogenesis in the males was observed. However, their libido appeared to be reduced. None of the males achieved a mating during and after the period of medication.     

Toxic and Carcinogenic Effects of Dimethylnitrosamine (Dmna) in the Blue Fox (Alopex Lagopus)

Single doses of DMNA from 8 to 15 mg/kg body weight (B.W.) were given in the feed, by stomach tube or by subcutaneous application to 37 foxes. The course and intensity of the disease was not influenced by the application route, but was directly related to the amount of DMNA given per kg body weight, and caused hemorrhagic centrolobular liver necrosis and acute vessel changes especially in the hepatic vein system. The possibility of liver regeneration after a single DMNA exposure depends on the degree of damage in the hepatic vein system. Some animals can recover from the acute disease caused by DMNA. But if the hepatic vessel changes are enough pronounced, progressive changes occur in the hepatic vein system eading to liver cirrhosis. The observation period of the foxes after a single exposure was from 13 to 380 days. LD50 should not be determined after a surviving time of 3 days but rather after 4 weeks. In our material LD50 was 10 mg DMNA/kg B.W. In an experiment over a longer period of time 18 foxes divided into 3 groups were given 2 weekly doses of DMNA in food. They were treated with daily estimated doses of 1.0, 0.2 and 0.1 mg DMNA/kg B.W., respectively. The foxes in Groups 1 and 2 developed ascites, jaundice and liver failure after intake of 45–70 mg DMNA/kg B.W. The foxes in Group 1 treated with 1 mg DMNA/kg B.W. showed centrolobular hemorrhagic liver necrosis and productive vessel changes in the hepatic vein system. The second group given 0.2 mg DMNA/kg B.W. developed hemorrhagic centrolobular necrosis which healed with fibrosis leading to cirrhosis and chronic occlusion in many of the hepatic veins. In addition noduli of chondroid lamellae and foci of hematopoietic tissue and early stages of hemagiomatous liver tumors were found in the liver. The group exposed with 0.1 mg DMNA/kg B.W./day did not develop hemorrhagic centrolobular liver necrosis, but thickening in the walls of the hepatic veins. After more than 3½ years of exposure multiple hemangiosarcomae were growing out from the changed vessel walls. In an experiment over a shorter time period with daily exposure of DMNA doses in the feed below 0.15 mg/kg B.W., all the foxes were completely healthy and only some showed beginning changes in the hepatic vein walls. Hematomae were often seen in foxes dying after a single DMNA dose. One fox treated with 0.1 mg DMNA/kg B.W. died of brain bleeding after 220 days of treatment. Chronic vessel changes were found in the heart and kidneys of the DMNA treated foxes. These results emphasize the fact that DMNA gives vessel changes of a more general nature.     

Metrifonate and dichlorvos: Effects of a single oral administration on cholinesterase activity in rat brain and blood

Cholinesterase activities in rat forebrain, erythrocytes, and plasma were assessed after a single oral administration of metrifonate or dichlorvos. In 3-month-old rats, the dichlorvos (10 mg/kg p.o.)-induced inhibition of cholinesterase reached its peak in brain after 15–45 min and after 10–30 min in erythrocytes and plasma. Cholinesterase activity recovered rapidly after the peak of inhibition, but did not reach control values in brain and erythrocytes within 24 h after drug administration. The recovery of plasma cholinesterase activity, in contrast, was already complete 12 h after dichlorvos treatment. Metrifonate (100 mg/kg p.o.) had qualitatively similar inhibition kinetics as dichlorvos, albeit with a slightly delayed onset. Peak values were attained 45–60 min (brain) and 20–45 min (blood), after drug administration. Apparently complete recovery of cholinesterase activity was noted in both tissues 24 h after treatment. The dose-dependence of drug-induced inhibition of cholinesterase in rat blood and brain was determined at the time of maximal inhibition, i.e., 30 min after dichlorvos treatment and 45 min after metrifonate treatment. The oral ED₅₀ values obtained for dichlorvos were 8 mg/kg for brain and 6 mg/kg for both erythrocyte and plasma cholinesterase. The corresponding oral ED₅₀ values for metrifonate were 10 to 15 times higher, i.e., 90 mg/kg in brain and 80 mg/kg in erythrocytes and plasma. In rats deprived of food for 18 h before drug treatment, the corresponding ED₅₀ values for metrifonate were 60 and 45 mg/kg, respectively, indicating an about two-fold higher sensitivity of fasted rats to metrifonate-induced cholinesterase inhibition compared to non-fasted rats. Compared to 3-month-old rats, 19-month-old rats showed a higher sensitivity towards metrifonate and dichlorvos. At the time of maximal inhibition, there was a strong correlation between the degree of cholinesterase inhibition in brain and blood. These results demonstrate that single oral administration of metrifonate and dichlorvos induces an inhibition of blood and brain cholinesterase in the conscious rat in a dose-dependent and apparently fully reversible manner. While the efficiency of a given dose of inhibitor may vary with the satiety status or age of the animal, the extent of brain ChE inhibition can be estimated from the level of blood ChE activity.     

Developmental toxicity of orally administered technical dimethoate in rats

BACKGROUND: Dimethoate (O,O-dimethyl-S-(N-methylcarbamoyl-methyl) phosphorodithioate), an organophosphate insecticide, was examined for its potential to produce developmental toxicity in rats after oral administration. METHODS: Pregnant Fischer 344 rats were given sublethal doses of 0 (corn oil), 7, 15, and 28 mg/kg/day dimethoate by gavage on gestation days (GD) 6-15. Maternal effects in 15 and 28 mg/kg/day dose groups included cholinergic signs such as tremors, diarrhea, weakness, and salivation, and depression in the maternal and fetal brain acetylcholinesterase (AChE) activities. Other maternal toxicity that included reduction in body weight and feed consumption was observed only in the treated group of 28 mg/kg/day. No maternal toxicity was apparent in the 7 mg/kg/day dose group. RESULTS: Maternal exposure to dimethoate during organogenesis significantly affected the number of live fetuses, early resorption, and mean fetal weight in the 28 mg/kg/day dose group. No external, visceral, and skeletal abnormalities were observed in any of the treated groups compared to the control. CONCLUSIONS: On the basis of the present results dimethoate can produce clinical signs of toxicity and significant inhibition of the maternal and fetal AChE activities in dose groups of 15 and 28 mg/kg/day and showed fetotoxicity without teratogenic effects at 28 mg/kg/day.     

Effects of Subchronic Administration of Metrifonate on Cholinergic Neurotransmission in Rats

The effects of subchronic oral administration of metrifonate, a long-acting cholinesterase (ChE) inhibitor, on cholinergic neurotransmission were assessed in young adult male Wistar rats. Animals were treated twice daily with metrifonate. In a pilot study testing a 100 mg/kg dose of metrifonate for up to 14 days, ChE activity was found to steadily decrease to reach maximum inhibition levels of about 55%, 80% and 35% in brain, erythrocytes and plasma. Steady-state inhibition levels were attained by the 10th day of treatment. When metrifonate-treatment was discontinued, ChE activity in plasma returned to control levels within another day, while erythrocyte and brain ChE activity took more than 2 weeks to recover. In subsequent dose-response studies, metrifonate treatment was given for 3 and 4.5 weeks at doses of 0, 12.5, 25, 50, and 100 mg/kg, to different groups of animals, respectively. Correlation analysis indicted that brain ChE inhibition was more accurately reflected by erythrocyte than by plasma ChE inhibition, although all effects were highly correlated. The changes in ChE activity were not paralleled by changes in other parameters of the cholinergic neurotransmission, such as acetylcholine synthesis rate or acetylcholine receptor binding. It is therefore concluded that repeated administration of metrifonate to rats induces a long-lasting inhibition of ChE activity in a dose-related and predictable manner, which is neither subject to desensitization nor paralleled by counterregulatory downregulation of muscarinic or nicotinic receptor binding sites in brain.     

Anticholinesterase effect and toxicity of bis(trichloromethyl) sulfone (N-1386 Biocide) in rats

The oral LD50 for bis(trichloromethyl) sulfone (N-1386 Biocide) in male rats was 691 mg/kg. Deaths occurred 1-5 days after treatment and signs of toxicity suggestive of an anticholinesterase effect were noted. However, neither plasma cholinesterase nor brain acetylcholinesterase was inhibited 2, 4 or 24 hours after a single, oral dose of 500 mg/kg. Atropine (300 mg/kg, s.c.) or scopolamine (670 mg/kg, s.c.) pretreatments did not protect against the acute lethality of bis(trichloromethyl) sulfone although signs of toxicity were alleviated by both pretreatments. Bis(trichloromethyl) sulfone produced in vitro inhibition of rat plasma cholinesterase and brain acetylcholinesterase. The inhibition was competitive in brain. IC50's for these 2 enzymes were 8 microM in plasma and 25 microM in brain. In summary, bis(trichloromethyl) sulfone produced in vitro cholinesterase inhibition not demonstrated in vivo. Doses of anticholinergic compounds that ameliorated many toxic signs did not protect against lethality produced by bis(trichloromethyl) sulfone.     

Comparative nutrient digestibility of arctic foxes (Alopex lagopus) on Svalbard and farm-raised blue foxes (Alopex lagopus)

Arctic foxes from Svalbard (n=4) and farmed blue foxes (n=4) was used in a digestibility experiment with a high-carbohydrate feed to add more information to the nutritional physiology of the arctic fox, and to compare its digestive capacity with that of the farmed blue fox. The arctic fox has a diet containing mainly protein and fat from mammals and birds, while farmed blue foxes have been exposed to an omnivorous dietary regime for more than 80 generations. The experiment showed in general no difference in digestive capacity for protein and fat between the foxes (P>0.05), but for carbohydrates, including starch and glucose, the blue fox revealed higher digestibility values. The superior digestive capacity for carbohydrates in blue fox might be a result of a long-term selection of animals digesting dietary carbohydrates more efficiently, or that an early age exposition to dietary carbohydrates has given permanent improvement of the carbohydrate digestion in the gut.     

Adiponectin and peptide YY in the fasting blue fox (Alopex lagopus)

Adiponectin (Acrp30) and peptide YY (PYY) are weight-regulatory hormones participating in the control of energy homeostasis. This study investigated the effects of long-term wintertime fasting on plasma Acrp30 and PYY levels in the carnivorous blue fox, a farm-bred variant of the arctic fox (Alopex lagopus). Plasma Acrp30 and PYY concentrations were determined with radioimmunoassays during a 22-day period of fasting, which led to a 20.3% reduction in body mass of the animals (n=32). Sixteen fed blue foxes served as the control group. Acrp30 and PYY were present in blue fox plasma at similar or lower levels as reported previously for other mammals. Fasting had no acute effects on Acrp30 or PYY concentrations of the blue foxes. However, the Acrp30 levels of the fasted blue foxes were 24%-48% higher than in the fed animals between days 8-22 of fasting. Fasted blue foxes also had 6.2-fold higher plasma PYY concentrations after 15 days of fasting. Acrp30 and PYY seem to play roles in the body weight-regulation of the blue fox during long-term fasting, but their specific functions and physiological significance remain to be determined.     

Endocrinological and behavioural effects of p-chlorophenylalanine (PCPA) oral administration to broody turkey hens (Meleagris gallopavo)

Changes in plasma levels of prolactin and LH, feed intake, water consumption, behavioural pattern and ovarian activity were recorded after oral administration of PCPA to broody turkey hens. A decrease in prolactin concentration was measured, from day 3, in 3 out of the 5 birds treated with 100 mg PCPA/kg body weight (BW) for 3 consecutive days. In these hens, broodiness was disrupted on day 6 and feeding activity subsequently increased to levels of photorefractory hens. Neither LH concentrations nor ovarian activity were affected after treatment with PCPA. Moreover, PCPA treatment was ineffective at a 50 mg/kg BW dose. These results confirm that a serotoninergic mechanism is probably involved in prolactin release and moreover suggest that prolactin is implicated in maintaining broody behaviour. However, the reductions in the plasma concentration of prolactin induced by PCPA were not sufficient to restore the hypothalamic-hypophyseal-ovarian axis to a physiological status characteristic of the laying hen. Therefore, PCPA does not appear to be a useful method of treating broodiness in commercial turkey hens.     

Evaluation of developmental toxicity induced by anticholinesterase insecticide,diazinon in female rats

Developmental toxicities, including birth defects, are significant public health problems. This study was planned to assess the cholinergic and developmental potentials of diazinon that is widely used as an organophosphate insecticide. Pregnant female Sprague‐Dawley rats were given diazinon orally at doses of 0, 1.9, 3.8, and 7.6 mg/kg body weight (b.w.)/day on gestation days 6 to 15. Maternal brain acetylcholinesterase activities, measured on gestation day20, were significantly decreased at 3.8 and 7.6 mg/kg b.w./day, but fetal acetylcholinesterase activity was not altered. Maternal toxicities, as evidenced by cholinergic symptoms including diarrhea, tremors, weakness, salivation, and decreased activities, were observed at the 3.8 and 7.6 mg/kg b.w./day dose groups. Net gravid uterine weight was decreased at a dose of 7.6 mg/kg b.w./day. No maternal effects were apparent in the 1.9 mg/kg b.w./day dose group. Maternal toxicity at a dose of 3.8 mg/kg b.w./day did not induce fetotoxicity or teratogeneicity. However, 7.6 mg/kg b.w./day doses significantly resulted in fetal toxicity and malformations in addition to maternal toxicity in animals. In conclusion, teratogenic disorders only outlined by doses that produced marked maternal toxicity. Since the malformations were not morphologically related, they were considered to be secondary to maternal toxicity; hence, the malformations were not related to cholinesterase inhibition. Birth Defects Res (Part B) 92:534–542, 2011. © 2011 Wiley Periodicals, Inc.     

Clinical Picture and Antibody Response to Experimental Sarcoptes scabiei var. vulpes Infection in Red Foxes (Vulpes vulpes)

Three red foxes (Vulpes vulpes) were experimentally infected with Sarcoptes scabiei isolated from a naturally infected wild red fox. A fourth red fox served as a control. The first signs of sarcoptic mange became evident on the 31st day post infection (dpi). The signs gradually increased thereafter and between dpi 49 and 77 characteristic lesions of hyperkeratosis developed. Two of the infected foxes developed severe sarcoptic mange, and one of these animals died on dpi 121. The third fox developed a chronic hyperkeratotic lesion on its back, at the site where the mites had been applied. On dpi 127 the surviving foxes were treated systemically with ivermectin, and within 4 weeks the skin lesions had healed except on the pinnae of one animal. Antibodies to S. scabiei var. vulpes were demonstrated in the infected foxes by an ELISA with which seroconversion was seen around 4 weeks post infection (wpi). Western blot analysis of sequential sera of the infected animals demonstrated antibody activity consistently after the 2nd wpi. The fourth, non-infected, fox did not show any skin lesions throughout the experimental period nor any specific antibodies to S. scabiei var. vulpes. kw|Keywords|k]sarcoptic mange; k]red fox; k]serodiagnosis; k]ELISA     

Mercury in wild terrestrial carnivorous mammals from north-western Poland and unusual fish diet of red fox

Total mercury concentrations were determined in the kidney (K), liver (L), and pectoral muscle (M) of 19 individuals representing wild carnivorous mammals from NW Poland: 10 red foxes Vulpes vulpes (Linnaeus, 1758), 3 raccoon dogs Nyctereutes procyonoides Gray, 1834, 2 badgers Meles meles Linnaeus, 1758, 3 pine martens Martes martes Linnaeus, 1758, and 1 polecat Mustela putorius Linnaeus, 1758. The sample of red fox included 3 immature specimens found on Mielin Island; the island supports a black cormorant colony, and the foxes found there had fed mostly on cormorant nestlings as well as on fish and their remains. In addition to the Mielin Island foxes, the group of foxes included 3 other immature and 4 adult individuals. The highest mean of mercury concentrations were revealed in the Mielin red fox juveniles: 5.11, 4.52, and 1.56 mg/kg d.w. being recorded in K, L, and M. No significant differences in mercury concentrations in the respective tissues were found between the remaining immature and adult red foxes; their mercury concentrations were several times lower than those of the Mielin individuals. In all the animals except the Mielin foxes, mercury concentrations in K, L, and M did not exceed 1.3, 1.0 and 0.5 mg/kg d.w., respectively, the highest values being in badgers (which feed mostly on soil invertebrates), followed by pine martens and then the canids (red fox and raccoon dog). Studies on common and widely distributed terrestrial animals, particularly red fox and badger, may provide numerous valuable comparative data on mercury contamination of different areas of the northern hemisphere.     

杜仲绿原酸对高脂小鼠血液流变学作用研究

旨以研究杜仲绿原酸对高脂高胆固醇诱导的高血脂模型小鼠血液流变学的影响,以昆明小鼠为实验动物,随机分成5组:阴性对照组,模型对照组和低剂量(25 mg/kg BW)、中剂量(50 mg/kg BW)、高剂量(100 mg/kg BW)杜仲绿原酸组,每组10只.后4组饲以高脂饲粮,同时小鼠灌胃杜仲绿原酸4周,实验结束,分别测定各组小鼠血液流变学参数、血清和肝脏的抗氧化酶活性和脂质过氧化产物MDA含量及其总抗氧化能力和羟自由基清除率.高脂血症小鼠的全血粘度、血浆粘度、红细胞压积、血沉、纤维蛋白原、红细胞刚性指数和聚集指数显著降低(P＜0.05),红细胞变形指数显著提高(P＜0.05),小鼠血清和肝脏SOD、GSH-Px水平、总抗氧化能力和羟自由基清除能力均显著升高(P＜0.05),MDA水平显著降低(P＜0.05).在高脂膳食条件下,杜仲绿原酸能有效提高血液的抗氧化防御功能(包括抗氧化力、抗氧化酶活性)、改变血液流变学参数等,降低血液粘度、红细胞刚性和聚集,增强变形能力,使细胞膜的流动性增高,其中以中剂量效果相对较好.     

Physiological adaptations to fasting in an actively wintering canid, the Arctic blue fox (Alopex lagopus)

This study investigated the physiological adaptations to fasting using the farmed blue fox (Alopex lagopus) as a model for the endangered wild arctic fox. Sixteen blue foxes were fed throughout the winter and 32 blue foxes were fasted for 22 d in Nov-Dec 2002. Half of the fasted blue foxes were food-deprived again for 22 d in Jan-Feb 2003. The farmed blue fox lost weight at a slower rate (0.97-1.02% body mass d(-1)) than observed previously in the arctic fox, possibly due to its higher initial body fat content. The animals experienced occasional fasting-induced hypoglycaemia, but their locomotor activity was not affected. The plasma triacylglycerol and glycerol concentrations were elevated during phase II of fasting indicating stimulated lipolysis, probably induced by the high growth hormone concentrations. The total cholesterol, HDL- and LDL-cholesterol, urea, uric acid and total protein levels and the urea:creatinine ratio decreased during fasting. Although the plasma levels of some essential amino acids increased, the blue foxes did not enter phase III of starvation characterized by stimulated proteolysis during either of the 22-d fasting procedures. Instead of excessive protein catabolism, it is liver dysfunction, indicated by the increased plasma bilirubin levels and alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase activities, that may limit the duration of fasting in the species.     

Effect of lorglumide (CR-1409) on pancreatic secretory and trophic response to caerulein in newborn rats.

The authors investigated whether lorglumide a specific CCK-receptor antagonist affects the pancreatic actions of caerulein in female newborn Wistar rats. Pancreatic secretory response (expressed as the decrease in specific trypsin activity in the pancreas) was studied in 11-day-old rats following acute administration of saline (control), caerulein (0.3, 1, or 3 micrograms/kg s.c.) either without or with lorglumide (10 mg/kg s.c.). Lorglumide was given 15 min before caerulein. In chronic studies rats were treated 3x/day for 10 days from the day of birth (Day 1) with caerulein and lorglumide as above. On Day 11 the rats were decapitated and exsanguinated, their pancreas removed and analyzed. Acute administration of caerulein induced a dose-dependent depletion of specific trypsin activity from the pancreas and this was antagonized by lorglumide. Chronic treatment with each dose of the peptide increased total pancreatic trypsin content. Besides, the 3 micrograms/kg dose caused to increase pancreatic protein, DNA, and amylase content and to increase plasma corticosterone level. Chronic administration of lorglumide did not influence normal pancreatic growth, while it strongly inhibited the increase in trypsin content evoked by caerulein. However, lorglumide, given alone or in combination with caerulein, induced a significant increase in pancreatic amylase content without affecting plasma corticosterone level.     

Incorporation of intravenously administered urea-15N into sheep plasma proteins and their amide groups.

Two sheep with a low and high nitrogen intake (7.6 and 24 g N/day respectively) were given a single intravenous dose of 15N-labelled urea (15.3 mg 15N/kg b.w.) The findings were as follows. The greater part of non-retained 15N from the administered dose was excreted during the first day after the intravenous administration of 15N-urea. Daily excretion in the faeces amounted to 1.35-2.37% of the 15N in the given dose. With a low N intake, more 15N from the given dose (59.4%) was retained in the N pool than with a high N intake (50.5%). The net passage of 15N into the rumen and 15N incorporation into the amide-N of the plasma proteins was likewise greater. 15N incorporation into the amide-N of the plasma proteins rose steadily for 3 days. The porportion of amidic 15N in the plasma proteins rose steadily for 3 days. The proportion of amidic 15N in the plasma protein total 15N changed on the second and third day after administering 15N-urea from 8% to 16%, with the maximum at the beginning of the second day. The amount of 15N incorporated into the proteins in 1 litre plasma attained up to 3% of the given dose. It is concluded from the results that the synthesis of amino acids and their amide groups is both a quantitatively and a qualitatively important metabolic route for the reutilization of blood urea nitrogen for protein synthesis in ruminants.     

Teratogenicity and Embryotoxicity of Orally Administered Fenchlorphos in Blue Foxes

Pregnant blue foxes (Alopex lagopus) were administered fenchlorphos (0-0-dimethyl-0-(2,4,5-trichlorophenyl) phos-phorothioate) orally at a dose of 100 mg/kg/day in different periods of gestation. The dose chosen represents the therapeutic dose for the treatment of parasitic lesions. At term the mean number of whelps were recorded, and they were killed and examined for external, visceral and skeletal malformations. Of 19 medicated vixens the mean number of live whelps at term was 1.2 per vixen versus 9.5 in the control group. There was an evident predominance of males in the medicated groups. Several malformations of the head were registered, among them incomplete ossification of the skull bones, cleft palate, hydrocephalus internus and externus. Minor malformations like extra ribs or missing ribs occurred in the medicated groups. Congenital alopecia, hypoplastic kidneys, and hydronephrosis were observed in all the whelps in 1 medicated group. No significant difference in total brain weight, cerebellum weight or the cerebellum-to-total-brain weight was observed. Histological examination of the cerebellum showed a narrowing or absence of the granular and the molecular layers of the cortical zone.     

Effects of juice from Morinda citrifolia (Noni) on gastric emptying in male rats

The effects of juice from Morinda citrifolia (noni) on gastric emptying, gastrointestinal transit, and plasma level of cholecystokinin (CCK) in rats were studied. Male rats were given noni by gavage at levels of 0.25, 1, or 4 ml/kg once per day for one or 7 days. The rats in the control group were given water, while the rats in the experimental group were fasted overnight before measurement of gastrointestinal motility. Gastrointestinal motility was assessed in rats 15 min after intragastric instillation of a test meal containing charcoal (10%) and Na251CrO4 (0.5 microCi/ml). Gastric emptying was determined by measuring the amount of radiolabeled chromium contained in the small intestine as a percentage of the initial amount received. Then, gastrointestinal transit was evaluated by calculating the geometric center of distribution of the radiolabeled marker. Finally, blood samples were collected for measurement of CCK by radioimmunoassay. The administration of noni at 0.25 ml/kg, but not at 1 ml/kg and 4 ml/kg, for 1 day significantly inhibited gastric emptying. In contrast, gastric emptying was significantly inhibited by oral noni (0.25, 1, or 4 ml/kg) for 7 days. Intraperitoneal injection of lorglumide (5 or 10 mg/kg), a selective CCK1 receptor antagonist, effectively attenuated the noni-induced inhibition of gastric emptying. The intestinal transit and body weight, food intake, water intake, urine volume as well as feces weight were not altered by the administration of noni either acutely or chronically, but the administration of oral noni (1 ml/kg) for 7 days increased the level of plasma CCK in male rats. These results suggest that oral noni inhibits gastric emptying in male rats via a mechanism involving stimulation of CCK secretion and CCK1 receptor activation.     

Diet of arctic foxes (Alopex lagopus) in Iceland

Arctic foxes, Alopex lagopus , live in low productivity arctic and northern tundra habitats, where they generally prey heavily on lemmings. In Iceland, however, no lemmings are present, and the foxes have a very varied diet, including plants such as seaweed and black crowberries, a wide range of birds and invertebrates, and carcasses of large mammals such as seals, reindeer, and sheep. Marked seasonal, geographical and inter-annual differences confirm arctic foxes in Iceland as opportunistic feeders. There are coastal and inland foxes: coastal foxes feed mainly on prey derived directly or indirectly from the ocean, particularly various seabirds and seals, while inland foxes feed largely on migrant birds, such as geese, waders and passerines in summer, and ptarmigan in winter. Despite their reputation for killing lambs, in this study, lamb carcasses were found at only 19.4% of 1125 fox dens, 44% of which had only one carcass. The distance to the nearest farm and the physical condition of lambs were major determinants of the number of carcasses found at a den. We discuss the implications of arctic foxes' diet for population dynamics and group formation, and for management practices.