Fumonisin B₁ (FB₁) is among the most common contaminants produced by Fusarium spp. fungus from corns and animal feeds. Although FB₁ has been known to cause physical or functional defects of embryos in humans and several animal species such as Syrian hamsters, rabbits, and rodents, little is known about the precise toxicity to the embryos and the underlying mechanisms have not been fully addressed. The present study aimed to investigate its developmental toxicity and potential mechanisms of action on sphingolipid metabolism in Brown Tsaiya Ducks (BTDs) embryos. We examined the effect of various FB₁ dosages (0, 10, 20 and 40 µg/embryo) on BTD embryogenesis 72 h post-incubation. The sphingomyelin content of duck embryos decreased (p < 0.05) in the highest FB₁-treated group (40 µg). Failure of neural tube closure was observed in treated embryos and the expression levels of a neurulation-related gene, sonic hedgehog (Shh) was abnormally decreased. The sphingolipid metabolism-related genes including N-acylsphingosine amidohydrolase 1 (ASAH1), and ceramide synthase 6 (CERS6) expressions were altered in the treated embryos compared to those in the control embryos. Apparently, FB₁ have interfered sphingolipid metabolisms by inhibiting the functions of ceramide synthase and folate transporters. In conclusion, FB₁-caused developmental retardation and abnormalities, such as neural tube defects in Brown Tsaiya Duck embryos, as well as are partly mediated by the disruption of sphingolipid metabolisms.

The present study investigated stocking density and genetic lines, factors that may alter the severity and incidence of angel wing (AW), in White Roman geese. Geese (n = 384) from two genetically selected lines (normal- winged line, NL, and angel-winged line, AL, respectively) and one commercial line (CL) were raised in four pens. Following common commercial practice, low-stocking-density (LD), medium-stocking-density, and high-stocking-density treatments were respectively administered to 24, 32, and 40 geese per pen at 0 to 3 weeks (1.92 m(2)/pen) and 4 to 6 weeks (13.2 m(2)/pen) of age and to 24, 30, and 36 geese at 7 to 14 weeks (20.0 m(2)/pen) of age. The results revealed that stocking density mainly affected body weight gain in geese younger than 4 weeks, and that geese subjected to LD had a high body weight at 2 weeks of age. However, the effect of stocking density on the severity score of AW (SSAW) and incidence of AW (IAW) did not differ significantly among the treatments. Differences were observed among the genetic stocks; that is, SSAW and IAW were significantly higher in AL than in NL and CL. Genetic selection generally aggravates AW, complicating its elimination. To effectively reduce IAW, stocking density, a suspected causal factor, should be lower than that presently applied commercially.

A 3-week feeding trial in a 3 × 2 × 2 factorial design was conducted with three concentrations (0, 0.5, and 5 mg/kg) of T-2 toxin (T-2) and two levels (0% and 0.5%) of green tea powder (GTP) supplements used in the diets of female brown Tsaiya ducklings (BTDs) and Kaiya ducklings (KDs), respectively. Breed had a significant effect on the growth performances and the relative weights of organs and carcass. In general, the growth performances of KDs were better than BTDs. The relative weights of organs and carcass of BTDs were typically heavier than those of KDs; however, the breast of KDs was heavier than those of BTDs. Both ducklings received 5 mg/kg of T-2 blended in the diet showed lower feed intake and body weight gain (BWG) in the second and the third week. The diet containing 5 mg/kg of T-2 and 0.5% GTP improved the BWG compared to those fed the diet supplemented with 5 mg/kg of T-2 without GTP in BTDs. Ducklings fed the diet containing 5 mg/kg of T-2 induced hypocalcemia and hypomagnesemia, as well as decreased concentrations of creatine phosphokinase and alkaline phosphatase. The concentrations of blood urea nitrogen (BUN) and glutamate oxaloacetate transaminase (GOT) were increased in KDs and BTDs fed the diet containing 5 mg/kg of T-2 without GTP, respectively. However, duckling diets containing 5 mg/kg of T-2 with 0.5% GTP lowered concentrations of BUN and GOT in the blood plasma of KDs and BTDs, respectively. The diet containing 5 mg/kg of T-2 increased the relative kidney weight but decreased the relative breast weight of ducklings. Enlarged gizzards and reduced relative leg weights were observed in BTDs fed the diets containing 5 mg/kg of T-2. In summary, BTDs are more sensitive than KDs in responding to T-2 toxicity and GTP detoxification. Green tea powder has detoxification ability and could potentially mitigate T-2 toxicity on BWG, BUN, and GOT in ducklings.

This study aimed to investigate ultrastructural changes of growing porcine oocytes and in vitro maturated oocytes. Light microscopy was used to characterize and localize the primordial, primary, secondary, and tertiary follicles. During oocyte growth and maturation, the morphology of mitochondria was roundish or ovoid in shape depending on the differentiation state, whereas their mean diameters oscillated between 0.5 and 0.7 µm, respectively, from primary and secondary follicles. Hooded mitochondria were found in the growing oocytes of the tertiary follicles. In addition to the pleomorphism of mitochondria, changes in the appearance of lipid droplets were also observed, along with the alignment of a single layer of cortical granules beneath the oolemma. In conclusion, our study is apparently the first report to portray morphological alterations of mitochondria that possess the hooded structure during the growth phase of porcine oocytes. The spatiotemporal and intrinsic changes during oogenesis/folliculogenesis are phenomena at the ultrastructural or subcellular level of porcine oocytes, highlighting an in-depth understanding of oocyte biology and impetus for future studies on practical mitochondrion replacement therapies for oocytes.

Two experiments, Trial 1 (in vitro) and Trial 2 (in vivo), were conducted to examine the effects of ionophores, monensin, laidlomycin, and laidlomycin propionate on whole-animal O₂ consumption, organ weights, jejunal glucose absorption, and O₂ utilization, as well as growth, feed and water consumption, and feed efficiency. In Trial 1, 30 male Swiss-Webster mice, 8 wk old, were used to measure the in vitro effects of each of the ionophores at concentrations of 1.62 or 16.2 mM. Six combinations of three ionophores at two concentrations resulted in a total of eight treatments. All eight treatments were exposed to jejunal rings from a single mouse for a total of 30 observations per treatment. Jejunal rings were exposed to each ionophore treatment for 15 min. Laidlomycin propionate (16.2 mM) decreased (P < 0.02) glucose absorption, as estimated by H³-3-O-methyl glucose uptake compared with all other treatments, whereas laidlomycin propionate (1.62 mM) increased (P = 0.032) jejunal DM content compared with 16.2 mM laidlomycin propionate. In Trial 2, 40 5-wk-old mice were allotted into four treatments—control and 16.2 mM each of monensin, laidlomycin, and laidlomycin propionate—for a total of 10 observations per treatment. Ionophores were administered via the drinking water for 14 d. No ionophore treatment had any effect on whole-mouse O₂ consumption. Monensin increased (P = 0.004) stomach size and decreased (P = 0.049) the efficiency of BW gain compared with controls. Laidlomycin propionate decreased (P = 0.032) the percentage of whole jejunum oxygen consumption due to oubain-sensitive respiration compared with control. The efficiency of intestinal glucose absorption was not changed due to treatment in either trial. Under the conditions of these studies, monensin, laidlomycin, and laidlomycin propionate had minimal and inconsistent effects on jejunal function and energy utilization in mice. This investigation suggests that changes in the energetic requirements of animals treated with ionophores are not an issue in animal production.

Two lines of mice, M16 selected for rapid growth and a randomly selected control ICR as well as their reciprocal crosses were used to study the effects of genotype on whole-body energetics and intestinal responses to monensin. Six mice, eight weeks of age, from each line or reciprocal cross were assigned to one of two treatments, 1) drinking water containing 20 mmol/L monensin dissolved in 0.5% V/V ethanol, and 2) drinking water containing 0.5% V/V ethanol (control) for two weeks. After 11 days (age of 9 weeks and 4 days), whole-body O 2 consumption was measured. At the end of two weeks, jejunal O 2 consumption, intestinal tissue composition and histomorphometrics as well as the rate and efficiency of glucose absorption were estimated. In comparison with the control, monensin administration in drinking water resulted in less daily water intake (13.4 vs. 15.5 ml/mouse, p<0.01), less protein to DNA ratio of jejunal mucosa (5.41 vs. 6.01 mg/mg, p<0.05), lower villus width (88 vs. 100 µm, p<0.05), and less jejunal tissue O 2 consumption enhancement by alcohol (7.2 vs. 10.5%, p0.05) effect on variables measured in either line of mice or their reciprocal cross. In contrast, the M16 line, selected for rapid growth, as compared to the ICR controls or the reciprocal crosses, had less initial (pre-monensin treatment) whole-body O 2 consumption per gram of body weight (1.68 vs. 2.11-2.34 µmol/min⋅g BW, p<0.01) as compared to the ICR and reciprocal crosses. In addition, the M16 mice exhibited greater growth (412 vs. 137-210 mg/d, p<0.05), better feed efficiency (41.7 vs. 19.9-29.3 mg gain/g feed, p<0.05), shorter small intestines adjusted for fasted body weight (1.00 vs. 1.22-1.44 cm/g FBW, p<0.05), wider villi (109 vs. 87-93 µm, p<0.05), more mature height of enterocytes (28.8 vs. 24.4-25.1 µm, p<0.05) and a lower rate (91 vs. 133-145 ηmol glucose/min⋅g jejunum, p<0.05) and less energetic efficiency (95 vs. 59-72 ηmol ATP expended/ηmol glucose uptake, p0.05) effect on whole-body O 2 consumption and jejunal function, whilst selection for rapid growth resulted in an apparent down-regulation of intestinal function. These data suggest that genetic selection for increased growth does not result in concomitant changes in intestinal function. This asynchrony in the selection for production traits and intestinal function may hinder full phenotypic expression of genotypic growth potential. (Asian-Aust.