Consequences of exposure to serum, with or without vitamin E supplementation, in terms of the fatty acid content and viability of bovine blastocysts produced in vitro

2003 ◽  
Vol 15 (5) ◽  
pp. 275 ◽  
Author(s):  
A. Reis ◽  
J. A. Rooke ◽  
G. J. McCallum ◽  
M. E. Staines ◽  
M. Ewen ◽  
...  

To determine whether serum supplementation influenced fatty acid content of bovine blastocysts and whether vitamin E addition to culture medium containing serum could improve development in vitro, cleaved eggs were cultured in synthetic oviduct fluid supplemented with bovine serum albumin (BSA, 0.4% w/v, fraction V) (SVBSA), fetal calf serum (FCS, 10% v/v) (SFCS) or FCS (10% v/v) plus 100 μM vitamin E (SFCS + E). Blastocyst yields were recorded and fatty acid composition was determined by gas chromatography. Day 7 blastocysts were incubated with [2-14C] pyruvate for 3 h and then fixed for cell counts. Yields of good quality blastocysts were greatest from cleaved eggs cultured in serum-free conditions (P < 0.01). In the presence of serum, supplementation with vitamin E increased both total and good quality blastocyst yields (P < 0.01). Presence of serum increased fatty acid content (mean ± SEM) of blastocysts (SVBSA v. SFCS = 57 ± 2  v. 74 ± 2 ng embryo−1; P < 0.001). In contrast, pyruvate metabolism was greater in blastocysts produced without serum (27 ± 3 v. 21 ± 3 picomoles embryo−13 h−1; P < 0.01) but, on a per cell basis, no differences were detected. Addition of vitamin E to the serum-supplemented formulation did not alter either the fatty acid content (73 ± 2 ng embryo−1) or pyruvate metabolism index (19 ± 1 pmol embryo−13 h−1) of SFCS + E blastocysts. Thus, despite lipid accumulation, supplementary vitamin E improved blastocyst yields in embryos exposed to serum.


1998 ◽  
Vol 1998 ◽  
pp. 221-221 ◽  
Author(s):  
R J Mansbridge ◽  
J S Blake ◽  
C Collins

The COMA report on The Nutritional Aspects of Cardiovascular Disease (1994) recommended that the intake of long chain n-3 polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), by the UK population should double. EPA and DHA in the human diet are derived principally from oily fish. The aim of this experiment was to determine the effect of increasing levels of fish oil in the diet at two levels of vitamin E supplementation, on intake, milk production, the extent of uptake of EPA and DHA into milk fat at levels exceeding those investigated to date, and the effect of a dietary supplement of vitamin E on fatty acid content.



2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 202-202
Author(s):  
Ding Wang ◽  
Young Dal Jang ◽  
G K Rentfrow ◽  
H J Monegue ◽  
M J Azain ◽  
...  

Abstract The study objective was to assess the contribution of fat source and vitamin E (VE) supplementation on tissue tocopherol concentration, antioxidant status, and fatty acid composition in the backfat of pigs at heavy slaughter weight (149.38 ±1.56 kg). A total of 64 individually-fed pigs (32 barrows, 32 gilts; 28.41 ±0.83 kg) were randomly assigned to 8 dietary treatments in a 4 × 2 factorial arrangement. Fat treatments included corn-starch (CS), tallow (TW), corn oil (CO) and coconut oil (CN). VE supplementation levels were 11 and 200 IU/kg. Loin muscle, backfat, and liver samples were collected at slaughter. Data analysis were performed by ANOVA using GLM in SAS. No interactions between dietary fat source and VE supplementation were observed. Increasing dietary VE level from 11 to 200 IU/kg increased (P < 0.001) the tocopherol concentration in both liver (4.73 vs. 21.06 ppm wet liver) and loin muscle (1.25 vs. 2.67 ppm wet muscle). Pigs from the CO group had higher liver SOD activity (P < 0.05) than the other treatments (CS 22.51, TW 22.67, CO 24.40, and CN 20.92 U/mg protein). Pigs from the CN group had the highest (P < 0.05) total saturated fatty acid content (CS 44.33, TW 40.33, CO 36.29, and CN 51.70%), but the lowest (P < 0.05) total polyunsaturated fatty acid content (CS 9.26, TW 9.80, CO 25.41, and CN 8.75%) and iodine value (CS 56.61, TW 60.66, CO 77.83, and CN 49.90) in the backfat. Pigs from the TW group had the highest (P < 0.05) total monounsaturated fatty acid content (CS 46.40, TW 49.87, CO 38.30, and CN 39.56%) in the backfat. Under conditions of this study, a higher level of VE supplementation increased liver and muscle tocopherol concentrations whereas dietary fat sources altered liver antioxidant activity and fatty acid composition in the backfat.



2014 ◽  
Vol 46 (5) ◽  
pp. 883-888 ◽  
Author(s):  
Claudia Delgadillo-Puga ◽  
Bernardo Sánchez-Muñoz ◽  
José Nahed-Toral ◽  
Mario Cuchillo-Hilario ◽  
Margarita Díaz-Martínez ◽  
...  


Weed Science ◽  
2020 ◽  
pp. 1-38
Author(s):  
Chad Brabham ◽  
Philipp Johnen ◽  
Janneke Hendriks ◽  
Michael Betz ◽  
Alexandra Zimmermann ◽  
...  

Abstract Methiozolin is a new herbicide for control of annual bluegrass (Poa annua L.) in several warm and cool season turfgrasses with an unknown mechanism of action (MOA). In the literature, methiozolin was proposed to be a pigment inhibitor via inhibition of tyrosine aminotransferases (TATs) or a cellulose biosynthesis inhibitor (CBI). Here, exploratory research was conducted to characterize the herbicide symptomology and MOA of methiozolin. Arabidopsis (Arabidopsis thaliana L.) and P. annua exhibited a similar level of susceptibility to methiozolin and arrestment of meristematic growth was the most characteristic symptomology. For example, methiozolin inhibited Arabidopsis root growth (GR50 8 nM), shoot emergence (GR80 ~50 nM), and at rates greater than 500 nM apical meristem growth was completely arrested. We concluded that methiozolin was neither a TAT nor a CBI inhibitor. Methiozolin had a minor effect on chlorophyll and alpha-tocopherol content in treated seedlings (< 500 nM) and supplements in the proposed TAT pathway could not lessen phytotoxicity. Examination of microscopy root images revealed methiozolin treated (100 nM) and untreated seedlings had similar root cell lengths. Thus, methiozolin inhibits cell proliferation and not elongation from meristematic tissue. Subsequently, we suspected methiozolin was an inhibitor of the mevalonic acid (MVA) pathway because its herbicidal symptomologies were nearly indistinguishable from those caused by lovastatin. However, methiozolin did not inhibit phytosterol production and MVA pathway metabolites did not rescue treated seedlings. Further experiments showed that methiozolin produced a very similar physiological profile across a number of assays as cinmethylin, a known inhibitor of fatty acid synthesis through inhibition of thioesterases (FATs). Experiments with Lemna showed that methiozolin also reduced fatty acid content in Lemna with a profile similar, but not identical, to cinmethylin. However, there was no difference in fatty acid content between treated (1 µM) and untreated Arabidopsis seedlings. Methiozolin also bound to both Arabidopsis and Lemna FATs in vitro. Modeling suggested that methiozolin and cinmethylin have comparable and overlapping binding sites to FAT. While there was a discrepancy in the effect of methiozolin on fatty acid content between Lemna and Arabidopsis, the overall evidence indicates that methiozolin is a FAT inhibitor and acts in a similar manner as cinmethylin.



2013 ◽  
Vol 4 (1) ◽  
pp. 21 ◽  
Author(s):  
Kun Liu ◽  
Suyun Ge ◽  
Hailing Luo ◽  
Dubing Yue ◽  
Leyan Yan


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