The critical dietary potassium concentration for induction of mineral disorders in non-lactating Welsh Mountain sheep

Diets with more than 30 g K/kg DM have previously been associated with hypomagnesaemia in grazing cattle, and to test whether such diets lead to mineral disorders in sheep, the absorption of Mg and other elements was investigated using experimental diets to which KC I had been added to provide 27, 29, 32 or 34 g K/kg DM. The apparent absorption, balance and apparent retention of Mg, and to a lesser extent Ca, were reduced for sheep offered the diets with 32 or 34 g K/kg DM. The absorption and retention of K, Na, P, Zn, Pb and Cd was not affected by treatment. The blood intracellular Ca concentration was reduced by the diets with 29, 32 or 34 g K/kg DM, compared to the diet with 27 g K/kg DM, but the concentration of other elements was unaffected. Blood plasma Ca concentration was increased at the highest level of K inclusion, providing evidence of mild hyperkalaemia and the involvement of Ca homeostatic mechanisms. It is concluded that Mg absorption by sheep will be impaired if the diet contains more than 30 g K/kg DM, equivalent to an intake of approximately 13 g K/d, but that a high K diet may be beneficial before parturition to accustom the sheep to Ca mobilization before lactation. (c) 2005 Elsevier B.V. All rights reserved.

The effectiveness of heat, cold and 6-dimethylaminopurine shocks for inducing tetraploidy in the Kuruma shrimp, Marsupenaeus japonicus (Bate)

In this study tetraploid Marsupenaeus japonicus (Bate) embryos were produced by preventing the first division in mitosis. The effectiveness of temperature and chemical shocks for producing tetraploid M. japonicus were assessed when applied at different times postspawning and for different durations. Tetraploid M. japonicus embryos (spawned at 27 degrees C) were produced by heat shocks at 35 degrees C and 36 degrees C in three and eight spawning samples respectively, and a cold shock at 5 degrees C in a single spawning sample. All temperature shocks inducing tetraploidy were applied 18-23 min postspawning for a 5-10 min duration. The percentage of spawnings successfully inducing tetraploid embryos (i.e., frequency of induction) ranged from 33.33% to 66.67% for the 21, 22 and 23 min postspawning heat shock treatment regimes. The percentage of tetraploid embryos within an induction (i.e., induction rate), as determined by flow cytometry, ranged from 8.82% to 98.12% (ave. S.E.) (34.4 +/- 21.4%) for the 35 degrees C shock treatments, from 13.12% to 61.02% (35.0 +/- 5.0%) for the 36 degrees C shock treatments and was 15% for the 5 degrees C cold shock treatment. No tetraploids were produced for spawnings that received heat shocks above 36 degrees C or below 35 degrees C, or for cold shocks above 5 degrees C for any of the tested postspawning treatment and duration times. Chemical shock with 150 mu M 6-dimethylaminopurine did not result in tetraploid M. japonicus embryos at any of the tested postspawning treatment times and durations. Tetraploid M. japonicus embryos were nonviable, with no tetraploid larvae being detected by flow cytometry. Based on our results heat shocking of M. japonicus embryos at 36 degrees C, 23 min postspawning for a 5-10 min duration is the most effective means to produce tetraploids through inhibition of the first mitotic division (taking into consideration the importance of frequency and induction rate equally).

The role of glucocorticoids in the induction of zinc-α2-glycoprotein expression in adipose tissue in cancer cachexia

Loss of adipose tissue in cancer cachexia in mice bearing the MAC16 tumour arises from an increased lipid mobilisation through increased expression of zinc-α2-glycoprotein (ZAG) in white (WAT) and brown (BAT) adipose tissue. Glucocorticoids have been suggested to increase ZAG expression, and this study examines their role in cachexia and the mechanisms involved. In mice bearing the MAC16 tumour, serum cortisol concentrations increased in parallel with weight loss, and the glucocorticoid receptor antagonist RU38486 (25 mg kg-1) attenuated both the loss of body weight and ZAG expression in WAT. Dexamethasone (66 μg kg-1) administration to normal mice produced a six-fold increase in ZAG expression in both WAT and BAT, which was also attenuated by RU38486. In vitro studies using 3T3-L1 adipocytes showed dexamethasone (1.68 μM) to stimulate lipolysis and increase ZAG expression, and both were attenuated by RU38486 (10 μM), anti-ZAG antibody (1 μ gml-1), and the β3-adrenoreceptor (β3-AR) antagonist SR59230A (10 μM). Zinc-α2-glycoprotein also increased its own expression and this was attenuated by SR59230A, suggesting that it was mediated through the β3-AR. This suggests that glucocorticoids stimulate lipolysis through an increase in ZAG expression, and that they are responsible for the increase in ZAG expression seen in adipose tissue of cachectic mice. © 2005 Cancer Research UK.

Antioxidants, reactive oxygen and nitrogen species, gene induction and mitochondrial function

Redox-sensitive cell signalling Thiol groups and the regulation of gene expression Redox-sensitive signal transduction pathways Protein kinases Protein phosphatases Lipids and phospholipases Antioxidant (electrophile) response element Intracellular calcium signalling Transcription factors NF-?B AP-1 p53 Cellular responses to oxidative stress Cellular responses to change in redox state Proliferation Cell death Immune cell function Reactive oxygen and nitrogen species – good or bad? Reactive oxygen species and cell death Reactive oxygen species and inflammation Are specific reactive oxygen species and antioxidants involved in modulating cellular responses? Specific effects of dietary antioxidants in cell regulation Carotenoids Vitamin E Flavonoids Inducers of phase II enzymes Disease states affected Oxidants, antioxidants and mitochondria Introduction Mitochondrial generation of reactive oxygen and nitrogen species Mitochondria and apoptosis Mitochondria and antioxidant defences Key role of mitochondrial GSH in the defence against oxidative damage Mitochondrial oxidative damage Direct oxidative damage to the mitochondrial electron transport chain Nitric oxide and damage to mitochondria Effects of nutrients on mitochondria Caloric restriction and antioxidants Lipids Antioxidants Techniques and approaches Mitochondrial techniques cDNA microarray approaches Proteomics approaches Transgenic mice as tools in antioxidant research Gene knockout and over expression Transgenic reporter mice Conclusions Future research needs