Effect of oxidized ß-carotene on the growth and feed efficiency of broilers.

Fully oxidized ß-carotene (OxBC) containing ß-carotene-oxygen copolymers is proposed as an alternative to antimicrobial growth promoters. Two trials were conducted to determine the efficacy of OxBC in enhancing growth and feed intake (FI) in male and female Ross × Ross 308 broilers in Ontario, Canada, and in Ross 308 male broilers in the United Kingdom. In the first trial, 0, 1, 2, or 5 ppm OxBC were added to diets in a 20% cornstarch premix, whereas in the second trial, 0, 2, or 5 ppm OxBC were added in a 1% cornstarch or 1% corncob grits premix. In trial 1, 2, and 5 ppm OxBC improved bird final body weights (BW) compared with the unsupplemented, nonmedicated (no bacitracin methylene disalicylate included), negative control birds after 39 d of feeding under commercial conditions (P < 0.05). All levels of OxBC improved feed conversion (FCR) during the finisher period (P < 0.05), whereas 2 and 5 ppm OxBC enhanced FCR relative to the negative control group during the full production cycle (P < 0.05). Average daily FI was not affected by OxBC, whereas 2 and 5 ppm OxBC increased broiler average daily gain (ADG) (P < 0.05). Oxidized ß-carotene did not affect bird mortality. The optimal OxBC dose was 2 ppm under the conditions used. In trial 2, 2 or 5 ppm OxBC on cornstarch and 5 ppm OxBC on corncob grits improved ADG, BW, and FI when fed for 35 d, as compared with the negative, nonmedicated control (P < 0.05). Feed conversion was not improved in the OxBC groups compared with the control group (P > 0.05). There were no differences among the 3 OxBC groups (P > 0.05). When birds were fed 2 ppm OxBC on corncob grits, the overall ADG, BW, and FI were lower than the respective control values (P < 0.001). Overall bird mortality was higher than expected for all groups, including the control group, but no dose effect was evident. Cornstarch was the preferred carrier for OxBC, and 2 ppm OxBC was the optimal dose under the conditions used.

Integrated responses of Na+/HCO3- cotransporters and V-type H+-ATPases in the fish gill and kidney during respiratory acidosis.

Using degenerate primers, followed by 3' and 5' RACE and "long" PCR, a continuous 4050-bp cDNA was obtained and sequenced from rainbow trout (Oncorhynchus mykiss) gill. The cDNA included an open reading frame encoding a deduced protein of 1088 amino acids. A BLAST search of the GenBank protein database demonstrated that the trout gene shared high sequence similarity with several vertebrate Na(+)/HCO(3)(-) cotransporters (NBCs) and in particular, NBC1. Protein alignment revealed that the trout NBC is >80% identical to vertebrate NBC1s and phylogenetic analysis provided additional evidence that the trout NBC is indeed a homolog of NBC1. Using the same degenerate primers, a partial cDNA (404 bp) for NBC was obtained from eel (Anguilla rostrata) kidney. Analysis of the tissue distribution of trout NBC, as determined by Northern blot analysis and real-time PCR, indicated high transcript levels in several absorptive/secretory epithelia including gill, kidney and intestine and significant levels in liver. NBC mRNA was undetectable in eel gill by real-time PCR. In trout, the levels of gill NBC1 mRNA were increased markedly during respiratory acidosis induced by exposure to hypercarbia; this response was accompanied by a transient increase in branchial V-type H(+)-ATPase mRNA levels. Assuming that the branchial NBC1 is localised to basolateral membranes of gill cells and operates in the influx mode (HCO(3)(-) and Na(+) entry into the cell), it would appear that in trout, the expression of branchial NBC1 is transcriptionally regulated to match the requirements of gill pHi regulation rather than to match trans-epithelial HCO(3)(-) efflux requirements for systemic acid-base balance. By analogy with mammalian systems, NBC1 in the kidney probably plays a role in the tubular reabsorption of both Na(+) and HCO(3)(-). During periods of respiratory acidosis, levels of renal NBC1 mRNA increased (after a transient reduction) in both trout and eel, presumably to increase HCO(3)(-) reabsorption. This strategy, when coupled with increased urinary acidification associated with increased vacuolar H(+)-ATPase activity, ensures that HCO(3)(-) levels accumulate in the body fluids to restore pH.

A putative beta2-adrenoceptor from the rainbow trout (Oncorhynuchus mykiss). Molecular characterization and pharmacology.

Extensive molecular characterization of mammalian beta-adrenoceptors has revealed complex modes of regulation and interaction. Relatively little attention, however, has focused on adrenoceptors from early branching vertebrates such as fish. Using an RT-PCR approach we have cloned a rainbow trout beta2-adrenoceptor gene that codes for a 409-amino-acid protein with the same seven transmembrane domain structure as its mammalian counterparts. This rainbow trout beta2-adrenoceptor shares a high degree of amino-acid sequence conservation with other vertebrate beta2-adrenoceptors. The conclusion that this sequence is a rainbow trout beta2-adrenoceptor is further supported by phylogenetic analysis of vertebrate beta-adrenoceptor sequences and competitive pharmacological binding data. RNase protection assays demonstrate that the rainbow trout beta2-adrenoceptor gene is highly expressed in the liver and red and white muscle, with lower levels of expression in the gills, heart, kidney and spleen of the rainbow trout. The lack of regulatory phosphorylation sites within the G-protein-binding domain of the rainbow trout beta2-adrenoceptor sequence suggests that the in vivo control of trout beta2-adrenoceptor signaling differs substantially from that of mammals.