We previously reported the production of limited quantities of biologically active recombinant human lactoferrin in the filamentous fungus Aspergillus oryzae. In the present study, we report a modification of this production system combined with a classical strain improvement program that has enabled production of levels of recombinant human lactoferrin in excess of 2 g/l. The protein was expressed in Aspergillus awamori as a glucoamylase fusion polypeptide which was secreted into the growth medium and processed to mature human lactoferrin by an endogenous KEX-2 peptidase. The recombinant protein retains full biological activity in terms of its ability to bind iron and human enterocyte receptors. Furthermore, the recombinant protein functions as a potent broad spectrum antimicrobial protein.
The effects of graded doses of dietary aflatoxin (0, 0.625, 1.25, 2.5, 5.0, and 10.0 mug./g.) on hemoglobin, packed blood cell volume, erythrocyte count, leucocyte counts, bone marrow lipid, and bone marrow nucleic acids of chickens were measured. The hemoglobin, packed cell volume, and erythrocyte count were reduced significantly (P less than 0.05) to about the same extent by any given dose. Microscopic examination of stained smears of the bone marrow revealed a hyperplastic response including the granulocytic elements. Chemical analyses of the marrow revealed a decreased lipid content and an increased content of ribonucleic acid and deoxyribonucleic acid. Total leucocytes were increased about three fold by aflatoxin (10 mug./g). Differential leucocyte counts revealed that the heterophils were increased while the eosinophils were unaffected and the basophils, lymphocytes, and monocytes were decreased. The increase in nucleic acids of the marrow and in circulating leucocytes occurred with doses which inhibit growth rate. These data suggest that aflatoxin causes a hemolytic anemia in chickens, that aflatoxin, by itself, is not involved in the hemorrhagic anemia syndrome of chickens, and that aflatoxin does not cause in chickens a general inhibition of ribonucleic acid and protein synthesis as assumed from studies on rats.
Aflatoxins, toxic metabolites of Aspergillus flavus or Aspergillus parasiticus, cause poor feed utilization, decreased weight gains, depressed immune function, liver dysfunction, coagulation abnormalities, and death in a wide variety of species including humans. Conservationists have become concerned that increasingly popular wildlife feeding or baiting practices could expose wildlife to toxic amounts of aflatoxin-contaminated grains. In particular, the effects of aflatoxins on the wild turkey (Meleagris gallopova silvestris) are of concern because the conspecific domestic turkey is highly susceptible to aflatoxins. To evaluate the effect of dietary aflatoxin on wild turkeys, four groups of 4-mo-old wild turkeys were fed diets containing either 0, 100, 200, or 400 g aflatoxin/kg feed for 2 wk in September and October 1996. Aflatoxin-fed poults had decreased feed consumption and weight gains as compared with control poults. Decreased liverto-body weight ratios, liver enzyme alterations, slightly altered blood coagulation patterns, and mild histologic changes indicated low-level liver damage. Compromise of cell-mediated immunity was indicated by decreased lymphoblast transformation. The effects were apparent in all treatment groups to variable levels, but significant differences most often were found at 400 g aflatoxin/kg feed. This study shows that short-term aflatoxin ingestion by wild turkeys can induce undesirable physiologic changes; therefore, exposure of wild turkeys to feeds containing aflatoxin levels of 100 g aflatoxin/kg feed or more should be avoided.
Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from less than .2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (less than 60 ppb) were found in suspect feed from two episodes. The main symptoms in turkeys were mortality (up to 59%), nephrotoxicity (pale, swollen kidneys that became tan colored in the sequel to acute toxicity), decreased feed consumption (as little as 20% of the normal feed intake) prior to death, and secondary air sacculitis. Histopathology revealed edema and necrosis of the proximal tubules of the kidneys and no changes in the liver or other organs. Suspect feed containing 2 ppm ochratoxin A increased uric acid levels in serum when fed to poults in the laboratory. The episodes in laying hens were characterized by reduced egg production, poor egg shell quality, and nephropathy. The episodes in broiler chickens were characterized by poor growth rate, poor feed conversion efficiency, poor pigmentation, nephropathy, and increased incidence of air sacculitis. Obtaining feed and ingredients free of ochratoxin, cleaning the feed and ingredient handling equipment, and adding antifungal agents to the feed proved beneficial. Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. Aqueous acetone was a better solvent for extracting ochratoxin than was the recommended phosphoric acid: chloroform. The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.