hugh l. tunison laboratory offish nutrition, riis ...€¦ · possibly affect cataractogenesis,...
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MFR PAPER 1348
Nutritionally Induced Cataractsin Salmonids Fed Purified andPractical Diets
HUGH A. POSTON, RONALD C. RIIS,GARY L. RUMSEY, and H. GEORGE KETOLA
Hugh A. Poston, Gary L. Rumsey,and H. George Ketola are with theTunison Laboratory of Fish Nutrition,U.S. Fish and Wildlife Service, Cortland, NY 13045 Ronald C. Riis iswith the Department of Clinical Sciences, Section of ComparativeOphthalmology, State University ofNew York College of VeterinaryMedicine, Cornell University, Ithaca,NY 14853. Data in this report hasbeen published in full in The CornellVeterinarian 67(4):472-509.
As in other areas of animal industry,the cost of feed is a major contributingfactor to the total cost of fish production. This is much more apparent forfish because they require 40-55 percentof their diet as protein, compared with18-22 percent for poultry, for example. This problem is accentuated by thefluctuating availability and costs ofanimal protein which carnivorous fishgenerally require in large amounts.
In searching for acceptable alternatesources of plant protein for fish foodat our laboratory, an 80-90 percent incidence of grossly discernible bilateralcataracts appeared in trout and salmonred a commercial isolated soy protein(lSP), at 40 percent of the diet, for atleast 8 weeks.
Reports from salmon and trout rearing facilities throughout the world indicate that fish cataracts, apparently ofdietary origin, are widespread andcause marked economic loss in fishproduction.
We initiated studies at our laboratoryto: I) determine some of the nutritionalfactors responsible for cataracts and reduction of growth in salmonids feddiets containing ISP as the major sourceof protein, and 2) characterize the development of the dietary-inducedcataracts.
Soybean products usually aredeficient in the total sulfur amino acids,methionine, and cystine. Also, alkalinetreatment during preparation of soy protein isolates possibly reduces the bioavailability of lysine, through conjugation of its bioactive sites such as the
October /978
opsilon groups, to below the minimallevel necessary to prevent cataracts infish.
Preliminary experiments eliminatedthe dietary form oflSP (i.e., isoelectricISP VS sodium proteinate ISP), thelevel of threonine, ascorbic acid, orchromium as possible causes for thelens opacity.
We conducted another experiment inwhich duplicate lots of I-gm lake trout,Salvelintls fontinalis, were fed, for 16weeks at 9°C, either a basal diet containing 38.7 percent ISP as the soleprotein, or the basal diet plus a supplement ofO. 9 percent DL-methionine and1.15 percent lysineoHCI. A practical,production-type diet that contained noISP was fed as a control diet.
We examined the intact eyes of livefish from each dietary group everymonth with a slit-lamp biomicroscope.Using the total amount of light transmitted through the normal lens as 100 percent, we assigned lenses the values of100,75,50,25, and 0 percent, according to the degree of opacity. Afterbiomicroscopic examination, the eyeswere enucleated and prepared for histological study of changes in lens structure.
Monthly biomicroscopic and histologic examination showed that,whereas fish fed supplementalmethionine and lysine had normallenses, those in fish fed the basal dietunderwent a series of degenerati vechanges (including replication of anterior lens epithelium, and opacification, vacuolation, liquefaction, and
hyalinization of fibers) progressingfrom the epithelium and outer cortex tothe nucleus.
In another experiment, duplicate lotsof 5-gm lake trout were fed a basal diet(40 percent ISP) or the basal diet plussingular supplements of 0.9 percentmethionine, 1.15 percent lysineoHCI,0.92 percent lysine (free base), or various combinations for 18 weeks at12.4 0c. Trout fed methionine, eithersingularly or with lysine, had normallenses, but those fed the basal diet orlysine without methionine had lenscataracts which progessed inward froman initial cortical opacification andepithelial replication to a deeper nuclear involvement with the same degenerative changes observed in the firstexperiment. These results show thatsupplemental methionine, but nolysine, prevented cataract formation inlake trout fed an ISP as the sole protein.
In other feeding studies with dietscontaining casein and gelatin, but notISP, a dietary riboflavin deficiency induced a lenticular-corneal abnormalityin fingerling rainbow trout, Salmogairdneri; a dietary vitamin A deficiency in swim-up brook trout, Salvelinus fontinalis, caused corneal andretinal, but not lenticular, abnormal ities.Supplemental dietary ~carotene prevented corneal and retinal lesions inbrook trout held in warm (12.4 0C), butnot in cold (9°C) water.
These results show the formation of anutritionally induced cataract whichcan be prevented by feeding supplemental methionine, but not lysine. Although our results do not show specifically how the deficiency of
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methionine metabolically induced thecataractogenesis, evidence of workwith other animals suggests that thesulfhydryl, rather than the methylgroup of methionine, is most importantin preventing methionine deficiencycataracts. One of the earliest detectablechanges in most cataract formations is arapid fall in concentration of sulfhydrylgroups. The sulfuydryl groups possiblyminimize conformational changes such
as unfolded proteins and the subsequentformation of disulfide cross-link bondsand insoluble proteins of high molecular weights.
Soybeans and soy proteins often contain antinutritional factors such as trypsin inhibitors and hemagglutininswhich interfere with normal intestinalabsorption of nitrogen and metabolismof methionine. Such factors, as theypossibly affect cataractogenesis,
growth, and composition, warrantfurther stud y.
In summary, these studies show thatat least three nutrient-related lesionsoccur in the eyes of salmonid fishes. Adeficiency of an amino acid caused lenscataracts; a deficiency of riboflavin induced a lesion involving cornea andlens. A vitamin A deficiency causedlesions in the cornea and retina, but notin the lens.
MFR PAPER 1349
MFR Paper 1348. From Marine Fisheries Review, Vol. 40, No. 10, October1978. Copies 01 this paper, in limited numbers, are available Irom 0822, UserServices Branch, Environmental Science Information Center, NOAA. Rockville,MO 20852. Copies of Marine Fisheries Review are available from the Superintendent of Documents, U.S. Government Printing Office, Washington, DC20402 for $1. 10 each.
Thomas L. Meade is with the Department of Animal Science, University of Rhode Island, Kingston, RI02881.
Environmental ParametersAffecting Fish Physiology inWater Reuse Systems
THOMAS L. MEADE
The incorporation of water reuse,based on microbiological treatment, inlarge-scale salmonid production systems a few years ago was widely regarded as a major breakthrough in production technology. Since that time,those of us who have been involved inthe development of water reusetechnology have seen the value of oureffort diminished by changing conditions and the appearance of physiological problems.
Innovative development work hasenabled us to offset some of the effectsof increased materials and energy costs,and meet the more stringent dischargecriteria. On the other hand, high mortalities experienced in some facil itieshave been a severe setback, and clearly
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illustrate that when the environment isappreciably modified we can expect aphysiological response. U nfortunatel y,physiological adaptation is not alwaysadequate to insure survival.
Experience gained in culturing onespecies in water reuse systems is notalways transferable to another species,and, similarly, problems encounteredin one area are not necessarily experienced in another. Most problems encountered are related to water quality.Such factors as pH, mineral content,metabolite levels, temperature, anddissolved gases may be critical. Ourmore recent research, which is multidisciplinary in approach, has centeredon the relationship between environmental factors and the well being of the
cultured species as judged by biochemical, physiological, and pathologicaldeterminative procedures.
It is generally accepted that toxicityof ammonia is due to the undissociatedfraction, with its concentration beingtemperature, salinity, and pH dependent. Thus, environmental pH manipulation can be employed to increase tolerance for ammonia. Since culturing inthe range pH 6.0-7.0 is not always desirable, we have endeavored to developa beller understanding of themechanism of ammonia toxicity. Datadeveloped to date suggests that impaired respiration resulting from an altered acid base balance, with a corresponding blood pH shift, is the primarycause of mortality.
In water reuse systems employingmicrobial nitrification, nitrite, a microbial metabolite, may also be toxic to thefish being cultured. A wide range ofLCso's of nitrite for various species hasbeen reported. In our work, we havedemonstrated that nitrite toxicity is related to temperature, oxygen concentration, and chloride ion concentration. Inhigh salinity environments, nitrite has alow order of toxicity , and, in freshwater
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