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

46

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

Marine Fisheries Review