Document NenyQBo3O65j5npRLMjo35qqV

; .4 ^ v. x.. * rt j y'Dietary Effects of PolychlqrinafecFBiplienyl, j I on;Mink/ --ft . v;wwi (0 Q>` N. S. Platonow ona"t: H. Karstod* ** * ABSTRACT rolionin; occurred in 32 mink fed diet* con taining meat from cows which had been fed a polychlorinated biphenyl (PCB). Arodor 1231. V--yp kit were produced and all adult mink died durinp a 103 day period of _fertting ft ra tion contalningjtjS?mt -ifa 0.64 nom of PCB in ration one of 12 mink pro duced three kits, all of which died daring thf fits! dav wftfr hiMh. CHixieal riM ww Un\- |M to weight loan and passage of black tarry feeea. The gross lesions seen were yellowish discoloration of the liver and hemorrhage into the abdominal cavity or gastrointestinal tract. Microscopic lesions were nephrosis, fatty de generation and necrosis of the liver, brsln edema, disseminated intravascular coagulation, and fibrosis or coronary arteries. It Is con cluded that mink are highly sensitive to smell Quantities of PCB fed for an extended period of time. . RfiSUMfi _ ' , On n empolsonnd 32 visone- en leor servant . une ration qul rontenalt do In vinnde de vnehes auxquelles on avail donnd un diphenyls poly1 ehlord (PCB), I'Aroclor 1234. On n'obtint ou- cun petit et taud* lea visone adultes mouiUrent an court d`uno pdriodo de 103 jours dursnt laquello on lcur servlt une ration contenant >37 ppm do PCB. A is concentration de 0.64 ppm de PCB dans la ration, une femelle. sur un to tal de 12. mlt bss trois petite qul moururent en moins de 24 heures spree leur naisssnee. U-t sfgnes cliniques se trsduisirent par uno perte de poids et le passage de fices d'apparenco goudronnfe. Lea kiions m&croscoplqucs conilstslent en une decoloration jaunstre du foie et en dcs hdmorragies Intra-nbdominates ou gastro-intestinales. Lea lesions microscoplques dtaient lea sulvants: nlphrose, degeseresetnee gralsseuso et ndcrose kepatlques, oedema edrd- brtl. coagulation intrs-vasculaire dissdmindeet fibrose dex artires coronslres. Lea auteurs en vlcnncnt k la eonelualon quo le vison eat tr> vulnerable k J'ingestloa prolongde de petites quantltds de PCB. . INTRODUCTION Polychlorinated biphenyl (PCB) com pounds art now recognised as widespread environmental contaminants of aquatic or terrestrial ecosystems. Since fish and vari ous biproducts made from domestic animal* are generally included In the diet of much- raised mink, it seemed to be important to know the effects of PCB compounds on mink, when included in the diet for an ex tended period of time. .. * MATERIALS AND METHODS AuStlMfRli f J|lnu/l (|/mn ,anS ruhiiur. .yUAbraiir #r rtwtsh 1 ^, TM* aaavr * prrMS In pail at iktfniuiMh Annual )Im(Ir( *t lb* Canadian I'aCaraiian at MiatacUal Sa* laUf*. QAm, QulSac, Jana 1T1. tkh (catarrh < financial!/ Sp |V Canada Mink i:c4fa* Aaaaeiaiian and tha Ontult Mialili; at AffliaUaif and >`ao4> BnbmUl'4 Avut i, im, Thirjy-two ranch mink approximately one year old were divided into two groups with four standard dark males, four pastel, females, and eight standard dark female* in each group. Each group of 16 mink was fed a separate ration. Rations were prcjmrvd from two Jersey cows which had been given orally ten consecutive daily doses of 1 and 10 mgm per kgm, respectively of a VC11. Vol.37 -- October. 1973 0 i->, clfk, F A ^ ' . S~ . 391 1. . m ---ryt * "-T-1 <*q--p"V 1*--- 'V'TT * '"T^T7^'k" * T! ' * . *r- ' *' -j. \\ c^?" * ,t 1 ` \ ., Od383i \' " . HQNS IS * * namely A roclor 3354', dissolved in,a small TABI.E'J. Lesions Seen In Mink Feed PCB amount of olive oil i<ml-mixed with "dairy concentrate. Twenty-four hours after the FCB <ppm> * 337 lost doses were given. the cows were killed; fat, musculature, liver and kidneys**, were removed, thoroughly ground and mixed with No of.mink Sex ** *No of deaths'/ * Mean survival . 12 F 12/12 commercial mink food cereal at a level of - 'days) , 74 24r.i cereal. The resulting: rations contained 0.64 ppm and 3.57 ppm of total PCB, re* Cross l.(iioni ` Weichi loss . * 8/12 spcctivcly. Hemorrhages 9/12 The cows did not have any clinical, gross ^ ellow liver 6/12 337 0.64 4 ' 12 MF 4/4 2/12 96 - ISt 2/4 0/12 3/4 0/t2 2/4 1/12 t or hlstopnthological signs of intoxication. If these animals had been slaughtered at an inspected orient plant, thy would without doubt have passed as fit for human con sumption. . Feeding ad libitum \ym begun two months before the breeding season, l.e. on January 7 and' continued until June 17, 1071 (ICO days). Beginning in early March the 12 females Microscopic Lesions Nephrosis 5/12 Liver ncerosis 2/12 Disseminated intra vascular coagu lation 2/12 Brain edema 3/12 Coronary arterio sclerosis 0/12 1/4 1/12 2/4 0/12 .50/4 1/12 a 0/4 0/12 1/4 1/12 1. AH mink in this group survived to the end of tf feedingperiod, 160 day* . . in each test diet group were presented daily for breeding to one of the four males in the group, until the female was found to be re ceptive and mating took place. The semen of each male, collected by vaginal aspiration from a just-bred female, was examined mi croscopically for motile sperm. The remaining 101 breeding female mink plus males and mink designated for other experiments in the institutional herd from- which the test mink were taken were main tained on a commercial mixed ration, pur chased locally. They were managed during the breeding and whelping seasons -just as were the experimental PCp-fad animals. For practical purposes, they were regarded as no-treatment, controls. During the course of the PCB experiments 50 to 60 mink from this herd were removed for Aleutian disease research, either killed at once for tissue cultures or maintained on other premises for infection experiments. All of these mink were examined for gross and histopathologicn] lesions. ding and sectioned at approximately 6 m crons. Hematoxylin-eoain stain was oat routinely. Whore necessary for study of I sions of blood vessels, selected tissue so tions were stained by the aUocbrome ptoc> dure (5). The PCB were extracted from vsrios tissues as well as from samples of ratios by the method of Grant it si (3) and subsi quently analyzed by the method of. Steelier brecker and Ecohlchon (12) using a Mien Teck. Model MT-2201/ gas chromatogropfe equipped with a **Nl high temperature tin tron capture detector. The quantitation o the PCB was performed by measuring tola peak arcaaas the detector response, using m Infotronics. Model 208*, .automatic digit* integrator equipped with a baseline trad ing and drift corrector. The PCB wet separated from DDT and its analogs by tb method described by Armour and Bunt U). . Xecroptieq were performed* on experi mental mink which died and those which, were killed after PCB feeding was discon tinued. Blood from the heart and samples of tissues from the major body organs and psoas muscle were taken for PCB analysis. Portions of brain, lungs, heart,, spleen, li ver, kidney, intestine, adrenal and reproduce tlvc organs were fixed in 20f& formalin,' processed for histology by paraffin embed- * RESULTS -1 Reproduction ./ / Fifteen of the 24 females were bred nor mully. Of the remaining nine, five on tb higher PCD diet which were not bred, fie Uwlir 1214 (Mlilw* *f luc i<r.v tMtfiti*) CuiO Ilk Vtltkli. OfiUffc, 392 blphtn'i* rsnUln. kr *! tTr(r tut, AwMIn, T*s VJSJL. *blilrMk U4. Uhimi, hlul ,Xan. J.`comp.--Med MONS 083833 I 7 f htt before oi' during* ttfe breeding pc-'1 f Two of the four on tho low PCB diet, jfed during May. In al! other cases, failure to breed was caused either by the female rejecting the male or because the..*female was too weak to participate. All males produced motile sperm, yet no litters were produced by the females fed the ration containing 3.57 ppm of PCS and only one of,the females fed 0.64 ppm PCD produced a litter. Three kits were born to this female but they died during their first day of life. Clinical Signs and Mortality Fit. I. LmImic ilMdtr to *f Hi. I In th# miMn rtr ( itoKltrl Sark ntto mink kill** ky tlkrr in* kilttU * Cr> * Ml pn rCW In4In. Allw dirann XIN. The first mink to die was an adult female fdd the ration with the higher level PCB which was dead on day 43 of tha experi ment. Deaths occurred sporadically there* after. All of the mink fed the 3.57 ppm PCB ration were dead by day 105. Two of the mink fed 0.64 ppm PCB died on days 122 and 129, respectively. The feeding of this ration was terminated on the 160th day, at which time four of the surviving mink, three males and one female, were killed with an overdose of ether so that specimens could be taken for PCB analysis and histopathology. From day 161 to day 277 the surviving mink which had been fed the 0.64 ppm PCB ration were fed the regular commercial ra tion which was fed to the no-treatment con trols. Three female and one male mink were killed for examination on eaeh of days 40 and 82 after the cessation of PCB feeding. The remaining two female mink were killed on day 277. - At both treatment levels, malts survived longer than females. There was a marked difference In survival between treatment levels (Table I). , Clinical signs were either absent or non specific. A few mink died suddenly while they were still in good flesh, but many of the mink became emaciated on the PCB rtf. I. Ln{ f (imiIi lanSart Ork mink which lit! wMiitlir with IIimmImM tknnhwli m 4*y IS! *f #41 larr* IT* pUteltl thrmhwa. |iN*Sl lh *tin E. Xf). tttilitilil kjr ` diets; they had poor appetites and In some cnscs became lethargic and very weak be fore they died. Some passed tarry feces, in dicating gastrointestinal hemorrhage. Cross Lesions * " rif. I. C*N"rf Mir)' ,f |t>* ttlnk Irnrlkil In fit. I. MmI ( the immUi mwtlt f the MnUt kw k#i * |hn4 hf Mrm iMKtif liwvt. Allwkiimt, N.'l). The gross lesions seen at necropsy were emacialion. blood in the gastrointestinal tract or intra-abdominal hemorrhage, and ycllowisli discoloration of the livers. They changes were not consistent In all cases. Their frequencies are given (n Table I. Hemorrhage* seemed to be more often chronic rather than massive and acute. It was not possible to relate the blood present In tho abdominal cavity to lesion* in the blood vessel* or visceral organ*. Bleeding Vol.37 --October, 1973 * 393 MOMS 003034 ?? n % z % % ' *i o o -H -H -H -H -H -H , 333'SS3 O* So =O5 -- -- -- w M -H -H p) o Sj t> S Q a s aBS.i H -H -H -H -H > e g| a tj 15 q t? ` ^ H O "* ** a o fe. } $ 8 t? !?. 3 <* 0 0 0 0 0 eR H -H ,-H -H -H -H JoT. .5 3 3 3 3 3 3' 3 **> 3o so *eS 2o se 8o a -H -H -H -H -0 t? C5 *5 8 Si R $} 2 -- o o o o o s e 8 3SI9SI 3 0 S 5 3 3 3 3 -2 II (I E pj ft .W W 31 i i n .S K.S si m 8" <S 5 .3 3.3 3 3 5s s3 t34 uemed to hi\ occurred by dlapcdeoio. It ` mllarly, the blood which wot promt hi tit gastrointestinal tracts of eight of Um % mink which died was not traceable to tihir or other gross'lesions. Usually the bleed vie partially digested. . Slight.spUnic enlargemont was foond 3 about half, the dead mink. Hydroptrfcar dtum and hydroperitoneum, seen In Hid poisoned with PCB, were never found, * Microscopic Lesions ** The most frequently observed mJcroecopfc lesions are listed in Table t, with their ire quencles of occurrence. Some degree of an phrosis was noted In about half of the mini which died. This consisted of vacuolar dip generative changes in tubular epitheMo ceils, flattening of the epithelium In aorae# the convoluted tubules, and dilatation of fco mens containing fibrin casts. Foamy eg flocculent eosinophilic exudates were times present in Bowman's capsules. Minimal to moderate focal liver was aeen in four mink on the high PCS diet. The yellow color seen on gross inepew tion was due to the presence of large frit vacuoles In msny hepatic cells. Brain v characterized by mild or moderate spongfc>- * sis and diffusely distributed, was seen hi three of the dead mink. . Disseminated intravascular coagulation was a prominent lesion In three mink. Thee* animals appeared to hare died of extent!** disseminated thrombosis followed by mulb pie hemorrhages in organs such as the hag .(Fig. l),-and brain and either hemerrhegn or irregular pooling of blood )n sinusoid* of the spleen and liver. Some of the ` had populations of megakaryocytes seemed to be greater than normal. * Fibrosis of the media of coronary arterkv (Figs. 2 and 3) was a lesion which rently developed late In the course of experiment. It was'found In two dark mink which died on days 105 and 123 of PCB feeding and in another which won killed for examination on day ICO. The mtafc which died on day 105 was on the high level FOB diet; the other two were pit the lower level diet. Healing and recent infarcts wero present in the l^ft .ventricular myocardium of the mink which died on day 105. No lesions were noted in the male and female reproductive organs. Many of the females hnd uterine hypertrophy, evidence of recent pregnancy, and the female mink . which died during latc March and April aV * iCon. J. comp. Med* MGNS 053835 MONS 083836 3. . \% * /Vr 2. mif Innr=-" A' 3* a. . ' jrrfT ".a r ,./*W Muirt * Co*3 Muoef* 4" 3. ' . T> 2. , nUTJc "T"...__ CD Llv.r. 4i. 3. . 2. 'dUf. _E3il*- Kldnov ;nnr=-T .. ' mi tCDTOld 396 TrTHill CD Btn,,4 n 'rn'rnTT Vi6*iT\5'iVi41 JYtf YFfb'poak fit. t, Katlv* |K m#i* rmrMtMi %| 9i> f 1h U,mm infill f Ihr |it9 tin* tW taliaa rMlill*i J.ii fCH, W 1M tf Ik* >nk I* IH* ISM Con. J. comp* T MQNS 083837 0.64 ppm tstlen / 0J corpora Icutca present/ In various dc- Igfett Of regrc.iMon. Ovarian follicles seemed . to be present in adequate numbers during . the breedins: period, although many of the follicle* were undergoing regressive changes in mink which died. Females which died be* Ln-LI 1 . ' ' fore or at the beginning of the breeding pc- rlod had quiescent uteri which were juvenile . in appearance. Male mink which died dur ing March *nd April had histological evl- . deace of spermatogenesis. Those which died dIor were killed later had testicular changes . typical of post-breeding regression. ` No lesions were observed in the adrenal ir. JUJ. " glands. ) aJlf Tissue Distribution op fCB ; - - -----------^, The concentrations of PCB in various lu u hji tissues of principal and control mink are 1given In Table II. * . In the group of mink fed the higher level : r-n nT ; of PCB, the concentrations of these com-' : pounds were lowest in the blood and highest U-' LP-II I------------ i In the liver. In the same group, the PCB ; concentrations in the brain were relatively 1high, especially when one considers that 4 they were higher than in the skeletal muscle. * The concentrations of PCB in kidneys were higher than In the brain, but lower than in i[jl__ r rTi=ujrLCCn__ lio*s ' the hearts and livers. In mink fed the ration containing 0.64 ppm.pt PCB, the PCB concentrations In OWLurr4"s*r*g`rL-J*rrmyijwu--whs**** tissues were similar in all organs analysed, Fir. I. Ratios tk< mm timMifN if ikiwi. except in blood, where the lowest levels (trapfcir *atf ( rari iliw idwli tf Mm iwm i were detected. Similarly, In mink fed the *<**n iiltin (ftlalninc Ml pn RCU. < act i tkt stmt Rak ia th Ataclar 1U4 ttaMitS. ! commercial control ration, the PCB conceit ' trations were nearly identical In the anal ysed'tissues, except in blood. The resolution by gns-chromatography of Aroclor 1264 standard as well as extracts of 'various feed or tissue.samples (under the operating conditions used in the present study) resulted in up to 18 distinct peaks. I Figure 4 depicts the chromatographic trac I* Ing of .tissue extract* from mink fed the ration containing 3.57 ppm PCB os well ns tho tracing of a standard Aroclor 1254. Note the decrease of early emerging peaks of tissue extracts, disappearance of peak 8 and increase of lute emerging peaks. values between unity and zero indicate the percentage decrease.of the peak; tho values higher than unity Indicate the increases in percentage above the value of tho standard. `The percentage reductions of the first eight peaks and the percentage Increases In the subsequent peaks In these two figure* are evident. Tho first eight emerging peaks were significantly reduced In Alt tissue*, except in blood, where the reduction was not always significant The second eight peaks were always significantly Increased pro portionally to the Aroclor 1254 stnmtmrl. The data depicted In Fig. 5 and Fig. 6' These changes were most pronounced in tho show the ratios between the mean percent- liver and least so in the blood. Pcuk 3 was i ages of peaks from each tissue extract of reduced to zero In all tissues, except in ; groups given 3.57 ppm and 0.64 ppm PCB blood; peak 7 was the next most strongly ; to tho percentages of the corresponding reduced. In peaks* emerging after p*k , peak of the standard Aroclor 1254, The base 'the prpikoctiona! percentage Increase wra . line Sn each case is unity. The zero value . nearly directly related to the retention time, . indicates the disappearance of the peak; the he. peak 16 increased more than peak D. Vol. 37 -- October, 1973 397 0#i838 'rhm-rn tct cipal PCB fed groups were not found in the several doacn ctfntrol mink killed for tissue culture purposes'end used in Aleutian dis ease research. ... r^rrn--!. i -q' * * >*" DISCUSSION rrflf mijVaVVn> i .... ......... riK. 1. lUtlM ittwttii tit* rcrnfert ff Me k f fitlnn r*Miln J.iT (Vpptf M Milan ttnUiaiin* *.** PCS <hW4I* fie*'*'. Tk k-fr tlgvrt. th*m Jar *amp*ian, ar* lh* ratiaa *( IM ll*t ( |S iMa *t atlnk f*4 1.11 aaat PCB. This tendency wse not observed In blood. On ell chromatograms e substentiel percent* age (ncrsaee was noted in peaks 17 and 13. These two peaks are below 0.1% in the Aroclor 1254 mixture. Figure 7 shows the ratios expressed si milarly to Fig. 5 and Fig. 6 but give the ra-< tios for both PCB rations fed, and (or com parison the values of livers of the group fed 3.57 ppm. .. Reproduction* and Health ' or Control hllNK . _ . The 101 mink which received the commer cial ration and which were regarded as no-treatment controls, produced only an average of 1.81 kits per female bred (satis factory production is considered to be four kits per female). When the commercial ration was analysed the following results were obtained. The data represent means of six samples taken at intervals during the experiment. Percent fat -- 13. - p,p' -- DDE -- 0.012 ppm . P.P' -- HDD -- 0.010 ppm ; o,p' -- .DDT -- 0.004 ppm p,p' -- DDT -- 0.008 ppm . Total DDT -- 0.033 ppm Dicldrin -- 0.006 ppm PCB ....-- 030 ppm Ko outbreak of Infectious disease was diagnosod in the herd during these experi ments. Lesions similar to those of the prin From the impaired reproduction and mortality observed, and the tiiaue concen- tratlons of PCB found, it can be concluded that the mink were very susceptible to the effects of. PCB compounds as dietary cew- taminants. The clinical and grosa and mL- croscoplc tissue abnormalities ware rather nonspecific, so that diagnosis in cases ad naturally occurring PCB poisoning would be very difficult. Reproductive failures weight loss and terry droppings could suggest either starvation or slautisn dis ease, a common disease of mink. The PCB- fed mink may have been on an Inadequate nutritional plane, but If so, it was not to cause the diet lacked eaientlal nutrients but rather that tha mink lost appetite am did not eat enough of tha feed that wa> put before them. Aleutian disease vrouli be ruled out on hialopathology, boweves since the severe hepatitis and nephritis u alcutian disease, marktd by proliferaUu of plasma edit, was not scan in the PCS poisoned mink. . ' - '- The occurrence of liver damage la miu which also developed hemorrhagic teudis eles suggests s breakdown in hemeatau in which prothrombin deficiency may to causative factor. Blood coagulation stud* should be made In future research on PC poisoning In mink. Splenic cnlargnau and increased numbers of megaksryoeyt in the spleen may represent compensate responses In attempts to maintain hew stasis. The causa of the disseminata* I travnscular coagulation scan in tha tha mink is unknown. Hormonal effects PCB may have beau responsible for t reproductive failure. The pretence at e> pora lutes In tha ovaries of the mink whi died during or immediately after tbu * mat gestation period indicates that an tion did occur but that gestation did continue to term. Fatty degeneration of the liver end H necrosis has been described in othar t ciee treated with PCB compounds, generative kidney lesions alto have I 398 Can. J. comp, h MOMS 083839 /^,/bcd In other specie* by tome work- Geissinger (8) reported on the effect o{ *%. Plutonow it at (9) have described pe ora! administration of PCB (Arnclnr rivascular hemorrhages * round coronary. 1254) in the adult boar. The doses of PCI! arteries In the hearts of chickens fed Aro- were such that no grots'or histological It- ctor. The coronary arterial lesions seen in sions could'be seen. However, the presence three of the mink in these experiments are of significant biochemical alterations were unexplained but thought to be related to the recorded. These changes consisted In dra*- - PCB feeding, since lesions of this typo have tic reduction of urinary levels of twv gotta- not been seen by the authors previously. dal hormones: dehydroepiandrosteronc and Their appearance in two of three mink estrogen, indicating that PCB have a dc- . which died between days 10$ and 129 of leterious effect upon reproductive activity. PCB feeding and in one of four mink killed The primary site of o.p'-DDD inhibition of on day 160 may mean that lesions in these ACTlI-induced steroidogenesis In the udrv- ' i vita! arteries develop as. a late response to nil cortex appears to be on the ACTii- low-level PCB ingestion. This should be in- regulated intramitochondri&l conversion of vestigated further in mink and also in cholesterol to pregnenolone (4). Since the other species. . chemical formulae of PCB's art similar to . , The poor reproduction In the no-treat that of DDT, It is possible that the hor ' ident controls may be referable to the low monal disturbances due to PCB are located . '(0.3 ppm) but significant amounts of PCB at the same site. At least this is a prob found in the control commercial ration. The able site of PCB effeet in the boar. W- controls, therefore, actually were an un* cauee pregnenolone is a precursor of do- 1 planned lower rCB treatment group of hydroepiandrosterone in ateroidognJ, ' mink. Lesions referable to the PCB con In comparison to domestic animals tg, . tent of the control ration were not seen in 9, 10, 13) mink seem to extensively meta , the mink from this herd which were used bolize the PCB, Aroclor 1254 used in this . ' for research on aleutian disease during experiment. The changes occurring on the . ' the course of these PCB experiments. Tho chromatograms of various tissue extructn ' ; low concentrations of dieldrin as well as indicated significant reduction of the first * . DDT and its analogs and metabolites In the eight- peaks, with simultaneous lnvrmrs control ration are for all practical purposes of the peaks emerging thereafter. The of no toxicological significance. order of appearance of peaks on the PCB * * . It has been suggested that PCB affect chromatogram is related to the extent of % enzyme systems that metabolize several chlorination of biphenyls. Thus, mwHt* ' ' ex hormones, which ultimately leads to chlorbiphcnyls appear before dlchlorobl- reproductive failure. Thus. Risebrough it phenyis. trlchlorobiphenyls before tetn- I (11) reported -that the PCB Induce the chlorobiophenyls,. etc., and decathlon*- activity of hydroxylnting enzyme which biphenyl (the completely ehlorinuled ^ metabolises estradiol. The estrogenic acti biphenyl) emerges as the last peak. The * vity* of various PCB mixtures upon the rat reduction of peaks of lower retention in uterus was described by Sitman and Cecil dicates that mink can metabolize PCI! of . ^ . (2). Platonow and Funnel (7. 8) reported lower chlorination numbers. Since this n- "f' ' that chronic feeding of PCB in cockerels ductfon in faster emerging peaks la much * resulted In anti-npdrogenlc effects, as less pronounced in the cow (13). pig fM*# ` assessed by decreased development of tes or chicken (S), one might'suggest that the ticles and comb. These signs appeared as extent of PCB metabolism Is related to the esrly as one week after the start of con extent of susceptibility to the toxic effect tinuous feeding of a PCB-contamlnatcd of PCB. Mink appear to be mere susceptible diet. to PCB than the domestic animals stutluM. It was recently demonstrated by No However, further studies are required to wick! and Norman (6) that the post-mito- confirm or reject the above hypothesis. chondrlnl hepatic fraction (microsomes ~f cytosol). from PCB-trentcd cockerels and i pullets metabolized testosterone, estradion' 17/J and 'l-androsteiic-3. 17-dione at in ACKNOWLEDGMENTS ' creased rates. The metabolic rates of these ( three natural steroid hormones were ln- The authors are grateful to Drs. Joan . creased approximately three-fold over ` Budd and Peter Lusis for assistance in nv- ! untreated birds. Platonow, Liptrap and cropsifs, to Mrs. N. Y. Chen for performing Vol. 37 -- October, 1973 399 MGNS 083840 .J I ,te analyses of'PCE, and to Mr. Hush Bel- : elicr fur curd of the experiment*) mink. The htstii|uithulo|c.v wu dune while the junior KOWIfKI H C,*an4 A. W. NONMaV. K^,.n^4 nritalic MrlsslwtM.fi of mtuMdone. t-rMnuni.l lis<1lRt. tail t*tradiMl0 in cMahvn ittHttaM Ilk i*DT or PCII. Slotnisla IM rVI'm). la*}. PI.ATONOW. N. ft. and II. ft. flNNLl.L. AniLnn. jiuthur was visiting professor at Utah v! 4ti*sAlf.||i,* afloat mf WrcMorieMtnl Ut*nrla I* Cnrltrrrlo. Vrl. M*r.>4li 104.110. W||, State' University. " -- PLATOXOW. >. S. and II. ft. PCNNEI.I. Tit* 41*. * trihuliwn ami avma rffr.to vf petiycMurinatad WfMtfk nyla lArarto 1994* in ctb#raia during ar.ilaniad (vnlinr trial. Can. 4. rama. MM. 941 rm.L i it] . PLATOXOW. ftH L. M. KARftTAO and f. W. HCrCREKCU ftASClIKNUHCrKitK. TU*u# dWiriWitnn f m4T thlaHnaiM blphssnyU (ArwhH 1394 in tMktnlai Krlalfcm la tit* durntitm of tiRwart and akaarva* lit-a nn rntMr. Con. J. f**mn. M4. 3Ti M.RJ. |tj. I AitMOrn. J. A> and J. As Il'RKL Method for 10. Pt.ATONOW, N\ 4, ft. >1. LIPTMAP and ft. . isatatiar *I>'rhlMiA*'i WphanyU from DOT and GCIftftlXCGK. THa eUatribwtlnn and ancratiam of , J. Aits off. inilfl Chem. Ot '(!?(). polyrMarinatrd bipkanrla tArualar IIi4i and Mart* tl.irt nn urinary uanadal steroid lavafo in tKa boar. niTMAN's J* ( CECIL- btrotmle *' ,,,-,iii,GTr*anoa>taoumM.aa ikaintiupoomlyeinMst.it-tfiimatrd. blfthcnyla. J. 11. lKltltfltlL. UrRnOvllr'.CHC.onKta.inW. .T,onri.c. ? 94k.9\ REICHK. 0. 1*19, R. PEAK. ALL. ft. C. HERMAN' and 91. X. KfftVRX. pl,. , 1.1`ast. n. u 'V. e. j. Phillips **< d. c. VILLEXEI'VL. Mataboliani ( p*bMurinaid Ll chlorinated blrhanyU in th* rtotal atuaratam. jiia. tut. Land. !J4t IMIUHt]. 1944. >krkl I Art*lor 1311* mUlori In tkt rat. livIL an* . IS. ftASCHLNVKCCKEIL P. W. and D. J. RCOfllCHOX. t<. Cam**. I: uS-lll. 1411. Extraction and raa chraRWltritiMt anabtlt f 4. MART. Ms Ms on# Is A. STRAW. Studln n the alia rblorlnatrd Jn.actlrMt* from animal tUaoo. J. aarta. Miloit tf o.ft'sDDD in tkt d*i adrenal carta*. |. Pd Clttm. 19: 1'.4.110. INI. laMbltl-m wf ACTM.*Jlntad preanamalane arntheoia. tt. SAUCIIKNUItECKtM. P. W,, ft. ft. PLATOXOW and H-erxI.la l?i MMII. 1**1. H. 8. FUN'NELL Mutkalit aittdy af paiyihlurlftniad I( LII.IC. R. D. Allatkramt tula. Am. J. din. Kalb. biphanyla In Witatin* aanra. pta*. Can. Kti Mai. l i 444. iUL Saa. 14* 44. Hit. / MOMS 083341 /