Document 1gZvyZ3Y5ZBey1MBZYX91YQ2o

Ing water * (^3 mg/day given for 10 wk)* inclusions are not observed by light oiieroscopy in the renal tubular cells. The Pb content of kidneys from such rats is only 2-3 mg/g of wet weight, while in this experiment (intake of 150 mg/day) the kidney was 30-70 pg/g of wet weight* Whether there is intranuclear complexing of Pb by proteins at a lesser dosage of Pb than that pro ducing observable inclusions may be important with regard to the cellular metabolism of environmental Pb or the chronic body burden of Pb endured by the present population, (26 references) 630. Hatch, R.C. > and F unriel 1, B.S, (Univ* Guelph, Ontario, Canada);?V/ LEAP LEVELS IN TISSUES AND STOMACH CONTENTS OF POISONED CAT^E: : A FIFTEEN-YEAR SURVEY. Canadian Veterinary journal 10:15^62 (Oct.), 1969. yT r Following a review of reported values of Pb in tissues of /ttle poisoned through various sources of Pb, the authors describe their' study designed to reassess the diagnostic significance of tissue pb odncentrations and to determine the need of testing rumen contents. During the period 1954-1969, random samples of/lngesta, liver and kidney from 175 cattle in Ontario whose death was mop likely due to pb poisoning were analyzed for Pb content, A modification of the method described by Sandell (1944) was used. Diagnosis was hUsed on reported clinical and postmortem findings: Diarrhea, colic,^Central.nervous system signs, motor abnormalities , congestion/r hemorrhages in the gastrointestinal tract, kidney, neart, brain, lungsy&t omentum, and "pulpy11 kidneys. Spleen or liver. No grphping of the capL& as to age, sex, breed or duration of 'Pb exposure was possible, For/^hls reason, the data of this survey were based on random samp1 eXfrom/the referrals. Among -the 175 referrals strong ly supporting pb poisonirfp/ 15$ kidney samples (cortex 4* medulla) averaged 137 ppiii Pb (2-2355); in/5,9%^ levels 425 ppm found in the cortex were re* garded as being of diagnostic Xignificance. Liver (170 samples) averaged 43 ppm (0* 1300) * Ipfiesta of 13JN^howed wide variation: av 3427 ppm (0(in 6/146,200)/ As tabulated, kidneys of 80%'of the dead cattle contain ed 1-200 ppm, 80% showed 0-50 ppm inOLiver, and no characteristic range of Pb levels could be associated with th/lngesta samples. The authors con* elude that the survey supportsthe opinibri that Pb accumulates predeminently in the kidneys of Pb-poisoned cattle. Liver and other tissue may be free of Pb despite fatal poisoning, Therefore, the mere presence of Pb in the kidney (or liver) and ingesta should lead to a presumptive diagnosis of Pb poisoning in cattle which die with signs, lesions, and histories character istic of Pb poisoning. Diagnosis may be confirmed by proof of access to,, or ingestion of, a source of Pb, 631, Hopkins, A* (Inst. Neurology, Queen Sq., London, England) : EXPERT- ' > / .MENTAL LEAD POISONING IN THE BABOON, British Journal of Industrial y Medicine 27:130-40 (Apr.), 1970. ------- ( This study" was undertaken because the nature of Pb palsy remains obscure f 4 in Spite of much animal experimentation. The reason for this is the differ ing response of different species to Pb, The author therefore chose the baboon as representative of a species .closer phylogenetically to man, Twelve baboons (7.2-13,6 kg weight), 9 females (judged to be >4 yr) and 3 males (on basis of weight, not full grown); and 3 infant females (2.8-3,3 kg) were 277 N37518 Abstr, 631 IV, Observations on Warm*Blooded Animals observed for at least 3 mp before Pb intoxication by intratracheal injec tion of a suspension of Pb carbonate, to assure the most complete absorp tion of Pb (suggested by Minot, 1924), The usual dosage was 1 g/ml, equiv alent to 50-135 mg/kg initial weight; the infants received smaller amounts, but dose/kg was the same; 1 baboon received a single dose of 105 mg/kg; in repeated dosage, 1 injection was given every 3 wk, although modified as required according to condition of animal or blood Pb, The procedures and methods used are described in detail; Pb was determined in hemolyzed whole blood by Pelves and Vinter *s method (1966), Ten animals were studied until death (39-265 days after 1st injection), mean survival was 120 days; 2 were killed after 336 and 362 days. Blood pb,'determined before Pb treatment oil these and 12 other healthy baboons used in other studies, gave a mean of 11,7 p.g/100 ml (3*-27, SO 5,5); 87% were <16 ug. In the baboon that received a single dose, blood Pb rose to a peak of 310 pg/lOO ml by the 4th day; it Remained at this level for 7 days, then declined exponentially, remaining >100 pg/100 mi for at least 24 days. The most striking finding in all animals receiving repeated injections was the loss of weight in spite of normal appetite (5 lost 40%, 1 lost 46%, and 5, 257*). Pb line was seen in none. Eight baboons had 1 or more fits (34 in all), and others may have occurred in the observers1 absence. The 13 fits seen by the author were of grand mal type; 2 began with focal seizure. The latter occurred in 1 baboon 149 days after beginning of poisoning* Paresis of limbs occurred in 3, associated with fits or other signs of encephalopathy, and thus were believed to be of central origin. Fits were particularly frequent 4-11 days after .an 'injection of Pb, when the blood pb reached its peak. All 5 baboons which began convulsing in this period died during .1 of a number of immediate* ly following seizures; in the 3 survivals, convulsions occurred 23-29 days after'injection, while blood Pb was falling. There was no clear relation ship between blood Pb, which rose as high as 4550 jig/100 ml, and other signs of poisoning, ie, weight loss * hemoglobin levels (Hb); as to the latter , results of 136 analyses of blood Pb, grouped into 100 ug/lOQ ml up to 10.00, 1000-1499, 1500-1999 and >2000, plotted against Hb levels showed that there was no significant decrease in Hb with increasing blood Pb. As determined by nerve conduction velocity (16 times) in the median, and anterror tibial nerves of 6 baboons 35-346 days after 1st Injection, electromyography, and preliminary histologic examination showed no abnormality of the peripheral nerves. In the 3 infant baboons, loss of weight occurred in all. They became, progressively more wasted and timid. No fits were observed, Mb decreased to 66 and 797. in 2; 1, still gaining weight, died in 5 wk, No Pb line or stippled cells were observed. The tolerance for high blood Pb levels ob served in the adults did not apply to the infants: 2 that died on days 75 and 117 had highest blood Pb of 560 and 140 pg/lOO ml; 1, sacrificed on day 150 with no signs save weight loss, showed 230 jj.g/100 ml. In discussing the results, the author reviews extensively the literature, pointing out the species differences; these are illustrated in a table, listing man, guinea pig, rabbit, rat, baboon, dog, cat, and their response to pb in anemia atid stippled cells, encephalopathy, palsy, changes in anterior horn cell, Wallerian-type degeneration, and segmental demyelination. In conclusion, he states that the findings in various species do 'not throw any light on the metabolic lesions produced by Pb in the red Cell 278 DUP050044016 Abstr, 632-634 IV, Observations on liariu-Blooded Animals . precursors and in the neurone or Schwann cell, Even animals with clear histologic lesions in the nervous system exhibit obvious species'differences> eg, guinea pig and rabbit that develop a mild paresis in spite of extensive lesions in the peripheral nerves, and humans in whom sudden severe palsy may occur with relatively slight changes in the peripheral nerves, (43 references) 632., Lucas., 11.F*> Jr,, and Markun, F, (Argonne Natl, Lab. , Ill;) : THOROTRAST: AN INTRAPERITONEAL INJECTION, In Radiological Physics Division Annual Report July 1967-June 1968. US Atomic Energy Com- I mission Document No, ANL- 7489, pp. 30-3, ^ Thorotrast was injected ip into a male rat in a comparatively^farge dose (4 ml) to determine whether this technique would offer opportunity to study the translocation of rad forme lid es in vivo. The animaPwas sacrificed 280 days after injection (1085 das^s of age), Resultspresented in tables for urine and feces samples collected throughovip^fhe period, foir 228j>a and 22Sxh excretion rates, whole^bod^content, and^l^Bi, 2l2pb, and 228xh ip bloody bone, lung, muscleiv 212pb^^3Ui^s'pCi/g were: bone, muscle,: 0,6; lung, 2#0j blood, 41, The/authors concluded that the experi ment was successful and that even largmdoses would permit accurate evalu ation of the complicated me tab oi l s (jyof Thbrotrast daughters accurately. It appeared that 228jh. produced in vivo is excise ted at a higher rate than fol lowing an iv injection, \ 633* Ha tone, S>, Conternov G* * Ramello, A., ar*4 Pich, p.G, (Univ, Turin, Italy): E f f etto^enlla peniclllamina sullXeserezione urinaria del piombo neliJxntossleaz i one sperlmentale .\ (EFFECT OF PENICILLA MINE ON URINARY LEAD EXCRETION IN EXPERIMENTALC POISONING) Gazzetta Medina Italiana 128, No. 12:673-8, 1969. After a discussion of the work of other authors in which D~penicillamine was used as a chelate in the treatment of Wilson's disease and occupational Pb poisoning, the authors report their own investigations in^Kich they used 8 rabbits (3-4 kg) poisoned by im administration of 2jp/mg of a Pb acetate solution, injected every other day up to a tota^of 200 mg. Peni cillamine was given in 1 dose of 60 mg in 5 ml of a physiologic solution, Iv, repeated after 24 hr* Urine samples were collected before and after penicillamine. After 10 days,during which interval the animals were left untreated, a 3rd dose of 60 mg peniciMamine was given and urine samples were collected before and 24, 48 and 72'Sshr after the last injection, The urinary Pb excretion before Pb intoxication was 9 ug/24 hr. After the Pb intoxication, the average daily ufinary Pb excretion was 85 fig. After the 1st injection of penicillamine, excretion was 855 and 805 }ig/24 hr, and after the 2nd injection, 216 hr (10 days later) , The 3rd produced urinary Pb excretion rates of 801,. 426 and 279 \g after 24, 48 and 72 hr, respectively. From these data it is concluded that in Pb-intoxicated rabbits the admin istration of penicillamine causes a significant increase in the urinary Pb excretion. (30 references) 634, Nilova, N. A* , and Mambeeva, A.A. (Inst. Norm. Pathol. Physiol., Acad* Med. Sci, USSR, Moscow): Porazhenie slizistoi obolochki zheludochno-kishechnogo trakta pri svintsovoi intoksikatsii v eks- 279 .* ' DUP050044017 IV Observations on. Warm-Blooded Animals Abstr. 636 corresponding figures were: 0.99, 5.94 and 0, thus shading a difference between the 2 groups of 105.71 and 1.85 jig/g in red cells and white muscle, respectively, The .average urinary CP and ALA excretion in the treated animals was 2.75 mg/1 and 2.60 mg/100 ml, respectively* Presence of ALA dehydratase activity was observed in the red muscles (supplied with myo globin) but it was absent in the white muscles (without myoglobin); there was also marked inhibition of ALA-D activity in the erythrocytes in Pb poisoned animals while the muscular ALA-D showed no significant change even after prolonged administration of Pb. The;authors explain the different behavior of the enzyme in erythrocyte and muscle by suggesting that ALA dehydratase is present in both in the form of 2 different iso-enzymes or, that in muscular tissue, substances exist which are capable of protecting the enzyme from the action of pb. 636. Sauer, R.M., Zook, B*G., and Garner, F#M. (Natl. Zoological Park, ; Washington, D.C.): PEMYEtlNATlNG ENCEPHALOMYELOPATHY ASSOCIATED j WITH LEAD POISONING IN NONHUMAN PRIMATES. Science 169:1091-3 (Sept. t J, 11), 1970* The cases of accidental Pb poisoning here described were: I, a female Bar bary ape (Hacaca sytvanus) born and housed in an outdoor all-season cage until found dead at the age of 22-1/2 mo after having suffered intermittent convulsions for 18 mo; IX, an adult ted** faced macaque (Macaca speciosa) that'had lived in an outdoor cage for 11-1/2 mo until death following 2 days of convulsions; XXI, a juvenile male red-faced macaque was placed in an in door cage after a 6-wk quarantine in a galvanized cage* He developed a convulsion 8 wk later and was taken to the hospital; he appeared blind and had frequent intermittent convulsions for'6 days. Euthanasia was performed after a 2-day coma. Case IV > an adult lesser spot-nosed guenon (Cercopithecus nictitans), housed in an indoor cage during the winter and an ad joining outdoor cage during the summer for 2 yr> suddenly became paraplegic. A prolapsed intervertebral disk (Ti2~Ll) was diagnosed and euthanasia perform ed 2 wk after the 1st clinical signs* Upon necropsy, gross findings were unremarkable in cases X and II; in III, swelling of the cerebral cortices were evident, and in IV, prolapsed inter vertebral disk was confirmed,, with no obvious compression of the spinal cord. In X, XX, and III, in which the clinical signs were primarily amaurosis and epilepsy, the histologic findings in the brain were characterized by prolif erative and degenerative vascular changes, edema, laminar necrosis, and demyelination. In Case IV, where sudden paraplegia rather than epilepsy was present, vascular lesions were minimum but bilateral symmetrical demy- elination was much more extensive. These were similar to those'found in idiopathic leukoencephalomyelosis of nonhuman primates occurring concurrent ly with amaurotic epilepsy. In the other organs, acid-fast intranuclear inclusion bodies were found in hepatocytes and renal px-oximal tubular epi thelial cells in all 4 cases. The Pb content in liver and kidney of cases X and XI was 110 and 65 and 120 and 90 ppm wet tissue, respectively; in III, 360 ppm in dehydrated, paraffin-embedded liver; in IV, 10 ppm in wet liver (spectrographic). The authors concluded that the findings suggest a new animal model for the study of demyelination and strengthen the supposition that Pb may be a fac tor in some idiopathic demyeiinating diseases. They also note that a de- 281 DUP050044018 Apscr, o3/ IV, Observations on Warm-Blooded Animals tailed study of a larger number of similar cases is being prepared for pub11 cation* (11 references) 637 > Schroeder, H.A,:, Kitchener, M, , and Nason, A,P,(Dartmouth Med, School, Hanover, N,B*): ZlRCONItM, NI0BIUM, ANTIMONY, VANADIUM] AND LEAD IN PJVTS: LIFE TERM STUDIES. Journal of Nutrition 100:/ 59-68 (Jan.), 1970, / To evaluate innate effects of the trace elements Zr, Nb, Sb, and V, and to reevaluate those of Pb, 603 rats of the Long-Evans strain were fed aydiet containing relatively small amounts of these elements in an enviromlent reasonably free of trace contaminants. Groups of 100 or morel diyoded as to sex, were given 5 ppm (as metal) of the 1st 4 ions, and 25 ppm Pb (males only) In drinking water from the time of weaning until naturai/neathj and compared with an equal number of controls. Cr, 1 ppm, was ir/the water. These doses were tolerable for growth which was enhanced fr^the male Nb group# Innate toxicity in terms of life span and 1ongevit/oc curred in the Sb groups. in these rats, nonfasting serum glucose level's were lower than fasting: levels. Serum cholesterol was abnormal in the db and V groups. Sb and pb accumulated in soft tissues, the former wlti/age, Considering the dose use'ifyNjie accumulation of Pb in soft tissues" was surprisingly small. Meqn values were, in pg/g: Kidney, 2,65; Liver, 2.06; heart, 1.28; lung, 1.04; spleenV 1.04; total mean accumulation yi.71 pg/g of tissue,, wet weight, \ / Glycosuria was found in 23% of 90 controls, kmi of 23 in the Sb group, 52% of 56 in the Zr grqup, 63% of 16 in the Pj/group, and in 717o of 24 in the V group. No significant differences in oteinurla were found between the several groups, \ / None of these 5 metals was tumorigenicy' There were more than twice as many tumors in females as inSmales. No/metal significantly suppressed the incidence of tumors, Blanehirik of inorsor teeth, which has occurred in a number of older rats, was found on the various groups with the following frequencies: Zr 7, Nb 5, Sb 5, PoSS, V 9 and controls 12. It was somewhat more prevalent in females than iiymaLes* There were no significant difference's from controls in Zr, Nb, Pb and V groups for survival and longevity. Pb-rfed males lost weight from 24-30 mo of age and their coats were poor, the onlySsigns of toxicity, A previous series of Cr-deficient rats/given the same abse of Pb showed early mortality, shortened life span and decreased longevity* rn the Cr-supplemented rats of this study, Pb was not: toxic to males in terms of growth and. survival (median age of 52 males^ 883 days). As mentioned^bove, there was a re markable resistance to^accumulation of Pb in the soff tissue of these rats* Although bone was not analyzed, this tissue probably\jtored Pb, as 91% of the Pb in the human body is in bone. Whether the Of-deficient rats of the 1st series of pb-fed rats can be compared with the present aeries of Cr-supple mented rats is problematical; however, the diets and regimens were identi cal, the rats were of the same type and other criteria were the same. If the profound differences in mortality between the 2 series can be accepted, it appears that Or protects against innate Pb toxicity. If any of the 5 trace elements in this study are essential for rats and mice, they are required at concentrations \!ess than those present in our diet. There is no evidence, however, that Sb and Pb are essential elements. (16 references) . ' ^ ^ 282 DUP050044019