Zinc Absorption, Metabolism, and Endogenous Excretion in Zinc-Deficient and Normal Calves over an Extended Time' W. J.

MILLER, D. M.

BLACKMON,% R. P. GENTRY, and F. M. PATE3

Depamnent of Animal and Dalry Science University of Georgia Athens 30602 ABSTRACT

INTRODUCTION

Zinc metabolism was studied in Zndeficient and control Holstein calves over a 2-mo period following a single oral or i.v. 65Zn dose. In both orally and i.v. dosed animals, all gastrointestinal tissue sections from &-deficient animals contained more 65% than comparable tissues of controls. Contents of proximal small intestinal sections of Zndeficient calves contained more 8 to 10 wk after dosing than did those from controls; however, the reverse occurred in the distal small intestine, cecum,and large intestine. With both dosing methods, Zndeficient calves retained more 652, throughout the study. Daily 6 5 2 , excretion rate as a percentage of that retained declined for 6 wk after dosing, indicating a constantly increasing biological halflife. For deficient calves, the biological half-life was about 500 d in the later weeks of the experiments. In orally dosed, Zndeficient animals, specific activity of fecal 65211 exceeded that of serum Z n throughout the study. This shows a shortcoming in the basic assumption of measuring endogenous Zn loss from fecal and serum specific activities and total fecal stable Zn. Thus, endogenously excreted Zn is not representative of that remaining. (Key words: zinc metabolism, endogenous zinc excretion)

Zinc deficiency has been characterized in ruminants, and 65Znhas been used in several studies to investigate its metabolism in normal and Zndeficient ruminants (4, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 18, 19, 20). Zincdeficient nuninants absorb a higher percentage of orally administered 6 5 ~ nthan do normal Znmplete animals (8, 9, 10, 12, 14, 19, 20). Endogenous fecal loss is reduced in the Zndeficient ruminant (8, 9, 10, 13). In normal animals, decreasing dietary Zn content increases 65Zn absorption and lowers endogenous fecal losses from i.v. injected 65Zn(8, 9, 10, 13). However, none of these studies extended beyond d 28 after administration of 65Zn. This study investigated 65Znand stable Zn absorption, metabolism in the gastrointestinal tract, and fecal excretion in Zndeficient calves in comparison with controls fed a Zn-adequate diet using both i.v. and orally administered 652, in separate experiments. The experiments continued for 8 to 10 wk following single oral or i.v. doses. Another objective was to determine whether the classical methods of studying endogenous mineral excretion based on specific activities in serum and feces (5, 24) are applicable to Zn. MATERIALS AND METHODS

Received February 28, 1991. Accepted M a y 31. 1991. 'Supported in part by state and Hatch funds allocated to the Georgia Agricultural Experiment Stations.

*Department of Large ~nimat~cdicine. 3Resent address: Agridtural Research Cmter, University of Florida, O m 33865. 1991 J Dairy Sci 7435353543

Two separate experiments, each involving a different group of six intact male Holstein calves, were conducted using tracer doses of SLSzn to study its metabofism in &-deficient and control animals. Three calves in each experiment were fed a Zn-deficient diet. Except for dilution with 5 kg of granular polyethylene/ 100 kg, which was added to improve handling properties of the feces, the basal deficient diet was the same as that described previously (17). It consisted of the following (per 100 kg):

3535

3536

MILLER ET AL..

glucose monohydrate, 19.5 kg; cornstarch, 25.0 kg; dried whole whey (spray process), 20.0 kg; cellulose, 10.0 kg; gelatin (flake,50 bloom), 10.0 kg; egg albumen (autoclaved), 3.0 kg; urea (feed grade, 42% N), .5 kg; KHCQ3, 1.5 kg; NaHCO3, 2.5 kg; dicalcium phosphate (anhydrous, food grade), 2.0 kg; CaCO3 (marble dust), 1.0 kg; lard (stabilized), 3.0 kg; NazS04 (anhydrous), 350 g; KCl, 550 g; NaCl, 484 g; MgO (56% Mg), 165 g; Fe2(S04)3,H20 (20% Fe by assay), 22 g; MnSO4H2O, 4.4 g; CuSO.4, 3.1 g; COCO, (45 to 50% Co by assay), 22 mg; KI, 18 mg; thiamheHCl, .9 g; riboflavin (50%), 2.0 g; dCa pantothenate (45%), 3.3 g; pyridoxineHCl, 1.1 g; nicotinic acid (USP), 2.2 g; folic acid (USP), .22 g; cyanocobalamin (1 mg vitamin B12 activity/g), 2.2 g; menadione sodium bisulfite (63%), .33 g; D-biotin, 26 mg; D-utocopheryl acetate (333 IU vitamin E activity/ g), 2.2 g; vitamin A palmitate (325,000 IU/g), 17.6 g; vitamin D3 (200,000 lU/g), 2.2 g; choline-Cl (70%), 264 g; and oxytetracycline (5.5%), 88 g. By analysis, the basal diet contained 4 ppm of Zn. The control diet was identical except for the addition of 40 ppm of supplemental Zn as ZnO. Prior to the experiments, animals were fed a practical diet, including milk replacer for 2 mo and calf starter until 2 to 3 mo of age, and the experimental diets thereafter. In the first experiment, 3 mo after animals were placed on the experimental diets, a single tracer dose of 65% was given orally via gelatin capsules. Likewise, in the second experiment, a single tracer dose was administered i.v. 4 mo after initiation of the experimental diets (13). Throughout both experiments, deficient animals were fed the Zndeficient diet with occasional limited amounts of control diet to prevent an extreme deficiency, which probably would have resulted in death. Within each study, the diets were fed in restricted amounts to limit weight gains so as to maintain the calves at relatively comparable sizes. Average Zn content in the diets fed to deficient calves after 65Zndosing was 6.7 and 8.2 ppm for the fist and second experiments, respectively; an average of 6.7 and 10.5% of their feed intake was the control diet. In each experiment, calves were adjusted to metabolism crates 7 d before dosing. The 65Zn content of the oral and i.v. doses were 540 and Journal of Dairy Science Vol. 74, No. 10, 1991

522 pCi, respectively, and each had greater than lo00 pCi of 652n/mg of Zn. Within each experiment, serum and tissue 65Znconcentrations for individual animals were adjusted to a uniform dosing level per unit BW of 107 kg (Experiment 1) and 150 kg (Experiment 2) as described reviously (12). Total 6pZn retention was determined by subtracting the fecal 65Znexcretion from the administered dose. This is feasible because the amount of 65% excreted via urine or other routes is very small (9). Total fecal collections doswere made daily for 17 d following ing. Subsequently, total fecal collections were taken for a 3 d period each week. At various intervals after dosing, jugular vein blood was obtained by gravity flow into glass tubes. Within 2 h after blood collection, serum was secured by centrifugation of the coagulated blood for 65Zn and stable Zn analyses. Calves used in Experiment 1 averaged 158 d of age and 107 kg of BW at dosing. They were killed at an average weight of 103 kg, 70 d after dosing. Animals used in Experiment 2 averaged 210 d of age and 150 kg of BW at the single i.v. dosing. When killed 56 d after dosing, they weighed 144 kg. Immediately after killing, designated sections of the gastrointestinal tract were carefully tied off to prevent movement of contents. Then contents of the reticulorumen, abomasum, duodenum (first 1.8 m of small intestine), small intestine 2 (second 1.8 m of small intestine), small intestine 3 (center of small intestine), cecum, and 1 e intestine were collected for drying and 3Zn analyses. To minimize mucosal cell sloughing, the intestinal contents were removed carefully from the intestinal tract sections with a very gentle milking action intended to resemble the natural peristaltic action (2). Gastrointestinal tract tissues were sampled as follows: 1) rumen, left aspect of dorsal sac; 2) abomasum, fundic; 3) abomasum, pyloric; 4) duodenum, first 1.8 m; 5) small intestine 2, section between 1.8 and 3.6 m from abomasum; 6) small intestine 3, 1.8 m from center; 7) cecum, 50 g from center, and 8) large intestine, 50 g from center. The intestinal tract tissues were M s e d thoroughly with .9% NaCl to remove any remaining contents. Total Zn concentration was determined by atomic absorption spectroscopy with nitric-

ZINC METABOLISM

3537

IN CALVES

TABLE 1. ?he 6%n of gastrointestinal tract times from a-deficimt and control animals 56 and 70 d after single i.v. or oral dosing.

Deficient

Control

Tissue

i.v. (56 d)

Rumen wall2 Abomasum. fundus

305 4%

D L I O ~ ~ wlm U ~ ~

.455 .602

small i n t e s ~23 small intestine 33

.382

CCCUm

585

Large intestine

.388

.415

oral (70 d)

Average

iv.

oral

(56 d)

(70 d)

(k of retained dose& of fresh tissue) .463 .634d 1.080 353 24.8 .372d 1.013 .627 250 .35Zd .854 M 8 .818 .455 .238 .42& 349 A38 .240 .31Ib 249 .33Zd .696 .467 A86 .932 .320 .45Zd .571 235 .31Zd $24

Average

SE'

CV

.96@

.061 .058 .@I5

13.3 17.0 13.9 15.7 26.9 13.4

.82@ .75@

.6W

.m

.048 .062 .035 .066

.69F

.068

.494'

.58F

16.8 23.5

4bSignatcant difference control versus deficient (P < .OS). c-dSipnircant dafcrence control versus deficient (P < .01). 1, = 3. %issue "Zn concentration data for individual animals wem adjusted to a uniform dosing level pes unit of BW (12). h o d m u m , first 1.8 m of small intestine. Small intestine 2,section between 1.8 and 3.6 m from p r o w end. Small intestine 3, 1.8 m from center.

perchloric-sulfuric acid wet ashing of samples. The 6sZn activity of samples was determined on an automatic gamma test tube changer system with NaI (TI) well crystal (model 709; Baird Atomic, Inc., Cambridge, MA). Specific activity data were calculated as the percentage of 65Zn excreted per unit weight of Zn, rather than in terms of absolute radioactivity, because of the greater usefulness in biological interpretation of the data. Data were subjected to a statistical ANOVA (23) using P < .05 and P < .01 to declare significance. The major source of variation of interest was control versus Zn-deficient diet within the i.v. and oral dosing experiments. Because the interactions between diets and dosing methods were not significant, the means for control and deficient diets were combined across experiments. The i.v. and oral 65Zn dosing data were confounded with other variables that differed between the two experiments. Because it is well known (8, 9) that a variable portion of orally given Zn is absorbed, determining effects between experiments was not an objective of this research. RESULTS AND DlSCUSSlON

The content in tissues of sections of gastrointestinal tract of Zndeficient animals

was substantially higher than in controls of

both oridly and i.v. dosed calves (Table 1). Each of these tissues from i.v. dosed animals had more %n than the comparable tissue in those orally dosed. The magnitude of the effect appeared to be similar in various tissues (Table 1). Specific activity on the gastrointestinal tissues shows the same treatment effects and patterns as the 6 5 ~ ndata (Table 21, because there were only minor differences in stable Zn values. Other research has shown that the total Zn concentration of most cattle tissues is not greatly affected by a Zn deficiency (9). The differences in 65Zn data between orally and i.v. dosed calves reflect the well-known fact that not all orally administered Zn is absorbed (9). Also, there were other differences between the two experiments, which were conducted at different times. The 6 5 2 concentrations in contents of various sections of the gastrointestinal tract at the time of killing are presented in Table 3. The duodenal contents contained much higher amounts of @Zn than did reticulorumen and abomasal digesta, suggesting far more endogenous secretion into the duodenum. Proximal sections of the small intestine from Zndeficient calves contained more 6 5 ~ nthan contents from control calves. However, contents from control calves had higher amounts in the distal portions of the small intestine, cecum, Journal of Dairy Science Vol. 74, No. 10. 1991

3538

MILLER ET AL.

TABLE 2. Specific activity of gastrointestinal tract tissues from Zudeficient and control animals 56 and 70 d after single i.v. or oral dosing.

Control Tissue

i.v. (56 d)

Deficient

oral (70 d)

(96 of retained Rumen wall Abomasum, fundus Abomasum, pylorus Duodenum3 small i n t a k 23 small intestine 33 CecUm Lame intestine

32.4 33.0 33.0 35.1 28.3 30.2 33.6 24.3

i.v. (56 d)

Average

16.2 14.9 19.3 15.4 17.3 17.0 20.5 16.8

24.3d 22.6d 26.2d 25.2d

22.8b 23.6d 27d 20.6d

%JI

oral (70 d)

dosJg of a)* 53.3 35.4 61.8 39.0 52.9 44.5 54.0 30.2 47.0 29.3 45.9 34.6 40.3 54.1 50.9 38.4

cv

Average

(96) 44.4' 50.4'

48.F 42.1' 38.2= 40.2' 47.2'

44.e

1.7 3.1 3.1 3.4 4.1 3.6 4.6 6.3

8.4 14.6 14.5 17.6 23.1 19.5 21.3 33.4

qbSignificant difference control verms deficient (P < .05). C*dSignificantdifference control versus deficient (P < .01). 1, = 3. specific activity data were adjusted to a uniform body size for individual animals (12). %issue "ZI 3Duodenum, first 1.8 m of small intestine. Small intestine 2. section between 1.8 and 3.6 m from proximal end. Small intestine 3. 1.8 m from center.

and large intestine. These data indicate a fecal Zn excretion by deficient calves. The higher endogenous 65Zn excretion into the up- substantial amounts of Zn reabsorption after per portions of the tract of deficient animals secretion into the gastrointestinal tract is conand higher subsequent reabsorption so that the sistent with results from other species (1). end result was a lower endogenous fecal excre- Likewise, the reduced endogenous fecal 65Zn tion of by deficient calves (Table 3). This excretion by deficient animals is in agreement does not necessarily infer that there is more or with earlier results in several species (1, 25). even as much total secretion of stable Zn into The lower endogenous 65Zn excretion sugthe upper small intestine of deficient animals. gested by the gastrointestinal content data for However, it does show that reabsorption is an Zndeficient calves (Table 3) is consistent with important factor in the reduced endogenous the much lower observed fecal 65Zn excretion

TABLE 3. The or oral dosing.

in gastrointestinal contents at k i u i in Zudeficient and control aaimals 56 and 70 d after single i.v Control

Tissue

i.v. (56 d)

Deficient

oral (70 d)

Average (% of

R W t l d C Ul Um

AbolMSW Duodenum2 Small intestine Z2 Small intestine 32 CeCUm h@ intestine

.022 .058 .3% .966 1.115 .286 .422

.150 .135 .%7 .860 .740 1.167 1.134

i.v. (56 d)

oral (70 d)

Average

SE'

CV

.132 .lo2 1.238 1.260 .819 342 .332

.039 .E7 .I59 .146 .161 .139 .163

62.1 47.2 28.6 23.2 31.8 45.0 50.8

rctaimd dose/kg of DM)

.086

.066

.o%

.034

.682 913

.932 .726 .778

.659 1.485 .433 .111 .197

.198 .171 1.818 1.034

1.205 .573 .468

(45)

'n = 3. No SigcSicant diffmnces of control verstls deficient (P .c .05). 2Duodernun,first 1.8 m of small m t t s k . Small intestine 2. section between 1.8 and 3.6 m fromproximal end. Small intestine 3. 1.8 m from center.

Journal of Dairy Science Vol. 74, No. 10, 1591

3539

METABOLISM IN CALVES

A

W v)

g 000

W v)

0

O.40

.c

I I

-0-

I

DEFICIENT CONTROL SE

w

LL

1

O

2z 6.00

g.30 -

5 4.00 w

I

LL -I

a

Q

I

.20 a

a 200

$!

ae

,,A'

i 'Z

--4,

k'

.I 0

0

20 30 40 50 60 DAYS A F T E R DOSING

.60

-

--c DEFICIENT

W 8-50 -9,

n 0.40 W

-

-0-

I

t

CONTROL SE

W LL

7 I

't

'

.A.

- 200 5

400

r . . . l

IO 20 30

DAYS AFTER DOSING Figure 1. Daily fecal excretion rate aftcr single oral or i.v. dosing in &deficient and normal calves expressad both as a percentage of retained dose and as biological @mot) half-life in days. Biological half-life in days was calculated asSaming that feces was the only route of 65Znloas. (A)Oral dosing, (B) i.v. dosing SE calculated from m o r mean squares, n = 3.

s

and longer biological half-life (Fi ure 1, A and B). However, endogenous fecal Zn excretion was negatively related to 6% concentration in the gastrointestinal tract tissues. Likewise, total stable Zn was not greatly or consistently different in gastrointestinal tract tissues of Zndeficient and control calves. Thus, it is apparent that amounts of endogenously excreted Zn

or 65Znwere not directly dependent on level of or 6 5 ~ nin gastrointestinal tract tissue. Rather, it would appear that amounts of readily exchangeable Zn may be the controlling factor (9, 10). This fraction is lower in deficient animals (3, 9, 10). Percentages of retained body burden of 15~Zn are shown in Figure 2, A and B. These Joamal of Dairy Science Vol. 74, No. 10, 1991

3540

MILLER ET AL.

at a slower rate for several weeks, indicating a constantly decreasing turnover rate. The slower m o v e r is caused by y t e r average tissue affinity for Zn. Daily Zn excretion did not reach relatively constant values until at least 4 to 6 wk after dosing. These data suggest that it takes a very long time for absorbed or injected Zn to equilibrate with the body Zn pool(s). The daily rate of 65% excretion, calculated as a pexentage of retained dose, also was expressed in terms of biological half-life (right-hand scales of Figure 1, A and B). Because feces were the only quantitatively important source of loss, this provides a relatively precise method of determining biological half-life. The biological half-life of 6%n was much longer in Zndeficient animals, and the effect was more consistent in i.v. dosed animals. The values are in reasonable agreement with those observed in humans (21, . x r . z x 22). The 65% specific activity, expressed as perDEFICIENT centage of the retained dose per gram of Zn,is I.V. --*CONTROL presented in Figure 3, A and B. Specific activ20 I SE ity of 6 5 ~ in n feces followed patterns similar to those for the m y 6 5 ~ nfecal excretion, because changes in fecal stable Z n did not exIO 20 30 4 0 5 0 6 0 hibit a definite time pattern. Serum %n speDAYS AFTER DOSING cific activity from an i.v. dose was consistently Figare 2. Total "20 retention with time after siagle higher in Zn-deficient animals, (Figure 3B), oral or i.v. dosing in Zn-dcfiiicnt and normal calves as from admiaistaed but the treatment effect was less consistent determined by suMrectiug fecal dose. (A) oral dosing, (B) i.v. do-, SE calculated from following oral dosing. During the 5 6 d period after i.v. dosing, specific activity of serum error mean sqaans, n = 3. 65Zn declined at a decelerating rate (pigure 3B) with a similar although less marked decreased in orally dosed animals (Figure 3A). data were derived from the total administered Other studies have established that peak serum dose less fecal excretion. This procedure is levels occuz very soon after 65Znreaches the justified because very little 65% was excreted duodenum and that here is a considerable in urine of this study (total urinary excretion decrease for several days after oral dosing (12, for the first 15 d following dosing did not 19, 20). exceed . l % of the dose) or previous studies (6, Throughout both experiments, fecal Zn ex9). With both oral and i.v. dosing, Zndeficient cretion was far higher in control than in Znanimals retained more 6% than controls. h- deficient calves. Endogenous fecal Zn on reptravenously dosed animals retained more @Zn resentative days during the experiment (Table than those dosed orally. These effects of ex- 4) was calculated using the classical formula perimental treatments and dosing method are (5, 24): in agreement with previous results fiom shortterm studies (8, 9, 10, 12, 13, 14, 20). endogenous fecal Zn = Daily fecal 65Znexcretim data, calculated as a percentage of retained dose, are presented specific activity of fecal Zn in Figure 1, A and B. Following peaks that specific activity of S c m zn occurred soon after dosing, % ' n excretion declined very sharply for several days and then x total fecal Zn.

'--P-'f

-

Jonmal of Dairy Science Vol. 74, No. 10, 1991

ZINC

METABOLISM IN CALVES

3541

-

specific activity of fecal 6% that was always higher than that of serum 65Zn (Figure 3A), SERUM DEF which is contrary to the basic assumptions z -0- SERUM CONT cited. Thus, either all the fecal @Zn did not come from serum, or that derived from serum 1 SE FECES c3 was not representative of the Zn remaining. The calculated endogenous fecal Zn values 60 during the first 2 wk after oral dosing are not given because, obviously, for some time following dosing, feces contained an unabsorbed portion of @Zn. However, it is not reasonable 20 to suspect that unabsorbed 65Znwould make a dominant contribution to fecal excretion 2 mo after dosing (Table 4, Figure 3A). Likewise, there is no indication that the calculated enDAYS AFTER DOSING dogenous Zu excretion was either approaching a reasonable value (Table 4) or that relative + FECES DEF specific activities of 65Znin serum and feces 4- FECES CONT -C SERUM DEF from Zndeficient animals were changing a p +- SERUM CONT preciably, especially after 28 d following dosing (Figure 3A). Accordingly, an explanation 3 - L f SE FECES other than unabsorbed @Zn is needed. I SE SERUM A cotollary to the basic assumptions and methods for determining endogenous mineral excretion is that specific activity of 2h in urine may be used instead of that in serum (5, 24). 301 In an earlier study from our laboratory, 65Zn - 20specific activity data on urine and feces 10- I Figure 3 of refemnce (13)] were available -,---* , from Zndeficient goats. The specific activity was far higher in feces than in urine even 28 d after dosing Figure 3, A and B of Figure 3. Specific activity of 6%n in blood semm and reference (13)]. When these data were pubfeces with time after single oral or i.v. dosing in Znlished, we elected not to discuss the fact that deficient and normal calves. (A) Orat dosing, (B) i.v. dosing, SE calculated from error mean squares, n = 3. they were in direct contradiction to classical methods of determining endogenous mineral DEP = Deficient; CONT = control. excretion with isotopes and specific activity until confirmatory and longer term studies were made. Results of this report and the earlier studies (13) are in agreement. These The basic assumptions in this calculation are studies were unlike most endogenous Zn exthat endogenous fecal Zn comes from the se- cretion experiments in that Zndeficient diets rum and that the specific activity is the same and animals were employed, resulting in a far as that of serum Zn. Calculated endogenous less than normal endogenous fecal Zn (1). This fecal Zn excretion means from control animals makes obvious a shortcoming of the basic of each experiment are possible and, pehaps, assumptions embodied in the classical method within a reasonable range (Table 4). However, of determinjng endogenous fecal mineral exseveral calculated endogenous fecal Zn values cretion (5, 24), which may not be apparent or for iv. dosed Zn-deficient animals, although quantitatively very important with usual diets having adequate mineral content. possible, are high relative to total fecal extion. Thus, their reasonableness is doubtful. CONCLUSIONS All calculated endogenous fecal Zn excretion values for orally dosed Zn-deficient animals Fecal endogenous 65Zn from Zndeficient are impossible (Table 4). This results from animals did not have the same specific activity I

#

L

A

+ FECES DEF

“i

*.

J o d of Dairy Science Vol. 74, No. 10, 1991

3542

MILLER ET AL.

TABLE 4. Calculated emlogenous fecal Zn e x d o n in Holstein calves fed Zn-ddicient or control m e d diets followinn i.v. and oral dosinn.

Intraveaoas dosing DW dosing

Fecal

zn

Endogulousl

d

m

Zn excretion

*

Days dosing

Oral dosing

al

Endogenous1

excrctim

Zn excretion

Fecal

(mg znld) Control 16 23 36 51 Deficient 16 23 36 51

(mg W d )

50.8 63.7 65.6 78.0

12.3 11.0 9.8 13.7

16 30 59

8.0 6.2 16.2 6.5

5.3 5.2 3.9 3.8

16 30 44 59

44

32.3 142 26.6 46.3

22.1 7.6 6.8 11.6

4.2

6.8 13.6 10.7 9.5

5.4

3.3 5.7

qndlic acrivity of fecal zn 'Calculated by the formala: endogenous fecal Zn = sptciticauivi~0faamnznx total fecal Zn (5, 24).

as that of serum or urine. It appears that the Zn secreted into the intestine probably did not have the same specific activity as that in the serum. However, one possibility is that a quantitatively important fraction of serum Zn has a very slow turnover rate and, thus, does not exchange with the 65Zn to a major degree, even over a 2-mo period. This is supported, indirectly, by several types of information indicating that adequate readily exchangeable Zn is most important to normal Zn metabolism but that this fraction is a minor part of total body Zn (3, 8, 9, 10, 11, 14). For example, in rats, there is a dramatic alleviation of deficiency symptoms within 2 to 4 h when dietary Zn in amounts less than 1% of that in the body are fed (9). Likewise, in many tissues, 6% turnover rate is reduced with a Zn deficiency (1, 8, 9, 10, 11, 14). REFERENCES

M.C.E. Casey,and N.F. Krebs. 1986. &.Page IinTraccelemeatsinhumanandanimal nutrition. 5th ad., Vol. 2. W. Mertz, ed. Academic Press. London, EngL 2Hiers, J. M,Jr., W.J. Miller. and D. M. Blackmon 1968. Endogenous seuetion and reabsorplion of % i l l C in ruminants as affected by zinc deficiency and feeding of ethylermlku&tetmetate or cadmium. J. Dairy Sci. 51:730. 3 King. J. C. 1990. Assessnent of zinc status. J. Nutr. 1201474. 4 Kirchgessner, M,and W.A. Schwan. 1976. meet of zinc deficiency and varying zinc supplements on the 1 Hambidge, K

Jovnal of Dairy Science Vol. 74, No. 10, 1991

rate of zinc absorption and zinc retention in dairy cows. Arch. Tiaernahr. 263. SKleiber, M 1961. Page 25 in 'Ihe fire of life. An introdaction to aoimal energetics. John Wiley & Sons,

Inc. New Yo& NY. 6Milla. J. K. and R. 0.Cragle. 1%5. Gastrointestinal sites of absorption and endogenous secretion of zinc m dairy cattle. 1. Dairy Sci. 48:370. 7Milla, J. K.. and W. J. Miller. 1962. Experimental zinc deficiemy and recovesy of calves. J. Nu@. 7 6 467. 8Milla, W. J. 1969. AbsorptiOn, tissue distribution, endogenorur excretion.and homeostatic control of zinc in nvninants. Am. J. Clin. Nu&. 221323. 9 Milla, W.J. 1970. Zinc nutrition of cattle: a review. J. Dairy Sci. 53:1123. 10 Milla, W.J. 1971. Zinc metabolism in farm animals. pasC 23 in Mineral studies with isotopes in domestic enhnals. Int. Atomic Energy Agency. Viema, Austria. 11 Miller, W. I., D. M.Blackawn, R. P. Gentry, and F. M.Pate. 1970. 65Zinc distribution in various tissues of ziuc-deficient and normal bull calves with t h e after single hmvenous or oral dosing. J. Anim. S a . 31: 149. 12Millff, W.J.. D. M. Blachmm, R. P. Gentry, W.J. Pias. and G. W.POWCU. 1967. Absorjttion, excretion, and retention of orally administered ziuc-65 in various tissues ofzinc-deficient and IIormal goats aod calves. J. Nntt. R 7 1 . 13MiIler. W. J., D. M. Blackmon, G. W.Powell, R P. Gcntry, and J. M Him, Jr. 1966. Effects of zinc deficiency per se and of dietary zinc level on nrinary endogenous fecal excretion of 6% from a single intravenous dose by J. Nutr. 90:335. 14MiIlff, W.J., Y.0.Msrtin, R P.Gentry,and D. M. BIWAUIOIL1%. 6% and stable zinc absorption, d o n and tissue CODCCntratiollS as affected by type of diet and level of zinc in normal Cahres. J. N u t 9 4 391. 15Milla; W.J.. J. D. Morton, W.J. Pins, and C. M. +

.

3543

ZlNC METABOLlSM IN CALVES

Clifton. 1%5. Effcct of zinc deficiency and restricted feeding on wound healing m thc bovine. Roc. SOC. Exp. Biol. Med. 118:427. 16Miller,W.J., W. J. Pins, C. M. Clifton, and S. C. Schmittle. 1964. Experhentally produced zinc deficiency in the pat. J. Dairy Sci. 47556. 17 Miller,W. J., G. W. Powell, D.M. Blachwn, and R. P. Gentry. 1%8. Zinc and dry matter conteat of tissues and feces of zincddicient and normal rnminnnh fed ethylcmdiaminetetraaceeate and cadmium. J. Dairy Sci. 51:82. 18 Pate, F. M.,W.J. Miller, D. M. Bkkmon, and R. P. Gentry. 1970.~ m l tissue y '52, distribution after duodenal dosing in &es fed zinc-deficient and control diets. Roc. Soc. Exp. Biol. Med. 135653. 19 Pate, F.M,W. I. Miller, D.M.Blackmon, and R. P. -try. 1 ~ 0 . 6 5 2 nabsorption rate following single duodenal dosing in calves fed zinc-deficient or control diets. J. Natr. 100:1259. ZOPowell, G. W., W. J. Miller,and D. M. Blackmon. 1967. Effects of dietary EDTA and cadmium on ab-

sc"ptiol& excretion,

tcrad

and rdention of orauy adminis-

Zn in varioas tissnes Of zinc-ddicht and

normal goats and calves. J. Nntr. 93203. 21Richmond.C. R.,I. F. F k u c h , G. A. %ifton, and W.€3. Laagbn. 1962. Comparative metabolism of ladiormctides m mrmmata. 1. Uptake and retention of orauy administered -5 by four lian species. Health Ws. 8:481. 22 Spcncer,H., B. Rosofl, A. Peldstein, S. H. Cobq and E. ~epmano.1965. Metabolism of zinc45 in man. Radiat. Res. W432. 23 Steel, R.G.D., md J. E€. Torrie. 1960. Principles and procadnrts of statistics. McGraw-Hill, New Yak,

NY. 24Undawood, E. J. 1%. Page 32 in The mineral rmtrition of livestock. The central R ~ SLtd., S Aberdeen, Scotland. 25 Wugand, E., and M. Kirchgesseer. 1980. Total hue cfncieocy of zinc utilization: determination and

hommstaticdepcndareuponthezincsupplystatosin young rat% J. NUQ. 110469.

J o d of Dairy Science Vol. 74, No. 10. 1991