Effect of prolonged supplementation with dailysupplements of selenomethionine and sodiumselenite on glutathione peroxidase activity inblood of New Zealand residents13

Christine D. Thomson, Ph.D., Marion F. Robinson, Ph.D., Dianne R. Campbell, B.Sc., and

Heather M. Rea, B.Sc., Dzp.Sci.

ABSTRACT Glutathione peroxidase (EC 1.11.1.9, GSH-Px) activities and selenium (Se)

concentrations in blood of 12 New Zealand residents were followed during prolonged supplemen�

tation with physiological doses (100 �tg Se) of sodium selenite (selenite-Se) or selenomethionine

(Semet-Se). OSH-Px activities increased in all subjects but at 17 wk the mean increase was not

significantly greater for Semet-Se (6.2 ± SD 3.2 units/g Hb) than for selenite-Se (3.7 ± 1.8 units!

g Hb). After dosing ceased, OSH-Px activities of most subjects returned to predosing values in 17

to 40 wk, but in some subjects activities remained high. Increases in Se concentrations in whole

blood, erythrocytes, and plasma were greater after Semet-Se than after selenite-Se. Se concentra-

tions tended to plateau after selenite-Se while after Semet-Se they continued to rise as long as

dosing continued. Enzyme activity of one of four subjects supplemented daily with 500 �cg selenite-

Se was unchanged, despite a great increase in plasma Se. Blood Se and GSH-Px of 23 New Zealand

residents who ingest regular large doses (0.5 to 3 mg Se) mainly of selenite-Se showed that those

who dosed weekly had greater values than the less frequent dosers. Three subjects showed extremely

high values. It is suggested that each individual might have an optimal level of GSH-Px activity,

so that the level reached is a balance between Se intake and other factors, including possible

stressor effect of selenite. Am J Clin Nutr 1982;36:24-3l.

KEY WORDS Selenium supplements, selenite, selenomethionine, glutathione peroxidase ac-

tivity, New Zealand residents, long-term self-dosers

Introduction

Two previous papers have reported theeffects on selenium (Se) metabolism of short-term supplementation of diets of New Zea-land residents with large doses of sodiumselenite (selenite-Se) or selenomethionine

(Semet-Se) (1) and the effects of prolongeddaily supplementation with physiologicaldoses of selenite-Se, Semet-Se, and fish-Se(2). Semet-Se was more effective in raisingblood Se than was selenite-Se. The seleno-enzyme, glutathione peroxidase (EC 1.1 1.1.9;GSH-Px) is the only known function of Se inanimals, and is therefore our only measure ofits bioavailability. A linear relationship wasdemonstrated between blood Se and GSH-Pxactivity for New Zealand residents, but notfor those with higher blood Se values such asNew Zealand residents on return from over-seas travel or overseas visitors to New Zea-land (3, 4).

Herein we report the effects of long-termsupplementation with both physiological andlarge doses of selenite-Se or Semet-Se onGSH-Px activities in New Zealand residents.Daily supplements of 100 �.sg Se raised theNew Zealand intake to US intake.

Methods

Sixteen apparently healthy adults (eight women and

eight men) aged 21 to 62 yr, volunteered for experiments

1 and 2. The subjects were all residents of Dunedin and

four of them (M, H, R, and S) had participated in earlier

studies (1, 2, 5). Informed consent was obtained from all

I From the Department of Nutrition, University of

Otago, Dunedin, New Zealand.2 Supported by the Medical Research Council of New

Zealand and the New Zealand Medical Research Distri-

bution Committee, and Roche Products Ltd, Welwyn

Garden City, U.K.

Reprints not available.

Received September 24, 1981.

Accepted for publication December 29, 1981.

24 The American Journal of Oinical Nutrition 36: JULY 1982, pp. 24-31. Printed in U.S.A.© 1982 American Society for Clinical Nutrition

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SE SUPPLEMENTS AND GSH-PX ACTIVITY 25

participants. The study extended over 4 yr. Details of

diet were recorded by most subjects.

Experiment 1-prolonged supplementation of diet withphysiological doses of Se

Experiment la-selenite-Se (1977 to 1978). Five fe-

male (f) subjects (OF, M, MG, HR, and H) and two

male (m) subjects (JR and 5) ingested daily for 12 to 32wk, 90 �g Se as sodium selenite in a capsule which also

contained 20 lU a-tocopherol acetate and lactose and

maize starch as diluent (Roche Products Ltd, Welwyn

Garden City, Hertfordshire, UK). Se content of capsules

by analysis was 90 and not 100 �tg Se as planned. The

subjects were followed during a postdosing period of at

least 17 wk.Experiment ib-Semet-Se (1978 to 1979). Three fe-

male subjects (OF, DC, ai�d R) and one male subject

(JR) ingested daily for 11 to 44 wk, 100 ,.tg Se as DL-

selenomethionine in a capsule which also contained 20

IU a-tocopherol acetate and lactose and maize starch as

diluent, followed by a postdosing period of 10 to 40 wk

for three subjects. Two subjects JR and OF participated

in both experiments la and lb. A fifth subject DF (m)

participated from 1976 for 80 wk, but his blood GSH-Px

activities are available only from wk 46. Plasma a-to-

copherol was measured at the beginning and at the end

of the dosing period.

Experiment lc-selenite-Se after Semet-Se (1978 to1980). Subjects JR and DF changed overnight from

dosing with Semet-Se in experiment lb to ingesting daily

a capsule of 90 �zg selenite-Se and 20 IU a-tocopherol

(experiment la) for 22 and 16 wk, respectively.

Experiment id-selenite-Se (1978). Subject GA (m)

ingested 100 ,.tg selenite-Se in solution daily for 22 wk

after a 4-wk period of dosing with 500 jzg selenite-Se

daily in solution (experiment 2a). There was a postdosing

period of 23 wk before dosing with 90 ,zg selenite-Se for

a further 21 wk.A blood sample was taken before dosing, on day 1, at

weekly intervals for 4 wk, two weekly intervals up to 16

to 18 wk, and then monthly during the remainder of the

dosing period and at 2- to 4-wk intervals during the

postdosing period. In experiment lb a 24-h urine collec-tion was made usually on the same day as the blood

collection.

Experiment 2-short-term supplementation with largedoses of Se

Four male subjects ingested 500 �zg selenite-Se in

solution daily for 4 wk, followed by a postdosing period

of 4 wk except for subject GA who continued dosing

with 100 �g selenite-Se daily (experiment ld).A blood sample was taken before dosing, at wk 1, 2,

and 4 during dosing, and at end of postdosing period.

Experiment 3-study of Christchurch and Hamilton“dosers”

Blood samples were taken from 23 New Zealandresidents in Christchurch and Hamilton, who ingest reg-

ular supplements of Se for relief of muscular pains.

Seven subjects were aged between 49 and 60 yr, and therest were over 60 yr.

Se was taken in the form of selenite, sodium selenate,

or Se-dioxide; the quantities taken varied from 1 to 3 mg

Se and were taken at varying intervals for 0.5 to 15 yr.

Each capsule of Se-dioxide contained 1.4 mg Se and also

50 mg a-tocopherol acetate. An elderly couple fromHamilton, subjects ED (m) and MD (f) had been ingest-

ing daily doses of 0.46 mg and 0.37 mg selenite-Se,

respectively, for 3 yr.

Techniques

Collection and storage of samples

Blood samples were collected and stored as described

previously (I). Whole blood, plasma, and erythrocyteswere analyzed for Se, and whole blood was assayed for

OSH-Px activity. Urine samples were collected and

stored as described previously (2, 5).

Analytical methods

Se was measured by a modification (6) of the diami-

nonaphthalene fluorimetric method of Watkinson (7).

Hemolysates of blood samples for enzyme assays were

prepared by adding to an appropriate dilution of whole

blood in physiological saline (9 g NaC1/l), an equalvolume of double strength Drabkin’s reagent 10.016 M

KCN, 0.00 12 M K3Fe(CN)6, 0.238 M NaHCO3] to convert

methemoglobin to cyanomethemoglobin, and four vol-

umes of 0.02 M phosphate buffer (pH 7) containing 0.5%

(v/v) Triton X-lOO to lyse cells. GSH-Px activities were

assayed by a modification (3, 8) of the coupled method

of Paglia and Valentine (9) using t-butyl hydroperoxide

as substrate. Each assay contained 2 iemol glutathione,

0.5 units glutathione reductase (Sigma Chemical Co, StLouis, MO) I �tmol NaN3, 0.1 �mol NADPH in 20 mM

phosphate buffer, and 6 m�i EDTA in a volume of 0.9

ml. The pH was adjusted to 7.3, 0.1 ml hemolysate was

added and the mixture was incubated for 10 to 15 mm

at 25#{176}Cafter which the reaction was initiated by adding

10 � 30 mt�i t-butyl hydroperoxide (Koch-Light and Co,

Cambrook, Bucks, England). The reaction was followed

for 4 mm and enzyme activity calculated from the linear

rate of NADPH oxidation between 2 and 4 mm. A small

nonenzymic rate of NADPH oxidation was substracted

from the overall rate. One enzyme unit of activity was

defined as I �mol NADPH oxidized/mm and results

expressed as units/g Hb. Twenty-four assays of onewhole blood sample on different days gave a mean

activity of 9.52 (SD 0.48) units/g Hb.

a-Tocopherol was measured using the thin-layer chro-matography method of Bieri and Prival (10), and lipidswere measured by the turbidimetric method of de Ia

Huega et al. (11).

Results

Experiment 1-prolonged supplementationwith selenite-Se and Semet-Se

Experiments la and lb. Initial enzyme ac-tivities were similar for subjects in both ex-periments la and lb (Table 1; Figs. 1 and 2).The lowest activities were found in the sub-jects who had not previously ingested Sesupplements, although subject GF had aninitial activity of less than 14 units/g Hb(experiment lb) 1 yr after dosing with sele-nite-Se (experiment la).

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>120 30 60 90 120period of experiment (days)

26 THOMSON ET AL.

TABLE 1

Se concentrations and GSH-Px activities in blood of Otago residents duringdaily supplementation with selenite-Se and Semet-Se and in blood

of Otago blood donors and of overseasvisitors to New Zealand (4)

Form ofsupplcmcni

Sccontcnt n

Durationof dosing

GSH.P X

Sc conccntration

Whoicbk�d

Erythrocytcs Plasma

�g v/c uni:s/g Fib ng/m/ ng/nil ng/ml

Experiment Ia 100 7 0 15.5 ± 2.6* 84 ± 15 102 ± 17 67 ± 12

Selenite 4

17t

17.1±3.2

19.2± 3.7

103±12

116±10

114±20

128 ±9

93±9

103±11

Experiment lb 100 4 0 14.9 ± 1.7 63 ± 16 77 ± 18 52 ± 14

Semethionine 4

l7�

16.1 ± 0.8

21.2 ± 1.9

114 ± 9

187 ± 38

106 ± 19

218 ± 66

114 ± 6

154 ± 14

Experiment 2 500 4 0 14.8 ± 3.4 70 ± 11 89 ± 6 49 ± 9

Selenite 4 17.6 ± 4.1 105 ± 10 99 ± 12 98 ± 17

Otago blood 104 12.5 ± 3.5� 59 ± 12 74 ± 97 48 ± 10

donors (4) (84) (97)

Overseas visitors 25 20.4 ± 5.3 153 ± 32 174 ± 37 98 ± 21

toNZ(4) (21) (22)

* Mean ± SD.

t Final blood values used for one subject who had ceased dosing at 12 wk.� Final blood values used for two subjects who had ceased dosing at 11 and 12 wk.

§ No. of determinations is given in parentheses where complete sets were not available.

In

C

‘Ia

0�

FIG. I. GSH-Px activities in whole blood: a, during daily supplementation with 90 �tg Se as selenite-Se and b.postdosing periods, for subjects HR (0), OF (#{149}),H (i�), iR (A), M (0), MO (I), and S ( ).

GSH-Px activities in whole blood of allsubjects increased with Se supplements ofeither selenite-Se (Fig. 1) or Semet-Se (Fig.2). The supplementation period has been di-vided into period 1, 17 wk (120 days), theapproximate average life span of the humanerythrocyte, and period 2, the remainingweeks of dosing. During period 1 the increasein enzyme activities with selenite-Se variedbetween 0.6 for subject H and 6.1 units/g Hb

for subject 5; and between 1.1 and 2.1 units!g Hb for period 2 (Fig. 1). The increases withSemet-Se during period 1 varied from 2.9 forsubject JR to 9 units/g Hb for subjects GFand DC, to reach 22.7 units/g Hb, a little lessthan the highest enzyme activities with sele-nite-Se of 25.2 and 27.2 units/g Hb at 17 to27 wk, respectively, for subject S. The meanincrease in GSH-Px activities was not signifi-cantly greater for Semet-Se than for selenite-

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30

26

22

18

14

10

“ >-izo 30 60 90 120

period of experiment)days)

400 -(a)

351

300 -

FIG. 2. GSH-Px activities in whole blood: a, during daily supplementation with 100 jzg Se as selenomethionine

and b, postdosing periods for subjects R (0), OF (S), DC (A), and JR (A).

(b(

.1

#{149}S.

0(250 -

200 -

E

8150 -

100

#{149}

A

50

.� �A

AL #{163} #{163}�I #{163}�

0

(C)

#{149}#{149}.

0

#{149}�.AA AA� 226�

� �

(4 ID

350 400 450 500 5501’

#{163}

0 50

�AA #{163}�

100 150 200 250 50 100 150 2(1) 250 300

SE SUPPLEMENTS AND GSH-PX ACTIVITY 27

Se at 17 wk (6.2 ± (SD) 3.2 versus 3.7 ± 1.8units/g Hb, respectively) or at the end ofdosing (6.3 ± 3.0 versus 4.9 ± 2.5 units/gHb).

During the postdosing period after selenite-Se most subjects initially maintained higherenzyme activities which had returned almostto predosing values at the end of the postdos-ing period of 17 to 40 wk. However, activitiesat 30 to 40 wk for two subjects S and M werestill 4.5 and 5.7 units/g Hb greater than pre-dosing values.

.a=

LIa

a-=I’,

After Semet-Se dosing, the higher enzymeactivity of subject GF was maintained for 9wk and then fell (Fig. 2); whereas that ofsubject DC continued to rise during 9 wkpostdosing to 30 units/g Hb and subsequentlyfell.

Whole blood, erythrocyte, and plasma Seincreased for all subjects, but increases weregreater after Semet-Se than after selenite-Se(Table 1; Fig. 3). Plasma Se initially rosemore rapidly than erythrocyte Se, and atabout wk 4 both had reached a plateau with

period of experiment (days)

FIG. 3. Selenium concentration (ng/ml) in whole blood (0), erythrocytes (#{149})and plasma (A) and GSH-Px

activities (units/g Hb; A) in whole blood of subject JR during daily supplementation with a, 90 yog Se as selenite-Se,

b. 100 yog Se as selenomethionine and followed by c, 90 yog Se as selenite-Se.

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selenite-Se; whereas with Semet-Se they con-tinued to rise throughout the dosing period-erythrocyte Se more rapidly than plasma Se.

The paired correlations between GSH-Pxactivities in whole blood and Se concentra-tions in erythrocytes were significant (p <

0.05) for all subjects except JR and S withselenite-Se, and between GSH-Px activitiesand plasma Se (p < 0.05) for all subjectsexcept subject S with selenite-Se.

Urinary output (7 to 11 �tg Se/day) in-creased immediately with Semet-Se by 6 to 8�.tg Se/day and at the end of dosing was 40 to65 j�g Se/day. There was a close relationshipbetween 24-h urinary Se and plasma Se (r =

0.91 to 0.97; p <0.001) for all subjects exceptsubject R (r = 0.77 for six samples).

Plasma a-tocopherol levels were within thenormal range for all subjects in experimentib, and increased with supplementation from1.1 ± 0.1 mg/g lipids to 1.4 mg/g lipids.

Experiment ic. For subjects JR (Fig. 3) andDF, for whom data are not given, enzyme

activities were unchanged during dosing withselenite-Se after Semet-Se even though therewas a dramatic fall in whole blood, erythro-cyte, and plasma Se for both subjects within

150 -(a) (b)

iioo -�

50 -

32 A

#{163} AL

AL

#{163}

�24-

�2 16- a

12 A _____________

1 wk after selenite-Se dosing commenced. Aplateau was reached for both subjects whichfor subject JR was similar to that reachedwith selenite-Se in the earliest experiment(experiment la).

Experiment ld. Subject GA showed a con-tinuing rapid increase in GSH-Px activitiesfrom 18.0 to 30.1 units/g Hb during 22 wk ofdosing with 100 �tg selenite-Se daily in solu-tion after 4 wk on 500 �tg selenite-Se daily(experiment 2, Fig. 4). Activities fell onlyslightly during 23 wk postdosing. In contrast,whole blood and plasma Se changed littleafter the initial 4-wk dosing period and eryth-rocyte Se showed only a small increase. Dur-ing the postdosing period, whole blood andplasma Se fell while the higher erythrocyteSe concentration was maintained.

Experiment 2-short-term supplementationwith large doses of selenite-Se

GSH-Px activities in whole blood rose inall subjects except one who showed the great-est increase in plasma Se from 50 to 118 ngSe/ml. The increases in enzyme activity werewithin the range shown in experiment la at4 wk by subjects receiving the smaller supple-

#{149} #{149}S0 0

0 A A

A

#{163}

#{163}

ALA

AL

1 1 1 1’! I

0 50 1� 150 200� 0 50 1�) 150

28 THOMSON ET AL.

period of experiment (days)

FIG. 4. Se concentrations (ng/ml) in whole blood (0), erythrocyte (5) and plasma (A) and GSH-Px activities

(units/g Hb; A) in whole blood of subject GA during daily supplementation a, with 500 yog Se as selenite-Se, b,followed by 100 �zg Se as selenite-Se, with an intervening nondosing period of 23 wk.

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52

48

44

�40

C

�32

>

a 24

1/)

�16

128

4

U

U

U

IIIIIIIiIi

0

0

0

1�L�L � I � I I

SE SUPPLEMENTS AND OSH-PX ACTIVITY 29

ments of selenite, except for subject GA (+5.4 units/g Hb). Further, the larger doses ofselenite increased the plasma Se, but not theerythrocyte Se, by more than the smaller doseand the increases were less than the respectiveincreases obtained with 100 �tg Semet-Se (ex-periment lb).

Experiment 3-study of Christchurch and

Hamilton “dosers”

Since no differences could be detectedwhich could be attributed to the form of Setaken, the results have been grouped accord-ing to the frequency of dosing. The once ortwice weekly dosers (n = 9) compared withthose dosing less frequently (n = 10) hadgreater enzyme activities (22.8 ± 4.0 versus18.4 ± 3.6 units/g Hb; p < 0.05) and bloodSe (121 ± 19 versus 94 ± 12 ng Se/mi; p <

0.01). Mean blood Se of the less frequentdosers was similar to that for 18 Christchurchresidents (“Lincoln dosers”) in an earlierstudy (89 ± 15 ng Se/mi) (1).

Dosing for over 1 yr was not associatedwith higher blood values for the less frequentdosers. However, one frequent doser with ablood Se of 129 ng Se/mi had, after 2 yr ofdosing, an enzyme activity of 49.5 units/gHb, which is the highest so far determined inour laboratory (Fig. 5) and is well above

enzyme activities for overseas visitors to NewZealand. Enzyme activity was a little lower 5months later (42.6 units/g Hb), when it wassimilar to GSH-Px activity for one of the twoHamilton elderly residents (MD and ED)(40.7; 34.2 units/g Hb) who dosed daily withselenite. Furthermore, their blood Se (186;173 ng Se/nil, respectively) were muchgreater than for all the Christchurch dosers.

A weak correlation (r = 0.45; p < 0.05) wasobtained between GSH-Px and blood Se forall the Christchurch dosers and inclusion ofthe Hamilton results gave a strong correlation(r = 0.65; p < 0.001).

Discussion

An increase in GSH-Px activity was ob-served in all but one of the subjects whoreceived extra Se. However, the increase wasnot great and after an initial rise during thefirst weeks of supplementation, enzyme activ-ities in some subjects plateaued while in oth-ers the levels increased more slowly. Morenotable was the variation in response of theseNew Zealand subjects, all of whom had hada lower Se status compared with overseasresidents [Fig. 5 (4)J.

Control subjects receiving placebo were notfollowed in this study. However, assays of

40 80 120 160 200 240 280 320 360 400 440

Se concentration (ng/mIwhole blood)

FIG. 5. Relationship between Se concentrations (ng/ml) in whole blood and GSH-Px activities (units/g Hb) for

subjects supplementing with 90 y�g Se/day (0) and 500 yag Se/day (#{149})as selenite-Se, 100 yog Se/day (A) as

selenomethionine, visitors from Tahiti (0) (4), Christchurch and Hamilton dosers (U). Mean ± SD for surgical

patients, blood donors, New Zealand travelers overseas, and overseas visitors to New Zealand. (From Table 1,

Reference 4.)

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30 THOMSON ET AL.

GSH-Px activity in six blood samples takenfrom a nondosing subject over a period of 2months gave a mean activity of 16.3 (SD 0.3)units/g Hb. Furthermore, in a previous dos-ing study (12), 37 subjects receiving a placebocapsule daily for 4 wk showed no changes inblood Se concentrations or GSH-Px activi-

ties, whereas significant increases were ob-served in those receiving selenite. None of thesubjects in the present study recorded anychanges in dietary patterns that might haveinfluenced Se intake.

The present studies distinguished betweenthe long-term response in blood Se concen-trations and enzyme activities to physiologi-cal supplements of Semet-Se and selenite-Se.These studies confirmed the findings fromprevious shorter studies which showed thatSemet-Se was more effective in raising bloodSe than was selenite-Se (1, 2). However, themean increases in GSH-Px activities for thetwo forms were not different at 17 wk, theaverage life span of erythrocytes, or at theend of dosing. Enzyme activities had changedlittle, although at times blood Se levels afterSemet-Se were well within the range for USresidents.

Ganther et al. (13) have pointed out thatthere are factors other than the Se intake thatmay influence enzyme activity by altering Semetabolism or by altering the “oxidant stress”of the cell itself. These might play a greaterrole when the Se intake is adequate, as in

these long-term and short-term dosing stud-ies. Thus each individual might have an op-

timal level of enzyme activity, so that thosewho showed a greater increase might havehad a higher optimal requirement determinedby a greater need for GSH-Px.

A rapid increase in GSH-Px activities withonly a minimal increase in blood Se concen-trations was found for subject GA, an activeperson participating in athletic training. Al-though exercise itself does not affect GSH-Pxactivities in erythrocytes of horses (14) or ofrats (15), a stressor effect of physical activitymay possibly increase the requirement forGSH-Px, which might be raised when extraSe is given. Furthermore, exercise has beenshown to increase lipid peroxidation in manas measured by pentane production (16). Onthe other hand, the older subjects, JR and H,showed very small increases in enzyme activ-

ities with supplements only, indicating per-

haps that a lower enzyme requirement hadbeen met. Moreover, enzyme activity for JRwas not altered by the two changes in theforms of Se supplements.

The greatest GSH-Px activities were forthe two elderly Hamilton residents takingregular frequent large therapeutic doses ofselenite and for a Christchurch doser takingselenium dioxide. Nothing has been found inthe literature to indicate that selenium diox-ide is handled differently from selenite (17)and no differences in urinary excretion werefound after doses of selenium dioxide andselenite (Thomson CD, Robinson MF,Campbell DR, Rea HM, unpublished re-sults). It is not clear whether these high activ-ities were an adaptive change to the oxidantstressor effect of excess selenite (18) orwhether they were a response to selenite-Seand/or other Se metabolites resulting from

an overloading of the erythrocyte mechanismthat deals with selenite-Se (19-22). Furtherwork is needed to determine whether suchhigh enzyme activities are desirable andwhether they are reached by any of the othersubjects regularly ingesting therapeutic doses.

Other workers have used therapeutic dosesof selenite, but for short periods of time, andin each case the enzyme (and blood Se whenmeasured) have reached normal ranges (21,23-25). Similarly a smaller dose of selenate(100 ,zg Se) had reversed a lowered enzymeactivity (26). Furthermore, Lombeck et al.(27) demonstrated that the extremely lowerythrocyte and plasma Se and GSH-Px ac-tivity of children on phenylketonuria dietcould be restored to normal ranges with yeastrich in Se (45 �tg Se/day). However, the samesupplement at treble the dose produced nochange in GSH-Px activity when given to USresidents, who therefore may be consideredSe adequate (28).

Some New Zealand residents may havehad inadequate or suboptimal enzyme activ-ities, which were enhanced with Se supple-ments, but whether they could actually bedescribed as Se deficient is not clear. Apartfrom the patient on total parenteral nutrition(29), no Se-responsive condition has beendetected among the New Zealand residents.Perhaps, like their sheep, New Zealandershave adapted somewhat to their low Se status!The principal function of GSH-Px is to main-tain the integrity of cell membranes, includ-

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SE SUPPLEMENTS AND GSH-PX ACTIVITY 31

ing those of erythrocytes, and peroxidativedamage is prevented by the interplay with theother factors, vitamin E, catalase, and super-oxide dismutase. These factors may compen-sate for a lowered GSH-Px activity and thisneeds to be investigated in New Zealanders.

LI

The authors are particularly grateful to the subjects

for their willing cooperation, Annabelle Duncan and

Gaylene Friend for technical assistance, and Dr. C. H.

Hassell, Roche Products, U.K.

References

I. Thomson CD, Burton CE, Robinson MF. On sup-

plementing the selenium intake of New Zealanders.

1. Short experiments with large doses of selenite or

selenomethionine. Br J Nutr I978;39:579-87.

2. Robinson MF, Rca HM, Friend GM, Stewart RDH,

Snow PC, Thomson CD. On supplementing the

selenium intake of New Zealanders. 2. Prolonged

metabolic experiments with daily supplements of

selenomethionine, selenite and fish. Br J Nutr

1978;39:589-600.

3. Thomson CD, Rca HM, Doesburg VM, Robinson

MF. Selenium concentration and glutathione per-

oxidase activities in whole blood of New Zealand

residents. Br J Nutr l977;37:957-62.4. Rca HM, Thomson CD, Campbell DR. Robinson

MF. Relation between erythrocyte selenium concen-

trations and glutathione peroxidase (EC 1.11.1.9)

activities of New Zealand residents and visitors to

New Zealand. Br J Nutr l979;42:20l-8.5. Thomson CD. Recovery of large doses of selenium

given as sodium selenite with or without vitamin E.

NZ Med J I974;80:163-8.

6. McKenzie RL, Rca HM, Thomson GD, Robinson

MF. Selenium concentration and glutathione per-

oxidase activity in blood of New Zealand infants

and children. Am J Clin Nutr 1978;3l:14l3-18.7. Watkinson JH. Fluorimetric determination of sele-

nium in biological material with 2,3-diamino-

naphthalene. Anal Chem l966;38:92-7.

8. Robinson MF, Godfrey PJ, Thomson CD, Rca HM,

van Rij AM. Blood selenium and glutathione per-

oxidase activity in normal subjects and in surgical

patients with and without cancer in New Zealand.Am J Clin Nutr 1979;32:l477-85.

9. Paglia OE, Valentine WN. Studies on the quantita-tive and qualitative characterization of erythrocyte

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