Jou nal
o Animal and
Feed
Sciences, 6, 1997, 343-351
Seasonal
a ia ion o glu a hione pe oxidase,
CK
and AST in
sheep
in a low-selenium egion
M.
Lopez Alonso, M.
Mi anda,
J.
He nandez, C. Cas illo, I. Ayala
and
J.L.
Benedi o
Depa men o Animal Pa hology, Ve e ina y Facul y o
Lugo,
Uni e si y
o San iago de Compos ela
27002
Lugo,
Spain
(Recei ed 27 Decembe 1996;
accep ed
19 Augus 1997)
ABSTRACT
Blood
glu a hione
pe oxidase
(GSH-Px; E.C.
1.11.1.9)
ac i i y,
a
measu e
o selenium
s a us,
as
well
as he plasma indica o s o muscle
damage
c ea ine
kinase
(CK; E.C. 2.7.3.2) and
aspa a e
amino ans e ase
(AST; E.C. 2.6.1.1) we e e alua ed in
sheep
in a egion
wi h
low selenium le els
du ing
he sp ing and he summe ,
because
his ime may be
c i ical
o su e ing selenium
de iciencies. GSH-Px ac i i y was highes du ing he sp ing, when
mean
alues
anged
om
74.16
and 90.51 Ul/g Hb,
descending
d as ically du ing he summe , below physiological le els (P < 0.001)
wi h
mean
alues
anging
om
43.33
o 50.01
Ul/g
Hb.
GSH-Px
ac i i y,
wi hin
he de iciency
ange,
egis e ed du ing he summe did no o igina e muscle
damage,
since
he muscle
enzymes
CK and
AST
we e
wi hin
hei no mal
ange.
KEY
WORDS:
enzymes,
selenium,
ewes
INTRODUCTION
The biochemical ole o selenium was demons a ed by Ro uck e al. (1973)
o be a componen
o
he enzyme glu a hione
pe oxidase
(GSH-Px. EC 1.11.1.9).
GSH-Px unc ions in cellula oxida ion- educ ion eac ions o p o ec he
cell
memb anes
om
oxida i e
damage
caused
by ee adicals and pe oxides (Flohe
e al.,1973).
Selenium de iciency in
sheep
mani es s
i sel
in
a a ie y o ways, he classical
one being whi e-muscle
disease,
bu i
also
b ings abou educed g ow h
a es,
ill
344
LOPEZ-ALONSO
M. ET AL.
h i ,
in e ili y,
subop imal
wool
yields and pe iodon al
disease
(Sanson,
1990).
These
mani es a ions equen ly occu
in
he
same
a eas
and chemical
analyses
o
he
pas u e
samples
sugges
ha he condi ions migh be
associa ed
wi h
low
le els o selenium in he
soil
(Zacha a e al., 1989).
Seasonal
a ia ions o Se le el in
pas u es
ha e
been
obse ed, being specially
low
o
c i ical
du ing he sp ing (Hun e e al., 1982; Blood e al., 1992),
since
a
his ime
pas u e
was ac i ely
g owing,
and Se is in a lowe a io in he
he bage.
O he
au ho s
ha e
also
epo ed
seasonal
ends
in he selenium
s a us
o
animals, showing ha
issue
and blood selenium concen a ions we e a
a minimum du ing he sp ing and he summe (B aun e al., 1991; Scholz, 1991;
Capaul e
al.,
1992; Koh e
al.,
1992). This
seasonal
in luence is specially ele an
in
egions
wi h
ma ginal o de icien Se le el in he soils, whe e his mine al
dec eases
d as ically in he
issues
o he animals
wi h
he
occu ence
o
clinical
mani es a ions o selenium de iciency (Whea ley and Beck, 1988;
Zacha a
e al.,
1989).
De e mining
he concen a ion o selenium in soils,
pas u es,
as
well
as in
blood
and o he animal
issues
is bo h ime consuming and cos ly. Howe e ,
selenium concen a ion and glu a hione
pe oxidase
a e highly co ela ed in he
blood
o
sheep,
wi h
his enzyme being in u n a apid and
cheap
indica o o
selenium
s a us
(Mackin osh e al., 1989;
Hamli i
e al., 1990).
The objec i e
o
his expe imen was o examine he selenium
s a us
o
sheep
in
a egion
wi h
low selenium le els (Lopez
Alonso,
1995),
du ing he sp ing and he
summe ,
since
his pe iod may be a
c i ical
ime o su e ing selenium
de iciencies. Fo his
pu pose
whole blood GSH-Px
ac i i y,
as a good indica o
o
he p o ec ion ha he animal has
agains
oxida i e
damage,
as
well
as he
plasma indica o s o muscle
damage,
c ea ine
kinase
(CK) and
aspa a e
amino ans e ase
(AST),
we e e alua ed.
MATERIAL
AND METHODS
Animals
Twen y
pu e na i e
ewes
o Gallega b eed anging
om
2 o 4
yea s
o age
we e
selec ed
a andom
om
a
lock
in a low-selenium
a ea
o he p o ince o
Lugo
(NW Spain). The animals we e examined
om
Ap il
un il
Sep embe
1994.
Fo he p e ious 3 mon hs and du ing he expe imen he
ewes
we e kep on
na u al
pas u es
(a mix u e o whi e clo e and
ye-g ass)
wi hou any
supplemen a y eed, mine als o i amins.
Blood
samples
we e d awn, by jugula enepunc ion, a mon hly in e als.
Each
sample
was placed in o hepa inized
ubes
and
ubes
o se um sepa a ion,
ENZYMES
ACTIVITY
IN SHEEP
WITH
Se
DEFICIENCY
345
and kep e ige a ed o anspo a ion o he labo a o y. All
samples
we e
assayed
wi hin
12 h o sampling.
Analy ic
p ocedu es
GSH-Px was
measu ed
wi h
a comme cial ki (Ransel, Randox,
UK),
based
on
he me hod o Plagia and Valen ine (1967). Enzyme
ac i i y
was
exp essed
in
in e na ional
uni s pe g am o haemoglobin (Ul/g Hb). Haemoglobin was
de e mined by he s anda d cyanme haemoglobin me hod
(Hainline,
1958).
Se um c ea ine kinase (CK) and
aspa a e
amino ans e ase (AST) ac i i ies
we e
exp essed
in in e na ional uni s pe
li e
(UI/1)
and we e
assayed
using
kine ic
p ocedu es
wi h
comme cial
eagen s
(Knicke bo cke , SAE; C oma-
es ®
Reagen s).
S a is ical
analyses
One-way analysis o a iance (Fishe 's F es ) was
used
o
es
o he
changes
o
he analysed
pa ame e s,
and o di e ences be ween
seasons
(Snedeco
and
Coch an, 1978). Di e ences we e conside ed signi ican a P<0.05.
RESULTS
GSH-Px
ac i i y
showed a s ong
seasonal
a ia ion (Table
1).
An
inc ease
o
GSH-Px
ac i i y
was obse ed du ing he sp ing,
om
74.16 + 7.20 Ul/g Hb a
he beginning o he expe imen , o a maximum alue o 90.5 + 8.66 Ul/g Hb in
June.
In he
ollowing
mon h his enzyme
dec eased
d as ically by 50%
TABLE
1
Changes
o GSH-Px
ac i i y
(Ul/g Hb) and se um CK and AST ac i i ies
(UI/1)
du ing he s udy
pe iod,
exp essed
as mean ± s anda d e o
Mon hs
Ap il
May
June
July Augus
Sep embe
GSH-Px
74.16
+ 7.20
85.11
±15.44
90.51+8.66
43.33
+
4.88*
49.90 + 6.10
50.01
+9.18
39.0 - 140.3 9.5 - 200.9 55.5 -198.1 14.4 - 78.0 10.4 - 111.6 3.7 - 137.0
CK
86.25+ 11.66
64.38±
5.22
59.39±
5.09 116.59+ 11.3* 81.38+ 9.23* 81.76+ 11.10
45.4 - 208.0 33.0 - 111.4 24.8 - 94.9 53.6 - 198.1 45.4 - 155.2 31.3 - 208.0
ASAT
85.56+ 2.65 81.31+ 3.35 71.82+ 2.74 72.44+ 3.39 69.75+ 3.06 64.25+ 1.85
62
- 104
61
- 104
55
-
92
50
-
99
55
- 104
56
- 82
*
P<0.05
346
LOPEZ-ALONSO
M. ET AL.
TABLE
2
Scales
in whole blood GSH-Px
ac i i y
and selenium concen a ion
used
o diagnosis selenium
s a us
in
sheep
(Saez
e al., 1995)
Selenium concen a ion GSH-Px
ac i i y
Selenium
jig/ml
UI/gHb
s a us
<0.05 <60
de icien
0.05-0.1 0-120
ma ginal
>0.1
>
120
adequa e
TABLE
3
Mean
alues o GSH-Px
(Ul/g
Hb),
CK and AST
(UI/1)
ac i i ies du ing he sp ing and he summe ,
exp essed
as mean + SE
GSH-Px
CK
ASAT
Sp ing
77.29
±4.90
70.01
±4.80
79.57+1.86
Summe 47.75
±3.96***
93.24±6.46**
68.81
±1.68***
**
P<0.01
***
P<0.001
ENZYMES
ACTIVITY
IN SHEEP
WITH
Se
DEFICIENCY
347
(P<0.05),
eaching he minimum alue (43.33 + 4.88 Ul/g Hb).
Du ing
he
subsequen
pe iod GSH-Px
ac i i y
showed a sligh eco e y, bu emaining a
de icien
le els o
sheep
(Table
2).
The wide
ange
o alues ound du ing
all
he
expe imen indica e la ge
indi idual
a ia ions o he GSH-Px
ac i i y.
Al hough
in
some
cases
he
ac i i y
o he plasma indica o s o muscle
damage,
CK and
AST,
was
abo e
he
physiological
le els (< 100
UI/1),
he mean
alues we e usually
wi hin
he no mal
ange
(Table 1), excep in July o CK
(P < 0.05), whe e he mean alue was 116.59 + 11.39, coinciding
wi h
he lowes
GSH-Px
ac i i y
egis e ed.
Du ing
he whole expe imen CK
ac i i y
showed
a ma ked
seasonal
a ia ion,
he e olu ion being in e se o he GSH-Px
ac i i y
(Figu e
1).
Finally,
GSH-Px
ac i i y,
as
well
as he plasma indica o s o muscle
damage,
CK
and AST, showed signi ican di e ences be ween bo h
seasons
(Table 3).
DISCUSSION
The majo i y o he selenium (75%) is in he e y h ocy es as glu a hione
pe oxidase (Oh e
al.,
1974). Fo his
eason,
a ia ions in he
le el
o selenium in
he
pas u e,
and he e o e in he animal die , a e going o show up in he blood
GSH-Px
ac i i y.
Ou
da a
indica ed a s ong
seasonal
end in GSH-Px
ac i i y;
while
in
he sp ing his enzyme
ac i i y
is
ma ginal,
du ing he summe
i
is below
he
physiological
le els o
sheep
acco ding o
Saez
e
al.
(1995).
These
esul s do
no
ag ee
wi h
Bedo e
al.
(1992) and And es e
al.
(1994),
who
ha e
egis e ed he
lowes GSH-Px ac i i ies in he sp ing,
wi h
hese
obse a ions coinciding
wi h
low
selenium le els in he
pas u es.
Ne e heless, we mus conside ha
while
selenium concen a ions in se um and plasma co ela ed
highly
wi h
he
a e
o
o al
o pa en e al adminis a ion and espond
quickly
o
changes
in Se in ake,
whole
blood selenium, as
well
as GSH-Px espond mo e
slowly
han se um (o
plasma) o
changes
in selenium in ake (Nicholson e al.,
1991;
S owe and He d ,
1992).
This is
because
he majo i y o he glu a hione pe oxidase in whole blood
is inco po a ed in o he ed blood cells a he ime o e y h opoiesis. So
a comple e
esponse
in whole blood Se, o GSH-Px
ac i i y,
o a Se
change
in he
die
will
equi e he e o e a ime
span
equal o he
a e age
li e
span
o he
e y h ocy es,
which,
in he
case
o
sheep
is app oxima ely 120 days. This ac is
specially e iden when a Se supplemen a ion is adminis e ed, since he whole
blood
selenium o GSH-Px
need
8 weeks app oxima ely o each maximum
ac i i y
(Whea ley and Beck, 1988;
Hamli i
e a ., 1993). Conside ing his ac we
could
explain he
adequa e
GSH-Px
ac i i y
showed du ing he sp ing,
which
would
co espond
wi h
high Se le els in
pas u e
du ing he win e (Hun e a al.,
(1982),
and hen, how in he summe he GSH-Px
ac i i y
was
low,
ep esen ing

348
LOPEZ-ALONSO
M. ET AL.
a
c i ical
Se concen a ion in
pas u e
du ing he sp ing in his
a ea.
Whea ley and
Beck (1988)
also
epo ed ha he GSH-Px ac i i y
dec eased
d as ically a he
end o he sp ing in a egion
wi h
low le els o selenium. This luc ua ion in
GSH-Px
ac i i y
sugges s
ha Se
s a us
o
ewes
canno be
assumed
o be
cons an
h oughou he
yea ,
and he e o e, o
diagnose
a
lock
as ma ginal o
adequa e
in
selenium, o in
need
o supplemen a ion, sampling mus occu when he
ewes
a e mos
likely
o be in a de icien
s a us.
Se e al
au ho s
(Whea ley and Beck,
1988; And es e al., 1994)
ha e
also
showed la ge indi idual a ia ions,
wi h
animals included a he de icien , ma ginal and
adequa e
ca ego ies
o GSH-Px
in
he
same
he d.
Al hough
in ou s udy GSH-Px ac i i y is below he physiological le els
du ing
he summe ,
wi hin
a de icien
ange,
i did no
cause
impo an muscle
damage,
since
CK and AST ac i i ies we e usually
wi hin
he no mal
ange.
This
de icien
GSH-Px
ac i i y
may be
compensa ed
by an
adequa e
le el
o
i amin
E
in
he o age. In his s udy
i amin
E
s a us
was no
assessed.
Howe e
ewes
we e
g azing on esh
he bage,
conside ed as an
adequa e
sou ce
o
i amin
E (Maas e
al.,
1984;
Hamli i
e al., 1993), sugges ing ha
i amin
E
s a us
was
adequa e.
I
is
well
known ha i amin E and
Se-GSH-Px
ac i i y a e he mos impo an
componen s
o
he an ioxida i e
de ence
mechanisms,
capable
o
subs i u ing o
one
ano he .
In his
sense,
Ga ce
and Cla ck (1991)
ha e
showed ha
Se- esponsi e
diseases
do no occu a he
same
selenium
s a us
in di e en
egions, sugges ing ha
hese
di e ences in Se equi emen s may be pa ly
explained by he a ying i amin E in akes. Ne e heless, i mus be conside ed
ha du ing si ua ions whe e an impo an oxida i e
s ess
occu s, such as
s ages
o
de elopmen , la e ges a ion o lac a ion, in ec ious
p ocesses,
e c.,
hese
wo
an ioxida i e
sys ems
could o e load,
wi h
he
appea ance
o
clinical
mani es-
a ions o selenium de iciency.
We
ha e
ound di e ences in CK and AST ac i i ies be ween bo h
seasons.
B aun e al. (1993) and And es e al. (1994)
ha e
also
desc ibed simila
seasonal
ends
o
hese
enzymes.
This a ia ions a e, in hei poin o
iew,
in ela ion
wi h
changes
o he die o he animals. The ac o
inding
CK ac i i ies sligh ly
abo e
he no mal
ange
when GSH-Px ac i i y showed a ma ked
descen
indica es ha his
c i ical
concen a ion
o
GSH-Px could
cause
sligh subclinical
pe oxida i e
damage
in
cell
memb anes.
As a
consequence
o
his,
al e a ions in
he pe meabili y o he
memb anes
occu s, b inging abou he libe a ion o his
cy osolic enzyme in o he blood s eam, and which
inally
esul s
in a sligh
inc ease
in plasma CK ac i i y. The AST e olu ion was di e en , showing he
lowes ac i i y du ing he summe , jus when he GSH-Px ac i i y was a he
minimum
alue. This beha iou con i ms ha AST is no as speci ic as CK as
ma ke o muscle
damage,
since
i is widely dis ibu ed in di e en
o gans
and
issues
(Blood
e al., 1992; Smi h e al., 1994). The in e se
changes
o
ENZYMES
ACTIVITY
IN SHEEP
WITH
Se
DEFICIENCY
349
GSH-Px-CK
ac i i ies could
also
indica e ha his la e enzyme may be
used
as
a good moni o o muscle
damage.
In his
sense
di e en au ho s
ha e
showed
ha CK is one o he mos speci ic
pa ame e s
o
acu e
muscle
damage
in all
species,
epo ing
also
ha CK
ac i i y
was
highly
co ela ed o muscle
damage
(Blood
e al., 1993; B aun e al., 1993; Smi h e al.,1994).
CONCLUSIONS
GSH-Px
ac i i y
egis e ed du ing he summe ,
wi hin
a de icien ange,
indica es ha he animals we e cons an ly a isk
om
selenium-de iciency
diseases.
Howe e , his low
ac i i y
did no o igina e muscle
damage,
since he
enzymes
CK and AST we e
wi hin
hei no mal ange, indica ing ha i may be
compensa ed
by an
adequa e
le el o
i amin
E in he die .
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ENZYMES
ACTIVITY
IN SHEEP
WITH
Se
DEFICIENCY
351
STRESZCZENIE
Sezonowe
zmiany ak ywnosci pe oksydazy glu a ionu, kinazy k ea ynowej i ans e azy aspa aginiano-
wej u owiec z ejonu niedobo u selenu
Oznaczono ak ywnosc pe oksydazy glu a ionu (GSH-Px;
E.C.
1.11.19), jako wskaznika
zaopa -
zenia o ganizmu w selen, o az kinazy k ea ynowej
(CK;
E.C. 2.7.3.2)
i
ans e azy aspa aginianowej
(AST;
E.C. 2.6.1.1), jako wskaznikow uszkodzen
mieini,
u owiec pochodz^cych z ejonu o niskiej
zawa osci selenu. Oznaczenia wykonano wiosna^ i la em, bowiem e po y
oku
sa, k y yczne dla
wys epowania niedobo u Se.
Ak ywnosc
GSH-Px byla najwi?ksza wiosn^; s ednie wa osci wahaly si? od 74,5 do 90,51 Ul/g
Hb,
obnizaj^c si? d as ycznie w
ciajm
la a do poziomow ponizej
izjologicznych
(P < 0,001), od
43,33
do 50,01 Ul/g Hb. Nie s wie dzono jednak w ym
czasie
uszkodzen mi?sni, gdyz
oznaczona
ak ywnosc enzymow CK i AST miescila si? w g anicach no m izjologicznych.