E ec s o die a y a s ( ish,oli e andhigh-oleic-acid sun lowe oils) on lipid
composi ion and an ioxidan enzymes in a li e
Valen ina Ruiz-Gu ie
´ ez
1
, Alonso Pe
´ ez-Espinosa
1
, Ca men Ma ı
´aVa
´zquez
2
and
Consuelo San a-Ma ı
´a
3
*
1
Ins i u o de la G asa y sus De i ados, CSIC, apdo 1078, Se illa, Spain
2
Depa amen o Fisiologı
´a y Biologı
´a Animal, Facul ad de Fa macia, c/ P o esso Ga cı
´a Gonza
´lez s/n, 41012, Se illa, Spain
3
Depa amen o de Bioquı
´mica, B oma ologı
´a y Toxicologı
´a, Facul ad de Fa macia, c/ P o esso Ga cı
´a Gonza
´lez s/n, 41012,
Se illa, Spain
(Recei ed 22 Sep embe 1998 – Re ised 12 Ap il 1999 – Accep ed 28 Ap il 1999)
The e ec s o wo oleic-acid- ich die s (con aining oli e oil, OO, and high-oleic-acid sun lowe
oil, HOSO) on plasma and li e lipid composi ion de oxi ica ion enzyme ac i i ies, we e
compa ed wi h hose o a ish-oil (FO) die and a con ol die . Compa ed wi h he con ol die ,
plasma and hepa ic o al iacylglyce ol concen a ions we e inc eased in he animals ed on he
HOSO and OO die s and dec eased in hose ed on he FO die . The animals ed on FO showed he
highes le el o choles e ol in he li e and had lowe plasma choles e ol concen a ions when
compa ed wi h hose ed on he wo oleic-acid- ich die s. In compa ison wi h he animals ed on
he die s en iched in oleic acid, he FO g oup showed highe hepa ic le els o polyunsa u a ed
a y acids o he n-3 se ies and lowe le els o a y acids o he n-6 se ies. Li e s o FO- ed a s,
compa ed wi h hose o OO- and HOSO- ed a s showed: (1) signi ican ly highe ac i i ies o
ca alase (EC 1.11.1.6) glu a hione pe oxidase (EC 1.11.1.9) and Cu/Zn supe oxide dismu ase
(EC 1.15.1.1); (2) no di e ences in he NADPH-cy och ome c educ ase (EC 1.6.99.3) ac i i y.
The HOSO die had a simila e ec on li e an ioxidan enzyme ac i i ies as he OO die . In
conclusion, i appea s ha changes in he li e a y acid composi ion due mainly o n-3 lipids
may enhance he e iciency o he an ioxidan de ence sys em. The wo monounsa u a ed a y
acids oils s udied (OO and HOSO), wi h he same high con en o oleic acid bu di e en con en s
o na u al an ioxidan s, had simila e ec s on he an ioxidan enzyme ac i i ies measu ed.
Fa y acids: An ioxidan enzymes: Oleic acid
Many clinical s udies ha e indica ed ha die s ich in ish
a e associa ed wi h ca dio ascula heal h (K omhou e al.
1985; He old & Kinsella, 1986). The esponsible compo-
nen o ish appea s o be he high con en o polyunsa u-
a ed a y acids (PUFA) o he n-3 se ies (Bang e al. 1986).
Howe e , he e is g owing conce n ha habi ual in ake o
la ge quan i ies o PUFA may induce ca cinogenesis, p ob-
ably because hey a e e y suscep ible o pe oxida ion and
p oduc ion o ee adicals (Kok e al. 1994; Fang e al.
1996). The p oduc ion o ee adicals has been associa ed
wi h ageing (Ha man, 1992); howe e , some s udies indi-
ca e ha ish oil (FO) seems o ex end he li e span in animal
models o au oimmune disease (Jeng & Fe nandes, 1989).
The ole o he an ioxidan de ence sys em, which
includes Cu/Zn supe oxide dismu ase (EC 1.15.1.1; Cu/
Zn SOD), ca alase (EC 1.11.1.6; CAT), and glu a hione
pe oxidase (EC 1.11.1.9; GSH-Px), in p o ec ion agains
oxida i e insul s is well cha ac e ized in he li e , and i has
been sugges ed ha his an ioxidan de ence sys em may be
in luenced by nu i ion (Huang e al. 1994).
Besides FO, oli e oil (OO), an oil ich in monounsa u-
a ed a y acids (MUFA), is also ela ed o ca dio ascula
heal h. OO is bene icial in lowe ing LDL-choles e ol bu no
HDL-choles e ol, and dec easing he suscep ibili y o he
LDL o oxida ion, which in u n educes he a he ogenici y
o he LDL and he de elopmen o CHD (Ma son &
G undy, 1985). I has been epo ed ha oleic acid is no
necessa ily he only componen esponsible o his e ec
and ha o he an ioxidan compounds con ained in he non-
glyce ide ac ion o OO, such as s e ols and polyphenols,
may con ibu e o hese bene icial esul s (Papadopoulos &
Boskou, 1991). Al hough he adi ional sou ce o die a y
MUFA is OO, o he sou ces a e now becoming a ailable
such as he new high-oleic-acid a ie y o sun lowe oil
B i ish Jou nal o Nu i ion (1999), 82, 233–241 233
Abb e ia ions: CAT, ca alase; FO, ish oil; GSH-Px,glu a hione pe oxidase; HOSO, high-oleic-acid sun lowe oil; MUFA,monounsa u a ed a y acids; OO,
oli e oil; PUFA, polyunsa u a ed a y acids; SOD, supe oxide dismu ase.
*Co esponding au ho : D Consuelo San a-Ma ı
´a, ax +34 95 423 3765, email [email p o ec ed]
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess
(HOSO), which has a simila a y acid composi ion bu
di e en an ioxidan con en (Pe ez-Jime
´nez e al. 1995).
Compa ed wi h FO, he a e o pe oxida ion and p oduc ion
o ee adicals in he MUFA oils is lowe .
The aim o he p esen s udy was o compa e he e ec s o
die a y FO, OO and he HOSO on plasma and hepa ic lipid
composi ion and on some hepa ic an ioxidan enzyme
ac i i ies. The esul s show ha he beha iou o CAT,
Cu/Zn SOD and GSH-Px seems o be ela ed o he n-3
con en o lipid in he li e . The FO die p o ided he
g ea es an ioxidan capabili y whils he OO and HOSO
die s beha ed simila ly wi h ega d o he an ioxidan
enzyme ac i i ies.
Me hods
Animals and die s
Male Wis a a s (Le ica, Ba celona, Spain), weighing abou
80g a he beginning o he expe imen s, we e used. The
animals we e housed in a well- en ila ed oom main ained
a 22628on a 12h ligh –da k cycle. The a s we e
andomly di ided in o ou g oups o en animals. Each
g oup was ed on one o he ollowing die s o 12 weeks: a
semipu i ied die (basal die ) con aining 20g unspeci ied
lipid/kg, pu chased om Panlab SRL (Ba celona, Spain)
(con ol g oup) o he basal die supplemen ed wi h 100g/kg
OO (OO g oup) o HOSO (HOSO g oup) o FO (FO g oup).
The composi ion o he expe imen al die s is shown in
Table 1. To minimize oxida ion, all die s we e p epa ed
once weekly and s o ed a 48unde an a mosphe e o N
2
un il needed. Changes in composi ion du ing s o age we e
no de ec ed.
The a y acid composi ions o he oils we e de e mined
and a e shown in Table 2. The non- a y-acid componen s o
he oils a e p esen ed in Table 3.
Blood sampling and issue p epa a ions
A comple ion o he s udy he animals we e killed by
ce ical disloca ion. To minimize diu nal a ia ions he
a s we e ou inely killed be ween 09.00 and 10.00 hou s.
Blood samples we e emo ed om he hea and collec ed
in o ubes con aining EDTA (1g/l). Plasma was sepa a ed
by low-speed cen i uga ion a 1500ga 48 o 30min and
was immedia ely analysed. Choles e ol, phospholipids and
iacylglyce ols we e de e mined using an au oanalyse and
con en ional enzymic me hods (Nelson, 1972; Bucolo &
Da id, 1973; Allain e al. 1974).
The li e s we e immedia ely insed in ice-cold 0⋅145M-
NaCl, immed and quickly weighed. A 2g po ion o li e
was used o lipid ex ac ion and he es was used o
de e mine enzyme ac i i ies. All subsequen p ocessing
p ocedu es we e ca ied ou a 0–48. Homogena es (100g/l)
234 V. Ruiz-Gu ie
´ ez e al.
Table 1. Composi ion o expe imen al die s (g/kg)
Ing edien s Con ol OO HOSO FO
Casein 209 203 203 203
Suc ose 450 374 374 374
Maize s a ch 202 180 180 180
Lipids 20 20 20 20
OO – 100 – –
HOSO – – 100 –
FO – – – 100
Cellulose powde 52 56 56 56
Mine al mix* 57 57 57 57
Vi amin mix† 10 10 10 10
To al ene gy (MJ) 15⋅217⋅117⋅117⋅1
P o ein (% ene gy) 23⋅119⋅719⋅719⋅7
Lipid (% ene gy) 4⋅926⋅326⋅326⋅3
Ca bohyd a e (% ene gy) 71⋅953⋅953⋅953⋅9
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
*Mine al mix con ained (mg/g): NaCl 139⋅3, K
2
HPO
4
389⋅1, CaCO
3
381⋅4,
MgSO
4
.7H
2
O57⋅3, FeSO
4
.7H
2
O27⋅0, MnSO
4
.H
2
O4⋅0, ZnSO
4
.7H
2
O1⋅25,
KI 0⋅8, CuSO
4
.5H
2
O0⋅5, CoCl
2
.6H
2
O0⋅02.
†Vi amin mix p o ided (/kg die ): e inol 5⋅9mg, calci e ols 0⋅15mg, hiamin
20mg, ibo la in 15mg, niacin 70mg, py idoxine 10mg, inosi ol 150mg,
cobalamin 50mg, ocophe ols 170mg, i amin K 40mg, choline 1⋅36g,
p e oylmonoglu amic acid 5mg,
p
-aminobenzoic acid 50mg, bio in 0⋅3mg.
Table 2. Fa y acid composi ion o die a y a s (g/100g o al
a y acids)
Fa y acids Con ol OO HOSO FO
14:0 – – – 3⋅8
16:0 13⋅211⋅84⋅313⋅9
16:1
n
-7 1⋅20⋅90⋅115⋅1
17:0 – 0⋅40⋅1–
18:0 3⋅12⋅84⋅70⋅9
18:1
n
-9 36⋅879⋅280⋅226⋅2
18:2
n
-6 41⋅73⋅59⋅45⋅1
18:3
n
-3 4⋅10⋅60⋅10⋅2
18:4
n
-3 – – – 2⋅5
20:0 – 0⋅30⋅4–
20:1
n
-9 – 0⋅20⋅22⋅4
20:2
n
-6 – – – 1⋅4
20:3
n
-6 – – – 0⋅4
20:4
n
-6 – – – 0⋅6
20:5
n
-3 – – – 13⋅8
22:4
n
-6 – – – 0⋅3
22:6
n
-3 – – – 12⋅7
24:0 – 0⋅40⋅4–
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
Table 3. Composi ion o he non- a y-acid componen s o he
expe imen al oils
OO HOSO FO
To al unsaponi iable ac ion (g/kg) 15 10 11
To al s e ols (mg/kg) 1696 1754 1500
Choles e ol (%) 0⋅15 0⋅01 100
B asicas e ol (%) – 0⋅32 –
Campes e ol (%) 3⋅80 10⋅25 –
S igmas e ol (%) 0⋅81 11⋅59 –
b-Si os e ol (%) 93⋅99 59⋅35 –
D-5-A enas e ol (%) – 2⋅88 –
D-7-S igmas e ol (%) 0⋅22 11⋅84 –
D-7-A enas e ol (%) 0⋅15 3⋅27 –
Squalene (mg/kg) 3000 90 7400
Tocophe ols (mg/kg) 47 10 300
a-Tocophe ols 34 10 300
g-Tocophe ols 13 – –
F ac ion o polyphenols (mg/kg) 470 – –
To al polyphenols (mg/kg) 430 – –
O odiphenol (mg/kg) 40 – –
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess
we e p epa ed in 0⋅25M-suc ose, 1mM-EDTA, 1mM-DL-
di hio h ei ol and 15mM-T is HCl (pH 7⋅4), using an all-
glass Po e El ehjem homogenize (Selec a, Ba celona,
Spain). Each homogena e was cen i uged o 20min
a 800g. The esul ing supe na an ac ion was used o
de e mine enzyme ac i i ies.
Ex ac ion and sepa a ion o lipids
Quan i a i e ex ac ion o o al lipids om 2g li e was
ca ied ou ollowing he me hod o Folch e al. (1957) in
he p esence o bu yla ed hyd oxy oluene as an ioxidan .
Tissue dissocia ion was achie ed by homogeniza ion in ice-
cold chlo o o m–me hanol (2:1, / ) con aining 0⋅1g BHT/l
using an Ul a-Tu ax model Type TP-18-1 (Ul a-Tu ax,
Vineland, NJ, USA).
The lipid ex ac was quan i ied g a ime ically and kep
in s oppe ed ubes unde N
2
a −308un il he assays. Lipid
composi ion was de e mined by means o he Ia oscan TLC
echnique wi h lame ioniza ion de ec ion (De Sch ij e &
Ve meulen, 1991). The Ia oscan MK-5 (Ia on Labo a-
o ies Inc., Tokyo, Japan) was used in combina ion wi h
Ch oma ods S, which ha e a p ecoa ed ac i e silica hin
laye . Samples o o al lipids (3ml) we e spo ed on o each
od, using a 10ml Hamil on sy inge. To sepa a e o al lipids,
ods we e de eloped in hexane–die hyl e he – o mic acid
(90:10:2, by ol.). Rods we e scanned unde he ollowing
condi ions: H
2
low, 150ml/min; ai low, 1750ml/min;
scanning speed, 47mm/s; cha speed, 42mm/min. An
Ia oco de TC-11 in eg a o was used o eco ding and
a ea in eg a ion.
Fa y acid analysis
Fa y acids (g/100g o al a y acids) we e de e mined by
GC, as p e iously desc ibed (Molina e al. 1989). The
samples we e saponi ied by hea ing o 25min wi h 5ml
0⋅2M-sodium me hyla e and hea ed again a 808 o 25min
wi h H
2
SO
4
in anhyd ous me hanol (60g/l). The a y acid
me hyl es e s hus o med we e elu ed wi h hexane
and analysed in a Hewle Packa d 5890 se ies II GC
equipped wi h lame ioniza ion de ec o and using an
Omegawak 320 used silica capilla y column (30m×
0⋅32mm i.d., 0⋅25mm ilm). The ini ial column empe a u e
was 2008, which was held o 10min, hen p og ammed
om 200–2308a 28/min.
Non- a y-acid componen s
Fo he ex ac ion o he unsaponi iable ma e , 20g oil was
saponi ied o 30min wi h 75ml o e hanolic KOH (100g/l).
The solu ion was ans e ed o a 5000ml decan ing unnel,
100ml dis illed wa e was added, and he mix u e was
ex ac ed wi h 100ml po ions o hexane. The hexane
solu ion was e apo a ed o d yness in a o a y e apo a o
a 308unde educed p essu e. The s e ol ac ion was
analysed by capilla y GLC (Ga cia Reguei o e al. 1994).
Tocophe ols we e analysed by HPLC (K ame e al. 1997).
Fo he assay o squalene, he hyd oca bon ac ion was
sepa a ed om he oil by column ch oma og aphy on silica
gel and analysed by capilla y GLC (Sulpice & Fe ezou,
1984). The composi ion o he polyphenols ac ion was
de e mined by capilla y GLC (A ce e al. 1998).
Enzyme ac i i ies
CAT ac i i y was assayed acco ding o he me hod o Bee s
& Size (1952). The inal concen a ions in he cu e es
we e 0⋅5M-KH
2
PO
4
(pH 7), 100mm H
2
O
2
and 0⋅05–0⋅1mg
issue sample. The dec ease in he abso bance a 240nm
a e he addi ion o he subs a e was ollowed spec o-
pho ome ically.
GSH-Px ac i i y was assayed wi h a coupled enzyme
sys em in which GSSG educ ion was coupled o NADPH
oxida ion by glu a hione educ ase (EC 1.6.4.1; Law ence &
Bu k, 1976). The assay mix u e con ained 0⋅1M-KH
2
PO
4
(pH 7⋅5), 5mM-EDTA, 2mM-NaN
3
,1mM-GSH, 0⋅2mM-
NADPH, 1U glu a hione educ ase and issue sample
(0⋅05–0⋅2mg). A e 5min p e-incuba ion (20–258), he
eac ion was ini ia ed by he addi ion o 0⋅05ml 5mM-
H
2
O
2
( inal olume 1⋅0ml). The dec ease in he abso bance
a 365nm was ollowed spec opho ome ically.
SOD ac i i y was measu ed using he xan hine oxidase
(EC 1.2.3.2)–cy och ome cme hod as desc ibed by McCo d
& F ido ich (1969). The inal concen a ions in he cu e es
we e 50mM-KH
2
PO
4
(pH 7⋅8), 0⋅1mM-EDTA, 10mM-
cy och ome c,50m
M-xan hine, 50mMo 2mM-cyanide,
1U CAT and 0⋅05–1⋅0mg issue sample. The eac ion was
ini ia ed by he addi ion o 1U xan hine oxidase. The
inhibi ion o xan hine oxidase was ollowed spec opho o-
me ically a 550nm. One uni o SOD ac i i y is de ined as
he amoun o enzyme equi ed o inhibi he a e o
cy och ome c educ ion by 50%.
NADPH-cy och ome c educ ase (EC 1.6.99.3) ac i i y
was measu ed as desc ibed by Ve milion & Coon (1978).
The 1⋅0ml assay mix u e con ained he ollowing com-
ponen s: 300mM-phospha e bu e (pH 7⋅7), 0⋅04mM-
cy och ome c,0⋅1mM-EDTA, 0⋅2mM-NADPH and issue
(0⋅05–0⋅2mg). The eac ion was ini ia ed by he addi ion o
he NADPH, and he educ ion o cy och ome cwas
ollowed spec opho ome ically a 550nm.
All spec opho ome ic measu emen s we e ca ied ou in
a Shimadzu 160 A ul a iole spec opho ome e (Shimadzu
Co po a ion, Kyo o, Japan) wi h 1⋅0ml qua z cu e es wi h
a ligh pa h o 1⋅0cm. All enzyme assays we e pe o med a
258. Speci ic ac i i ies we e exp essed as nmol/min pe mg
p o ein. P o ein concen a ions we e de e mined by he
me hod o Low y e al. (1951).
S a is ical me hods
All esul s we e subjec ed o one-way ANOVA, and ep e-
sen means, wi h hei s anda d e o s, o en animals pe
g oup. Di e ences in mean alues be ween g oups we e
assessed by he wo- ailed S uden ’s es and we e con-
side ed s a is ically di e en a P,0⋅05.
Resul s
In he p esen s udy, a s in he ou expe imen al g oups
consumed simila amoun s o ood (Table 4). Animals ed
on die s con aining OO o HOSO had simila body weigh s,
235E ec s o die a y a s on a li e
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess
bu hese we e highe han hose o animals ed on he
con ol o FO die s. Animals ed on he die con aining FO
had signi ican ly lowe body and li e weigh s when com-
pa ed wi h he o he g oups; howe e , he li e :body
weigh alues we e simila in all he g oups. Li e lipid
con en was highe in animals ed on he OO and HOSO
die s han in hose ed on he con ol o FO die s.
Table 5 shows he e ec o die a y a ea men on
plasma lipid con en . When compa ed wi h he con ol
die , he HOSO and OO die s led o signi ican inc eases
and he FO die led o a signi ican dec ease in plasma
iacylglyce ol le el. Consump ion o he FO die esul ed in
a dec ease in he o al choles e ol and phospholipid con-
cen a ions in plasma in compa ison wi h he high-oleic-
acid die s. The HOSO and OO g oups did no di e in
plasma lipid concen a ions, bu hese we e highe han
hose in he con ol g oup.
To al iacylglyce ol concen a ions in li e a e shown in
Table 6. The OO- ed g oup showed he highes alues and
he FO- ed g oup he lowes . To al hepa ic choles e ol was
lowes in he con ol g oup and highes in he FO g oup.
OO- and HOSO- ed g oups showed in e media e alues,
and no di e ence was ound be ween hese wo high-oleic-
acid die s. The hepa ic phospholipid con en was lowes in
he animals ed on he con ol die . The animals ed on he
oil-en iched die s showed simila hepa ic phospholipid
con en s.
Table 7 shows he p opo ions o a y acids (g/100g o al
a y acids) in li e lipids in a s ed on he di e en die s.
The highes p opo ions o he wo majo sa u a ed a y
acids, palmi ic (16:0) and s ea ic (18:0) acids, we e ound in
a s ed on he FO and con ol die s as compa ed wi h he
high-oleic-acid oil g oups. Thus, he le els o o al sa u a ed
a y acids in li e we e highe in he con ol and he FO- ed
g oups in compa ison wi h he animals ed on he die s
en iched in oleic acid. The p opo ions o 18:1n-9 we e
simila in he OO- and HOSO- ed g oups and highe han in
he con ol- o FO- ed animals. The MUFA:sa u a ed a y
acids a io was consequen ly inc eased in animals ed on he
wo oleic-acid- ich die s compa ed wi h he o he g oups.
The FO g oup had a highe p opo ion o long-chain PUFA
o he n-3 se ies (20:5, 22:5 and 22:6) han he con ol, OO,
o HOSO g oups. The FO g oup also had lowe p opo ions
o long-chain PUFA o he n-6 se ies (20:4, 22:4 and 22:5)
wi h espec o he o he g oups. The e o e he n-6:n-3 a io
and he 20:4/18:2 a io we e ma kedly lowe in he FO
g oup.
The animals ed on he FO die exp essed highe CAT
ac i i y in he li e (5⋅06 (SE 0⋅27) U/mg p o ein) when
compa ed wi h he o he g oups (Fig. 1(a)). The CAT
ac i i y was simila in he OO and HOSO g oups (app oxi-
ma ely 3⋅70U/mg p o ein). The GSH-Px ac i i y in animals
ed on he con ol die was 0⋅63 (SE 0⋅01) U/mg p o ein.
Feeding he FO die inc eased his ac i i y o 0⋅74 (SE 0⋅05)
U/mg p o ein and eeding OO o HOSO dec eased he
ac i i y o 0⋅39 (SE 0⋅02) U/mg p o ein and 0⋅47 (SE 0⋅08)
U/mg p o ein espec i ely (Fig. 1(b)).
The Cu/Zn SOD ac i i y was highes in he FO- ed g oup
(3⋅51 (SE 1⋅12) U/mg p o ein) and was signi ican ly highe
han in he o he g oups. The oleic-acid-en iched oils had no
e ec on Cu/Zn SOD ac i i y compa ed wi h he con ol
die (Fig. 2(a)). The ac i i ies o NADPH-cy och ome c
236 V. Ruiz-Gu ie
´ ez e al.
Table 4. E ec o di e en die a y a s, ed o 12 weeks, on body weigh , ood in ake, li e weigh and li e lipid con en in a s*
(Mean alues wi h hei s anda d e o s o en a s pe g oup)
Die ... Con ol OO HOSO FO
Mean SE Mean SE Mean SE Mean SE
Food in ake (g/d) 20⋅81⋅121⋅00⋅922⋅81⋅919⋅11⋅2
Body w (g) a en y 85⋅12⋅377⋅63⋅278⋅33⋅186⋅82⋅4
a 12 weeks 302⋅4
a
7⋅8 325⋅9
b
6⋅1 331⋅1
b
13⋅2 260⋅4
c
6⋅6
Li e w (g) 9⋅3
a
0⋅810⋅4
a
0⋅89⋅4
a
1⋅27⋅5
b
0⋅6
Li e w (g/kg body weigh ) 31 2 30 3 31 2 29 4
Li e lipid con en (g/kg) 21
a
545
b
444
b
332
c
2
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
a,b,c
Mean alues wi hin a ow no sha ing a common supe sc ip le e we e signi ican ly di e en :
P
,0⋅05.
*Fo de ails o die s and p ocedu es, see Tables 1–3 and pp. 234–235.
Table 5. Plasma lipid concen a ions in a s ed o 12 weeks on die s con aining di e en a s*
(Mean alues wi h hei s anda d e o s o en a s pe g oup)
Die ... Con ol OO HOSO FO
Plasma lipid Mean SE Mean SE Mean SE Mean SE
T iacylglyce ols (mmol/l) 1⋅25
a
0⋅23 1⋅72
b
0⋅12 1⋅68
b
0⋅17 0⋅89
c
0⋅14
Choles e ol (mmol/l) 2⋅02
a
0⋅41 2⋅55
b
0⋅22 2⋅44
b
0⋅23 2⋅20
a
0⋅21
Phospholipids (mmol/l) 1⋅29
a
0⋅12 1⋅44
b
0⋅15 1⋅46
b
0⋅21 1⋅23
a
0⋅15
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
a,b,c
Mean alues wi hin a ow no sha ing a common supe sc ip le e we e signi ican ly di e en :
P
,0⋅05.
*Fo de ails o die s and p ocedu es, see Tables 1–3 and pp. 234–235.
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess
educ ase we e simila in li e s o a s ed on he oil-
en iched die s, and we e highe han ha o he con ol
animals (Fig. 2(b)).
Discussion
The p esen s udy was designed o de e mine whe he
eeding a PUFA oil (FO) o wo MUFA oils, p epa ed
om wo di e en sou ces (OO and HOSO), a ec s he
li e lipid composi ion and he an ioxidan de ence sys em;
he plasma lipid composi ion was also s udied.
Li e lipid iacylglyce ol le els we e lowes in FO- ed
a s (Table 6). This may ha e been due o inhibi ion o
hepa ic iacylglyce ol syn hesis (Wong e al. 1984; F oy-
land e al. 1997), and s imula ion o hepa ic pe oxisomal
b-oxida ion (Yamazaki e al. 1987) p oduced by he FO
die . Dec eases in lipop o ein lipase (EC 3.1.1.34) and
iacylglyce ol lipase (EC 3.1.1.3) ac i i ies in he li e
a e FO consump ion ha e also been desc ibed (Hu e al.
1993), and his may be an adap i e esponse o he low
concen a ions o subs a es ( iacylglyce ols) o hese
enzymes. The low le els o iacylglyce ols in li e a e
FO consump ion may also be ela ed o he educed le els o
plasma iacylglyce ols ound in ou s udy (Table 5) and
also desc ibed by o he s in man (Phillipson e al. 1985) and
a s (Yamazaki e al. 1987).
The OO die esul ed in a highe li e iacylglyce ol
con en han he HOSO die . This ac has been ecen ly
co obo a ed by o he s udies om ou g oup (Pe ona &
Ruiz-Gu ie ez, 1998), in which i has been epo ed ha he
237E ec s o die a y a s on a li e
Table 6. Li e lipid concen a ions in a s ed o 12 weeks on die s con aining di e en a s*
(Mean alues wi h hei s anda d e o s o en a s pe g oup)
Die ... Con ol OO HOSO FO
Li e lipid Mean SE Mean SE Mean SE Mean SE
T iacylglyce ols (mg/g) 5⋅5
a
0⋅812⋅3
b
1⋅78⋅3
c
0⋅91⋅9
d
0⋅6
Choles e ol (mg/g) 3⋅1
a
0⋅34⋅4
b
0⋅64⋅7
b
0⋅56⋅7
c
0⋅6
Phospholipids (mg/g) 13⋅4
a
1⋅329⋅6
b
3⋅732⋅3
b
3⋅826⋅5
b
3⋅2
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil; FO, ish oil.
a,b,c,d
Mean alues wi hin a ow no sha ing a common supe sc ip le e we e signi ican ly di e en :
P
,0⋅05.
*Fo de ails o die s and p ocedu es, see Tables 1–3 and pp. 234–235.
Table 7. Fa y acid composi ion (g/100g o al a y acids) o he li e lipids o a s ed o 12 weeks on die s
con aining di e en a s*
(Mean alues wi h hei s anda d e o s o en a s pe g oup)
Die ... Con ol OO HOSO FO
Fa y acid Mean SE Mean SE Mean SE Mean SE
14:0 0⋅40⋅10⋅30⋅10⋅40⋅10⋅40⋅1
16:0 21⋅1
a
0⋅415⋅4
b
2⋅017⋅3
b
0⋅722⋅3
a
1⋅0
16:1
n
-7 1⋅80⋅31⋅10⋅11⋅50⋅11⋅10⋅1
18:0 18⋅5
a
3⋅313⋅9
b
0⋅713⋅3
b
2⋅119⋅7
a
1⋅8
18:1
n
-9 13⋅1
a
1⋅327⋅7
b
0⋅524⋅6
b
2⋅78⋅4
c
0⋅2
18:1
n
-7 1⋅40⋅11⋅50⋅41⋅70⋅11⋅00⋅1
18:2
n
-6 13⋅11⋅711⋅90⋅513⋅31⋅113⋅91⋅6
18:3
n
-3 0⋅3
a
0⋅00⋅2
b
0⋅00⋅2
b
0⋅00⋅3
a
0⋅0
20:0 0⋅5
a
0⋅10⋅2
b
0⋅10⋅3
b
0⋅00⋅3
b
0⋅0
20:1
n
-9 0⋅1
a
0⋅00⋅4
b
0⋅10⋅3
b
0⋅00⋅1
a
0⋅0
20:4
n
-6 23⋅2
a
1⋅621⋅9
a
1⋅521⋅6
a
1⋅615⋅6
b
0⋅7
20:5
n
-3 0⋅2
a
0⋅00⋅1
a
0⋅00⋅1
a
0⋅03⋅0
b
0⋅9
22:0 0⋅6
a
0⋅10⋅5
a
0⋅10⋅7
a
0⋅10⋅9
b
0⋅0
22:4
n
-6 0⋅5
a
0⋅00⋅4
a
0⋅10⋅3
a
0⋅10⋅6
b
0⋅0
22:5
n
-6 0⋅6
a
0⋅20⋅4
a
0⋅10⋅4
a
0⋅10⋅2
b
0⋅0
22:5
n
-3 0⋅7
a
0⋅10⋅3
b
0⋅10⋅4
b
0⋅11⋅7
c
0⋅4
22:6
n
-3 3⋅8
a
0⋅63⋅6
a
0⋅83⋅3
a
0⋅411⋅1
c
1⋅8
SFA 41⋅1
a
3⋅430⋅3
b
2⋅831⋅9
b
2⋅943⋅5
a
2⋅8
MUFA 16⋅5
a
1⋅730⋅8
b
1⋅128⋅1
b
2⋅410⋅6
c
0⋅5
PUFA 42⋅4
a
3⋅439⋅0
b
2⋅339⋅7
b
1⋅345⋅9
a
1⋅7
To al
n
-6 37⋅4
a
3⋅934⋅7
a
2⋅235⋅7
a
3⋅729⋅9
b
2⋅2
To al
n
-3 5⋅0
a
0⋅44⋅3
a
0⋅44⋅0
a
0⋅416⋅1
b
2⋅9
n
-6:
n
-3 7⋅5
a
1⋅98⋅1
a
1⋅78⋅9
a
2⋅31⋅9
b
0⋅6
MUFA:SFA 0⋅4
a
0⋅31⋅0
b
0⋅30⋅9
b
0⋅20⋅2
a
0⋅1
20:4/18:2 1⋅7
a
0⋅41⋅8
a
0⋅51⋅6
a
0⋅31⋅1
b
0⋅2
OO, oli e oil; HOSO, high-oleic-acid sun lowe oil;FO, ish oil; SFA, sa u a ed a y acids; MUFA, monounsa u a ed a y acids;
PUFA, polyunsa u a ed a y acids.
a,b,c
Mean alues wi hin a ow no sha ing a common supe sc ip le e we e signi ican ly di e en :
P
,0⋅05.
*Fo de ails o die s and p ocedu es, see Tables 1–3 and pp. 234–235.
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess

consump ion o OO esul s in a g ea e amoun o li e
iacylglyce ol when compa ed wi h consump ion o HOSO.
These esul s sugges ha ac o s o he han he oleic acid
con en o he oils may be esponsible o enhancing
iacylglyce ol syn hesis in he li e o he animals ed on
he OO die . Fu he mo e, he same au ho s in he p esen
s udy obse ed di e en dis ibu ions o iacylglyce ol
molecula species in a li e ; OO led o a highe con en
o dioleoacylglyce ol species while he HOSO die led o
an inc ease in sa u a ed iacylglyce ol species, sugges ing
ha hese e ec s may be due o an enhancemen in he
syn hesis o such molecula species. In plasma we did no
obse e di e ences in iacylglyce ol con en o he wo
high-oleic-acid die s s udied.
Choles e ol le els in li e we e inc eased in animals ed
on he lipid-supplemen ed die s compa ed wi h he con ol
g oup (Table 6). The FO die led o highe alues han he
HOSO and OOdie s. The inc eased li e choles e ol con en
in he FO- ed a s migh ha e been due o he inc eased
squalene con en in his die compa ed wi h he o he s
(Table 3). The die a y e ec o his p ecu so o choles e ol
biosyn hesis is no clea , bu i has been shown o inc ease
bilia y choles e ol sec e ion (Ulloa & Ne i, 1985). In
plasma we ound a lowe choles e ol le el in he FO
g oup han in he OO and HOSO g oups. I has also been
desc ibed ha FO consump ion educes choles e ol le els in
blood, and ha i is mo e hypocholes e olaemic han OO
(Masi e al. 1986). Ga g e al. (1988) epo ed ha
PUFA lowe choles e ol le els in man and animals due o
a edis ibu ion o choles e ol om blood o issues.
We ound high choles e ol le els in bo h li e and plasma
ollowing oleic acid eeding compa ed wi h he con ol die .
This hype choles e olaemic e ec o a die high in OO in
se um and li e o a s has been epo ed p e iously by
Yaqoob e al. (1995). Je e y e al. (1996) con i med he
238 V. Ruiz-Gu ie
´ ez e al.
Fig. 1. Speci ic ac i i ies o (a) ca alase and (b) glu a hione pe oxi-
dase in he li e s o a s ed o 12 weeks on a con ol die o die s
con aining 100g/kg o oli e oil (OO), high-oleic-acid sun lowe oil
(HOSO) o ish oil (FO). Values a e means o en a s pe g oup, wi h
s anda d de ia ions ep esen ed by e ical ba s.
a,b
Mean alues no
sha ing a common le e we e signi ican ly di e en :
P
,0⋅05.
Fig. 2. Speci ic ac i i ies o (a) Cu/Zn supe oxide dismu ase and (b)
NADPH-cy och ome
c
educ ase in he li e s o a s ed o 12 weeks
on a con ol die o die s con aining 100g/kg o oli e oil (OO), high-
oleic-acidsun lowe oil (HOSO) o ish oil (FO). Values a e means o
en a s pe g oup, wi h s anda d de ia ions ep esen ed by e ical
ba s.
a,b
Mean alues no sha ing a common le e we e signi ican ly
di e en :
P
,0⋅05.
h ps://doi.o g/10.1017/S0007114599001415 Published online by Camb idge Uni e si y P ess
e ec on se um o al choles e ol concen a ions in a s ed
on die s con aining OO o HOSO. In man, howe e ,
hypocholes e olaemic e ec o MUFA is well es ablished
(Ma son & G undy, 1985) al hough he mechanism by
which i is b ough abou emains unclea .
Analysis o he a y acid composi ion in a li e homo-
gena es showed a signi ican inc ease o 18:1 in li e lipids
ob ained om OO- and HOSO- ed a s. We also ound
lowe sa u a ed a y acid le els in bo h g oups. This
inc ease in oleic acid con en was p obably ela ed o he
highe con en o oleic acid in he die o hese animals. I
has been epo ed ha when endo helial cell cul u es a e
di ec ly supplemen ed wi h oleic acid, an inc ease in i s
con en is ound, accompanied by a dec ease in he sa u a ed
acid con en (Spec o & Yo ek, 1985).
Wi h espec o he FO die , we ound a ma ked inc ease
in he p opo ion o o al n-3 a y acids (mainly 20:5 and
22:6), and a concomi an dec ease in n-6 (20:4, 22:4 and
22:5) a y acids in he li e . As a consequence, a signi ican
educ ion in he a io n-6:n-3 was ound in hese animals.
O he au ho s ha e epo ed a dec ease in a achidonic acid
in li e (Venka aman e al. 1994) and lung (A che e al.
1987) in animals ed on FO.
Animals ed on he FO die had highe ac i i ies o GSH-
Px, CAT and Cu/Zn SOD compa ed wi h hose ed on he
con ol die and he oleic-acid-en iched die s. Because he
lipid composi ion o he li e o a s e lec ed he lipid
composi ion o he die , he li e lipids o he a s ed on he
FO die con ained highe le els o PUFA. This ac migh
ende he li e s o a s ed on he FO die mo e suscep ible
o lipid pe oxida ion and he ac i i y o an ioxidan enzymes
migh be induced. A po en ial mechanism o he induc ion
o hepa ic an ioxidan s ollowing FO eeding migh be an
inc ease o he exp ession o hei genes; induc ion o he
exp ession o an ioxidan enzymes has been epo ed in
ci cums ances whe e an inc ease in ee adicals is p o-
duced, such as ageing (De Haan e al. 1992) o se e al
pa hologies (Ce iello e al. 1996; La ea e al. 1998). I is
also well known ha ee adicals may egula e he an-
sc ip ion o many o he genes (C ame e al. 1995; Roche &
Rome o-Al i a, 1995).
This g ea e ac i i y o an ioxidan enzymes may con-
ibu e o he hypo hesis ha consump ion o FO ex ends
li espan. This ac has been desc ibed in animal models o
au oimmune disease (Jeng & Fe nandes, 1989). An ioxi-
dan s ha e been closely linked wi h he p ese a ion o
heal h and longe i y in bo h mice and a s (Semsei e al.
1989; Rao e al. 1990).
Yamazaki e al. (1987) ound ha eeding FO o animals
inc eased he ac i i ies o some li e enzymes ( a y acyl-
CoA syn he ase (EC 2.3.1.85), CAT and GSH-Px) when
compa ed wi h sa lowe -oil- ed animals. Venka aman e
al. (1994) desc ibed an inc ease in he ac i i ies and mRNA
exp ession o CAT, GSH-Px and SOD in mice ed on a die
ich in FO compa ed wi h o he die s ich in n-6 lipids.
Recen ly, he same g oup has epo ed inc eases in CAT and
GSH-Px ac i i ies in seden a y and exe cised Fische -344
a s espec i ely, a e consump ion o FO, and non-signi i-
can changes in memb ane lipid pe oxida ion (Venka aman
e al. 1998). In con as , L’Abbe e al. (1991) epo ed ha
die s high in n-3 a y acids ele a e he lipid pe oxida ion in
hea and li e , due in pa o dec eased SOD and GSH-Px
ac i i ies. Nalbone e al. (1980) epo ed ha he GSH-Px
ac i i y o a s ed on FO die s emained unchanged in li e .
Be ge & Thomassen (1985) showed ha CAT ac i i y was
a ec ed only sligh ly by a FO die , and Van Noo den (1995)
desc ibed a mode a e inc ease in CAT ac i i y.
Less a en ion has been paid o he e ec o oleic-acid-
en iched die s on an ioxidan enzymes. In ou s udies we
ha e no ound di e ences in he ac i i ies o he an iox-
idan enzymes be ween he wo high-oleic-acid die s es ed.
The non-glyce ide ac ions o hese oils a e di e en (Table
3); polyphenols, which ha e ee- adical-sca enging p op-
e ies, a e only p esen in OO, and ocophe ols, which also
ha e an an ioxidan e ec , a e highe in OO. These di e -
ences in he na u al an ioxidan con en in he wo oils seems
no o a ec he ac i i y o he hepa ic an ioxidan enzymes
s udied.
NADPH-cy och ome c educ ase pa icipa es in he
de oxi ica ion o d ugs and xenobio ics. Simila ac i i ies
o NADPH-cy och ome c educ ase we e obse ed in a s
ed on he OO, HOSO and FO die s in he p esen s udy, and
each oil die suppo ed highe ac i i y han he con ol die .
Hepa ic NADPH-cy och ome c educ ase ac i i y was no
signi ican ly a ec ed by he FO die in compa ison wi h a
low- a die o die s en iched in n-6 PUFA (Van Noo den,
1995). The concen a ion o cy och ome P450 and a es o
oxida i e d ug me abolism we e g ea e when polyunsa u-
a ed a s we e inco po a ed in o he die han when a - ee
die s o sa u a ed a s we e gi en (Smi h & Willis, 1981).
In summa y, i appea s ha changes in he li e a y acid
composi ion, due mainly o n-3 lipids, may inc ease he
ac i i y o some an ioxidan enzymes, compensa ing he
isk o ca cinogenesis due o he pe oxida ion o PUFA and
ee- adical p oduc ion. On he o he hand, he wo MUFA
oils s udied (OO and HOSO), in spi e o hei di e en
con en s o na u al an ioxidan s, ha e simila e ec s on he
an ioxidan enzyme ac i i ies s udied.
Acknowledgemen s
This s udy was suppo ed by G an ALI96-0456 om he
Comision In e minis e ial de Ciencia y Tecnologı
´a, Spain.
We wish o hank Koipe S.A. and Acei es Toledo. We a e
g a e ul o Fe nanda Leo
´n and Manuel Rod iguez-Aguila
o expe echnical assis ance.
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