BioI. Med. Uden S., Schofield D., Miller P.F., Day J.P., Bottiglieri T. & ... 1992,6: 229-240. Bolton-Smith C., Woodward M. & Tunstall-Pedoe H. Eur. J. Clin. Nu@.
Biochemical Society Transactions ( 1 996) 24
E f k t of oral suppkmentation with micronutricnt antioxidants on t n m s fatty acid content of lipoproteins in healthy humans
--.,
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.... . ..._..,... .. .
~~
19 1 S
-...I--........I_.-."
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Low-Density High-Density "......" . , _.. LkW!!!5k! ...............m ..........."Fh9.!?!5 ,.".... Pre AORx Post AORx Pre AORx Post AORx
CHRISTOPHER CHALONER, MICHAEL I MACKNESS, PAUL N DURRINGTON and JOAN M BRAGANZA
PL YoMRLA
Department of Medicine, Royal Infirmary, Manchester, MI3 9WL,
PL Linoleate (pmoVmg protein)
217k38
178f18
186f34
130f18
PL Arachidonate (pmoVmg protein)
74f12
49k6
71k11
48f9
PL Oleate (pmoVmg protein)
90k 10
57+5*
78k34
49k5**
a Carotene (pmollmg protein)
268 f 66
731 f 119**
46 k 9
126 f 36*
13.0k1.3
5.5k0.5
5.8f0.4
L.01 k0.13 0.79f0.11 1.43f0.18 2.10f0.16*
UK Recent studies [I] showing little or no trans fatty acids in adipose tissues of paheats dying 60m myocardial infarction should not be
taken as evidence that trans isomerisation is irrelevant to the genesis of atherosclerosis. Exposure of linoleic acid (9Z, IZ-octadecadienoic acid) to ultraviolet radiation preferentially yields a stable diene-cojugated 9Z,11E isomer [2]. The same cis hm.s isomer OCCUTS in viw, as shown by ~apiUaryg a ChO~tOgraphy-mass ~ S ~ ~ ~ ~ ~ O S [3]. C O PThis Y speclficlty, when four isomers are possible (Z, Z; Z, E; E, Z; E, E), suggests the involvement of an isomerase that is activated by free radicals, and thwarts chain propagation towards lipid peroxidation [2]. Dietary and microbiological souTces cannot account for the very high serwn lev& of the 9Z, 11E isomer in oxidative stress-linked conditions such as pancreatitis, nor its normalisation by supplements of m i c r o d e n t antioxidants [4]. F'rmohid deficiencies of micronutrieat antioxidants have been implicated in a predisposition to atherosclerosis[5]. Therdore, lipidphase antioxidants were measured in low- (LDL) and high- (HDL) density lipoprotein 6actions before and after daily treatment for 20 days With selenium 200 pg, Dcarotene 1800 iu, vitamin C 180 mg, vitamin E 90iu. The results, and also the fatty-acid profiles of the particles' phospholipid coats, were examined in relation to previously published data on copper-stimulated production kinetics of lipid peroxides [6]. nK results (table) showed: (a) a threefold increase in B carotene, but no change in a tocopherol, in LDL and HDL 6actions, (b) reduced total unsahuated fatty acids in each -on; and, most i n t e r m , (c) sel&e concentration of 9Z, 1 1E within HDL after antioxidant supplements. The tindings suggest one way in which antioxidant-replete HDL may protect LDL against oxidation in viw,favouring isomerisation rather than propagation of a 6ee radical attack along the peroxidative pathway: this should stabilise LDL and hence thwart its uptake by scavenger macrophages (regarded as a prerequisite for the atheroscleroticprocess). Finally, the results help to explain the previously noted reduction in 'diem coyugates' but not in lipid peroxides within LDL after this antioxidant regimen [6], since 9Z, 11E accounts for the bulk of DC products in Vivo [2].
10.6k1.5 a Tocopherol (nmoVmg protein)
Table: Trans fat&yacid (%MRLA) and other parameters of oxidative stress in lipoprotein subfractions before @re AORx)and after @ost AORx) oral antioxidant supplements. *=p