Argan oil's benefits on cardiovacular diseases

Argan oil: Which benefits on cardiovascular diseases

M. Cherki et al.

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In spite of the high content of antioxidants in argan oil, little is known about its action. Recently, some laboratories have investigated in vitro the effect of argan oil minor compounds (tocopherols, sterols and polyphenols) at different concentrations on human-oxidized LDL by incubation with CuSO4 [22,37]. LDL lipid peroxidation was evaluated by conjugated diene and malondialdehyde(MDA) formation as well asVitamin E disappearance. In both studies, results showed that incubation of LDL with tocopherol, sterol and phenolic extracts of argan oil significantly prolonged the lag-phase of LDL peroxidation. Also, the phenolic extracts lowered the rate of lipid peroxidation and reduced the disappearance of Vitamin E in a concentrationdependent manner [22,37]. Incubation of HDL with phenolic extract significantly increased the fluidity of the HDL phospholipidic bilayer and the HDL-mediated cholesterol efflux from THP-1 macrophages. Cherki et al. [38] have also observed an increase (3.7%) of theHDLfluidity of subjects consuming argan oil for 7 weeks without being significant [38].

In parallel, other interesting ex-vivo studies have investigated whether the consumption of argan oil could improve antioxidant status in healthy men [22,39]. The first study showed that a regular consumption of argan oil significantly decreases plasma lipid peroxides (58.3%) and increases significantly the molar ratio of .-tocopherol/total cholesterol (21.6%) as well as .-tocopherol concentration (13.4%) when compared to a nonconsumer group [22]. In the second study, the results showed that 25 ml/day of argan oil during 3 weeks in healthy men induces a significant increase in the paraoxonase 1 (PON1) activities (29–45%) and Vitamin E concentration (16%) and decrease significantly the lipid peroxides and conjugated diene formation (18 and 8%, respectively) compared to the baseline values. Susceptibility of LDL to lipid peroxidation as well as the maximum diene production (MDP) were significantly reduced (8 and 13%, respectively). These findings confirm the beneficial effect of argan oil on plasma antioxidant status in vitro and show the same effect for argan oil supplementation in men. Thus, argan oil offers an additional natural food supplement to reduce cardiovascular risk.

The protective effect of argan oil is probably due to its high contents of powerful antioxidants, particularly polyphenols, tocopherols and sterols, which are known as powerful antioxidants [10]. These products act by several mechanisms: (1) scavenging of peroxy radicals, which break the peroxidation chain reaction; (2) chelating free Cu2+ to form redox-inactive complexes and thus reducing metal-catalyzed oxidation of LDL; and (3) inhibiting the binding of Cu2+ to apolipoproteins and subsequently preventing the modification of amino acid-apo-B protein residue. These hypotheses are also supported by the extended lag-phase and the reduction in the maximum diene production. Thus, LDL may be enriched with different antioxidants of argan oil, which might reduce their susceptibility to lipid peroxidation [40,41]. Gimeno et al. [42] showed that an intake of 25 ml/day of olive oil could increase the resistance of LDL to oxidation. Similarly, several in vitro and in vivo studies in humans as well as in animals have demonstrated that Vitamin E and phenolic compounds extracted from olive oil inhibited oxidation of LDL [6,11,43]. In the case of argan oil, the diminution of LDL susceptibility to lipid peroxidation, could be explained partially by an enrichment with oleic acid that reduce the oxidation potential [44]. In the same time, the marked increase of plasma Vitamin E may be due to abundance of tocopherols in argan oil (636 mg/kg), although the main tocopherol present in this oil is the .-tocopherol form [12]. The increase of plasma .-tocopherol levels with argan oil could be consequence of an eventual conversion from .- to.-tocopherol because of the close similarity between chemical structures of both molecules [45]. Indeed, .-tocopherol supplementation simultaneously increases .- and .-tocopherol levels. Recent epidemiological, experimental and mechanistic evidences suggest that .-tocopherol may be a more potent antioxidant and cancer chemopreventive agent than .-tocopherol [46–48]. For example, it was found that .-tocopherol have more potent interaction to reactive nitrogen oxide species than .-tocopherol [49]. In addition, because Vitamin E is the major natural antioxidant among those present in LDL, it is considered as the first line of defence against lipid peroxidation [6]. This was confirmed by the finding of Nigdikar et al. [50] which showed that the increase in lag-phase withVitamin E was four- to five-fold greater than with red wine polyphenols.

Also, the antioxidant activity of argan oil could be attributed to its capacity to induce a significant increase in the PON1 activities [39]. Indeed, dietary habits with a high content of vegetable oil could affect paraoxonase and arylesterase activities [51–53]. Nguyen and Sok [54] have demonstrated that the increase of PON1 activities is associated with the unsaturated fatty acid content. Indeed, they showed that monoenoic acids or their phospholipid derivatives play a beneficial role in protecting PON1 from oxidative inactivation as well as in stabilizing PON1 [54]. On the other hand, atherogenic diets have been demonstrated to reduce PON1 activities [51]. Shih et al. [51] showed that C57BL/6J mice fed with a high saturated fat, cholesterol (1.25% (w/w)), and cholate (0.5% (w/w)) diet exhibited reduced serum PON1 activities and hepatic PON1-mRNA levels.

Furthermore, antioxidant substances such as flavonoid quercetin, were shown to reduce the amount of lipoproteinassociated lipid peroxides and preserved PON1 activity [55]. Also, polygonatum extract and Vitamin E reduced oxidative stress and increased serum PON1 activity, but had no effect on PON1-mRNA expression in rabbit fed a high-cholesterol diet [56]. Similarly, Vitamin E supplementation in rats with propylthiouracil-induced hypothyroidism resulted in decreased lipid peroxide levels in plasma and significantly increased serum PON1 activity compared with propylthiouracil alone [57]. The minor polar components of argan oil could also be involved in this change. Thus, increasing plasma PON1 activities potentiate the anti-atherogenic effect of argan oil.
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