hydroxyl-free radicals and serve as potential antioxidants (Toure and Xueming
2010). Human body produces free radicals during fat, protein, and carbohydrate
oxidation, which damages tissues, membrane lipids, nucleic acids, etc. leading to
various diseases like cancer, neurological disorder, aging, etc. Lignan can scavenge
free radicals thus reducing oxidative stress (Hu et al. 2007). Under in vivo and
in vitro conditions, SDG, enterodiol, and enterolactone act as antioxidants by
inhibiting peroxidation of polyunsaturated fatty acids and decrease oxidation of
LDL cholesterol (Kitts et al. 1999). Also, SDG has been found to be a plateletactivating factor antagonist (Hall et al. 1993).
10.6.1.3 Effects of Omega Fatty Acids
Through several mechanisms such as decreasing inflammatory response, inhibiting
platelet aggregation and thrombosis, decreasing blood pressure, improving serum
lipids, and preventing cardiac arrhythmias, omega-3 fatty acids prevent cardiovascular diseases (Lanzmann-Petithory et al. 2002). These fatty acids interfere with the
production of pro-inflammatory and pro-aggregatory eicosanoids (prostaglandin E2,
thromboxane Ax2, and leukotriene B4) and protect against cardiovascular diseases.
Since ALA and linoleic acid (LA) are essential fatty acids, they need to be supplied
through diet. Upon ingestion, LA and ALA yield different classes of the eicosanoids.
Such eicosanoids have beneficial effects in case of inflammation, platelet aggregation, and vasoconstriction (Bloedon and Szapary 2004). Alternatively, omega-3 fatty
acids are involved in alteration of enzyme synthesis, regulating gene transcription
and expression, and modification of risk factors for coronary heart diseases (Chen
et al. 2007).
One of the prime requirements for the development of atherosclerosis is the
production of oxygen-free radicals. These free radicals are produced in the body
due to several metabolic reactions causing endothelial dysfunction which is the
causative agent for the development of hyperchoestrolemic atherosclerosis which
causes ischemic heart disease, stroke, and peripheral vascular diseases (Prasad
2000). The effect of flaxseed consumption on serum lipid levels had been studied
in several animal models and has been reported to have positive results. Similar
studies have been conducted in humans where flaxseed has been found to have
beneficial effect in CVDs and hypocholesterolemic activity.
Regular consumption of flaxseed has been found to decrease atherosclerosis
(by 46%) and lowered the number of inflammatory polymorphonuclear leukocytes
in rabbits (Prasad et al. 1998). Further, it was reported that when purified SDG
(15 mg/kg) was added to an atherogenic diet in rabbits (for 8 weeks), levels of aortic
malondialdehyde were also reduced (Prasad 1997). In a study involving 40 female
weaning Wistar rats fed with 200 g flaxseed oil/kg body weight for 4 weeks,
MacDonald-Wicks and Garg (2002) reported that flaxseed produced the lowest
concentration of 8-iso-PGF 2α (an in vivo oxidative stress marker) when administered
with an oxidative stress inducer (CCL4) as compared to rats that received either
saturated fat or linoleic acid containing diets. SDG isolated from flaxseed reduced
10 Flaxseed (Linum usitatissimum)
261
2010). Human body produces free radicals during fat, protein, and carbohydrate
oxidation, which damages tissues, membrane lipids, nucleic acids, etc. leading to
various diseases like cancer, neurological disorder, aging, etc. Lignan can scavenge
free radicals thus reducing oxidative stress (Hu et al. 2007). Under in vivo and
in vitro conditions, SDG, enterodiol, and enterolactone act as antioxidants by
inhibiting peroxidation of polyunsaturated fatty acids and decrease oxidation of
LDL cholesterol (Kitts et al. 1999). Also, SDG has been found to be a plateletactivating factor antagonist (Hall et al. 1993).
10.6.1.3 Effects of Omega Fatty Acids
Through several mechanisms such as decreasing inflammatory response, inhibiting
platelet aggregation and thrombosis, decreasing blood pressure, improving serum
lipids, and preventing cardiac arrhythmias, omega-3 fatty acids prevent cardiovascular diseases (Lanzmann-Petithory et al. 2002). These fatty acids interfere with the
production of pro-inflammatory and pro-aggregatory eicosanoids (prostaglandin E2,
thromboxane Ax2, and leukotriene B4) and protect against cardiovascular diseases.
Since ALA and linoleic acid (LA) are essential fatty acids, they need to be supplied
through diet. Upon ingestion, LA and ALA yield different classes of the eicosanoids.
Such eicosanoids have beneficial effects in case of inflammation, platelet aggregation, and vasoconstriction (Bloedon and Szapary 2004). Alternatively, omega-3 fatty
acids are involved in alteration of enzyme synthesis, regulating gene transcription
and expression, and modification of risk factors for coronary heart diseases (Chen
et al. 2007).
One of the prime requirements for the development of atherosclerosis is the
production of oxygen-free radicals. These free radicals are produced in the body
due to several metabolic reactions causing endothelial dysfunction which is the
causative agent for the development of hyperchoestrolemic atherosclerosis which
causes ischemic heart disease, stroke, and peripheral vascular diseases (Prasad
2000). The effect of flaxseed consumption on serum lipid levels had been studied
in several animal models and has been reported to have positive results. Similar
studies have been conducted in humans where flaxseed has been found to have
beneficial effect in CVDs and hypocholesterolemic activity.
Regular consumption of flaxseed has been found to decrease atherosclerosis
(by 46%) and lowered the number of inflammatory polymorphonuclear leukocytes
in rabbits (Prasad et al. 1998). Further, it was reported that when purified SDG
(15 mg/kg) was added to an atherogenic diet in rabbits (for 8 weeks), levels of aortic
malondialdehyde were also reduced (Prasad 1997). In a study involving 40 female
weaning Wistar rats fed with 200 g flaxseed oil/kg body weight for 4 weeks,
MacDonald-Wicks and Garg (2002) reported that flaxseed produced the lowest
concentration of 8-iso-PGF 2α (an in vivo oxidative stress marker) when administered
with an oxidative stress inducer (CCL4) as compared to rats that received either
saturated fat or linoleic acid containing diets. SDG isolated from flaxseed reduced
10 Flaxseed (Linum usitatissimum)
261