The Role of Vitamin E and Selenium on Arachidonic Acid Oxidation by way of the 5‐Lipoxygenase Pathway

Reddanna, Pallu; Whelan, Jay; Burgess, John; Eskew, Mary Lou; Hildenbrandt, George; Zarkower, A.; Scholz, Richard W.; Reddy, C. Channa

doi:10.1111/j.1749-6632.1989.tb14914.x

Cited by 69 publications

(18 citation statements)

References 23 publications

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“…Another pathway by which LPS could stimulate IL-1␤ release is through the leukotriene pathway. Leukotriene B4 has been shown to increase IL-1 activity from monocytes (57) and it is possible that alpha tocopherol could reduce the release of IL-1␤ from monocytes by decreasing levels of leukotrienes (58). Furthermore, Shapira et al (59) have shown that LPS-induced IL-1␤ production from human monocytes involves both PKC and protein tyrosine kinase.…”

Section: Discussionmentioning

confidence: 99%

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Devaraj¹,

Li²,

Jialal³

1996

J. Clin. Invest.

334

186

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Low levels of alpha tocopherol are related to a higher incidence of cardiovascular disease and increased intake appears to afford protection against cardiovascular disease. In addition to decreasing LDL oxidation, alpha tocopherol may exert intracellular effects on cells crucial in atherogenesis, such as monocytes. Hence, the aim of this study was to test the effect of alpha tocopherol supplementation on monocyte function relevant to atherogenesis. Monocyte function was assessed in 21 healthy subjects at baseline, after 8 wk of supplementation with d-alpha tocopherol (1,200 IU/d) and after a 6-wk washout phase. The release of reactive oxygen species (superoxide anion, hydrogen peroxide), lipid oxidation, release of the potentially atherogenic cytokine, interleukin 1 ␤ , and monocyte-endothelial adhesion were studied in the resting state and after activation of the monocytes with lipopolysaccharide at 0, 8, and 14 wk. There was a 2.5-fold increase in plasma lipid-standardized and monocyte alpha tocopherol levels in the supplemented phase. After alpha tocopherol supplementation, there were significant decreases in release of reactive oxygen species, lipid oxidation, IL-1 ␤ secretion, and monocyte-endothelial cell adhesion, both in resting and activated cells compared with baseline and washout phases. Studies with the protein kinase C inhibitor, Calphostin C, suggest that the inhibition of reactive oxygen species release and lipid oxidation is due to an inhibition of protein kinase C activity by alpha tocopherol. Thus, this study provides novel evidence for an intracellular effect of alpha tocopherol in monocytes that is antiatherogenic. ( J. Clin. Invest. 1996. 98:756-763.)

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Section: Discussionmentioning

confidence: 99%

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Devaraj¹,

Li²,

Jialal³

1996

J. Clin. Invest.

334

186

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“…Although no uniform opinion about a deficiency of the antioxidant defences has been formed, it appears likely that in chronic HD patients an increased demand for some non-enzymatic antioxidants, and particularly vitamin E, AA and GSH, can be present [6,11,17,23]. For this reason several approaches to an antioxidant supplementation have been tried in HD.…”

Section: The Use Of Non-enzymatic Antioxidants In Combatting Oxidativmentioning

confidence: 99%

“…In addition to its antioxidant function, vitamin E is known to stabilise the polyunsaturated fatty acids within the cell membrane, thus assuring the correct fluidity of the lipid bilayer [10], and to control lipooxygenase activity [11]. Moreover, vitamin E has been demonstrated to control the cell proliferation by affecting cell signalling [5], inhibiting the protein kinase C (PKC) activation [12], and to decrease leukocyte apoptosis [13].…”

Section: Figmentioning

confidence: 99%

Biological Effects of Oxidant Stress in Haemodialysis: The Possible Roles of Vitamin E

1999

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Oxidative stress has been proposed to play a role in many disease states, including cardiovascular and infectious diseases, cancer, diabetes and neurodegenerative pathologies. The fact that these diseases have an increased incidence in uremia, and particularly in dialysis patients, suggests an increased exposure to oxidative stress in this condition. In haemodialysis (HD), the absence of a complete correction of the uremic toxicity together with the untoward effects of the dialysis, malnutrition and the progressive worsening of the clinical condition, can lead to a high susceptibility to oxidative stress by an abnormal production of oxidants – including reactive oxygen species (ROS) and uremic toxins with prooxidant function – and defective antioxidant protection. One of the most investigated biological effects of the oxidative stress in the HD patients is lipid peroxidation in plasma and blood cell membranes. Moreover, we have recently described how abnormal apoptosis in peripheral blood leukocytes is associated with cell oxidative stress (intracellular thiol depletion). Vitamin E, in both in vitro and in vivo conditions, has been proposed to partially correct these effects. In this review we evaluated some features of two new dialysis strategies using an antioxidant approach to the protection against the oxidant stress in HD. Their rationale is based on the emerging role of vitamin E in counteracting some biological effects associated with oxidant stress namely lipid peroxidation and apoptosis. These techniques use: 1) the recirculation of the dialysate through a suspension of vitamin E-enriched liposomes combined with the supplementation by the dialysate with ascorbic acid, this method has been called hemolipodialysis; 2) the coating of the dialysis membrane with vitamin E (vitamin E- modified dialysis membranes). These unconventional approaches to the antioxidant therapy in HD open a widely unexplored and promising field in the evolution of the biomaterials and dialysis quality.

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“…29 Moreover, oxidative cytotoxic products produced by vessel injury may enhance the inflammatory process, impair cellular repair and accelerate cell death, and favor prostaglandin and leukotriene synthesis and platelet aggregation. 7,[37][38][39][40] The severity of the inflammatory stage might predict the severity of wound healing and therefore the total amount of collagen and matrix formation produced as a result of an injury. 3,4,7 Interestingly, a recent study has shown that the acute inflammatory changes peak at 24 hours after endarterectomy and disappear by the fifth day.…”

Section: Mezzetti Et Al Oxidative Stress and Vascular Remodeling 2663mentioning

confidence: 99%

Increased Systemic Oxidative Stress After Elective Endarterectomy

Mezzetti¹,

Guglielmi²,

Pierdomenico³

et al. 1999

ATVB

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Abstract-It has been reported that systemic and local redox state may have an important role in the functional and organic changes characterizing the process of vascular response to injury. Carotid endarterectomy to remove atherosclerotic plaque is followed by a long lasting healing and remodeling process that can be carefully followed over time with noninvasive ultrasonography. Plasma vitamin C concentration and native LDL (n-LDL) content in lipid peroxides, vitamin E, ␤-carotene, and lycopene as well as LDL susceptibility to peroxidation were assessed in 45 patients undergoing elective endarterectomy for internal carotid stenosis, at baseline, 24 hours, 3 and 15 days, and 1 month after surgery. Serial duplex scans were performed in all patients postoperatively and 3, 6, and 12 months. The changes in far wall thickness (FW) and % renarrowing from postoperatively to 12 months were used as remodeling indices. Plasma antioxidant vitamins and lag-phase showed a sharp and significant decrease during the first 24-hours after surgery remaining unchanged until the third day, whereas, an opposite trend was evidenced for n-LDL content in lipid peroxides and serum ceruloplasmin. After the third day all the parameters returned progressively to baseline within one month from endarterectomy. Interestingly, the n-LDL lipid peroxide content, the serum ceruloplasmin and the plasma vitamin C concentration, measured at 24 and 3 days from surgery, were significantly associated to the change in % renarrowing from postoperatively to 12 months. The higher the LDL content in lipid peroxides, the higher the serum level of ceruloplasmin, the lower the plasma content in vitamin C and the higher the % of vessel renarrowing.

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The Role of Vitamin E and Selenium on Arachidonic Acid Oxidation by way of the 5‐Lipoxygenase Pathway

Cited by 69 publications

References 23 publications

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Biological Effects of Oxidant Stress in Haemodialysis: The Possible Roles of Vitamin E

Increased Systemic Oxidative Stress After Elective Endarterectomy

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