Oxygenation of polyunsaturated fatty acids and oxidative stress within blood platelets

Abstract

The oxygenation metabolism of arachidonic acid (ArA) has been early described in blood platelets, in particular with its conversion into the potent labile thromboxane A that induces platelet aggregation and vascular smooth muscle cells contraction. In addition, the primary prostaglandins D and E have been mainly reported as inhibitors of platelet function. The platelet 12-lipoxygenase (12-LOX) product, i.e. the hydroperoxide 12-HpETE, appears to stimulate platelet ArA metabolism at the level of its release from membrane phospholipids through phospholipase A (cPLA) and cyclooxygenase (COX-1) activities, the first enzymes in prostanoid production cascade. Also, 12-HpETE may regulate the oxygenation of other polyunsaturated fatty acids (PUFA) by platelets, especially that of eicosapentaenoic acid (EPA). On the other hand, the reduced product of 12-HpETE, 12-HETE, is able to antagonize TxA action. This is even more obvious for the 12-LOX end-products from docosahexaenoic acid (DHA), 11- and 14-HDoHE. In addition, 12-HpETE plays a key role in platelet oxidative stress as observed in pathophysiological conditions, but may be regulated by DHA with a bimodal way according to its concentration. Other oxygenated products of PUFA, especially omega-3 PUFA, produced outside platelets may affect platelet functions as well.

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

“…The pro-oxidative conditions observed in both forms of psoriasis should result in ROS reactions with nucleophilic compounds, including lipids and proteins, causing their oxidative modifications. Particularly susceptible to oxidative modifications are PUFAs, which occur either bound to phospholipids or as free molecules, in biomembranes and are metabolized in ROS-dependent and in enzymes-catalyzing reactions [4]. The results obtained in our study have shown that levels of PUFAs decrease in both forms of psoriasis, but more in the case of PsA, which had more pronounced onset of oxidative stress, as discussed already.…”

“…Therefore, cellular redox homeostasis plays a key role in physiology of the cells as well as in numerous pathophysiological processes. Elevated ROS levels that cannot be counteracted by the cellular antioxidant abilities induce redox imbalance leading to oxidative stress [1,3], further causing oxidative modifications in the structure and function of cellular components, in particular of the unsaturated biomembrane lipids [4]. The consequence is an increase of the products of ROS-dependent oxidative fragmentation as well as cyclisation of fatty acids [5,6].…”

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

“…The pro-oxidative conditions observed in both forms of psoriasis should result in ROS reactions with nucleophilic compounds including lipids and proteins, which causes their oxidative modifications. Particularly susceptible to oxidative modifications are PUFAs, which are either bound to phospholipids or as free molecules, in bio-membranes and are metabolized in ROS-dependent and in enzyme-catalyzing reactions [ 4 ]. The results obtained in our study have shown that levels of PUFAs decrease in both forms of psoriasis but more in the case of PsA, which had more pronounced onset of oxidative stress, as discussed earlier.…”

“…Therefore, cellular redox homeostasis plays a key role in physiology of the cell as well as in numerous pathophysiological processes. Elevated ROS levels that cannot be counteracted by the cellular antioxidant abilities induce a redox imbalance that leads to oxidative stress [ 1 , 3 ], which further causes oxidative modifications in the structure and function of cellular components especially of the unsaturated bio-membrane lipids [ 4 ]. The consequence is an increase of the products of ROS-dependent oxidative fragmentation as well as cyclization of fatty acids [ 5 , 6 ].…”

Oxidative Stress Response of Aspergillus oryzae Induced by Hydrogen Peroxide and Menadione Sodium Bisulfite

“…When the level of ROS exceeds the antioxidant capacity of cells, lipids can react with ROS to reinstate the cellular redox homeostasis as well. Under oxidative stress, oxidants attack lipids containing C-C bond(s), particularly polyunsaturated fatty acids [19,20]. Since yeast does not contain polyunsaturated fatty acids, there is no lipid peroxidation process in its cells.…”