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Figure 6 | Particle and Fibre Toxicology

Figure 6

From: Ultrafine particles affect the balance of endogenous pro- and anti-inflammatory lipid mediators in the lung: in-vitro and in-vivo studies

Figure 6

Schematic representation of arachidonic acid-derived lipid mediators. Particles and/or OVA challenge interfere with cell membranes to activate cytoplasmatic phospholipase A2 (cPLA2), which cleaves arachidonic acid from membrane phospholipids. Due to the oxidative potential of UFCP [23], arachidonic acid is non-enzymatically oxidized to 8-isoprostane, used as a marker for redox imbalance. Arachidonic acid serves as a substrate for the downstream pathways of COX (cyclooygenase), 15- and 5-LO (15- and 5-lipoxygenase), leading to formation of prostaglandins such as PGE2, 15(S)-HETE, leukotrienes such as LTB4 and to LXA4 via PGE2 activated 15-LO [23, 26, 35]. Because these processes are predominantly located in the nuclear membrane or perinuclear space, these products of these pathways may influence gene expression. LTB4 activates the inflammation, whereas PGE2, 15(S)-HETE and LXA4 are immune-modulating, anti-inflammatory and pro-resolving lipid mediators, respectively.

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