ABSTRACT
In the highly oxygenated environment surrounding neurons, DHA chains are degraded, yielding a variety of oxidation products. Chemical oxidation occurs when oxygen attacks the multiple double bonds of DHA (Figure 8.1a). Warm temperatures (i.e., 37°C) and traces of metals such as iron and copper facilitate oxidation (Frankel, 2005). One of the most intriguing classes of oxidation products is named truncated or chain-shortened derivatives (Figure 8.1b). A DHA chain at the point of attack by O2 or its reactive oxygen species (ROS) derivatives can be severed or truncated, yielding a chain-shortened fragment of the DHA chain still attached to its phospholipid head group. The truncated phospholipid usually contains a second long-chain, saturated fatty acid resistant to oxidation. The long acyl tail of the saturated chain €rmly anchors the damaged phospholipid to the membrane (Gugiu et al., 2006). It has been proposed that the water-loving properties of chain-shortened DHA cause this stubby chain to exit the oily membrane interior where an intact DHA chain is normally located; the chain instead moves to a location in the aqueous layer above the membrane surface (Greenberg et al., 2008). According to the lipid whisker model proposed by these authors, oxidatively truncated chains stick out of the membrane surface like tiny molecular hairs or whiskers. The whisker model is important for understanding how DHA membranes of neurons age, as follows:
• Lipid whiskers are reporters of oxidative damage to membranes. • Membrane repair lipases can recognize and access these hairs as being defec-
tive and clear them from the surface (Farooqui et al., 1997; Leslie, 1997). • Lipid whiskers are exposed to receptors of phagocytic cells, which are trig-
gered into a state of phagocytosis for recycling old membranes and returning useful building blocks such as DHA.
