Fig. 6.3 The absorption spectra for A2E and the total Folch extract of human RPE (HL)

where it undergoes nitration, presumably by NO [55]. This reaction is possibly due to inflammation and is specific to the BM, since nitro-A2E is not found in the RPE.

It has been established that A2E can kill RPE cells once a critical quantity has accumulated. The absorption spectrum for A2E resembles that of lipofuscin indicating that A2E and structurally related compounds are the major components. However, the relationship between the concentration of A2E and RPE dysfunction has not been determined. Previous studies regarding this relationship have yielded inconsistent findings [12, 13, 51, 56]. Also, the state of A2E within the RPE has not yet been established. Simon and colleagues showed the presence of a variety of components within a lipofuscin granule under atomic force microscopy (AFM) [57].

6.1.3Formation of Higher Molecular Weight Material

Besides A2E, there are numerous components in RPE lipofuscin that are structurally related to A2E as determined by their absorption spectra and fragmentation pattern with losses of 106, 190, 174, and/or 150 amu from the parent ion and the formation of fragments of circa 592 amu. Figure 6.3 gives the absorption spectra of A2E (inset) and the total Folch extract of human RPE (HL). Clearly, there are more components in this mixture, but in terms of absorptions above 400 nm, A2E is a major component. The shoulder at 430 nm in the mixture is due to A2E and A2E like components. Additional evidence that it is a major component is that in cells it