{'fraction_non_alphanumeric': 0.04060913705583756, 'fraction_numerical': 0.029285435376805936, 'mean_word_length': 5.056737588652482, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Formation of a nonaoxirane from A2E, a lipofuscin fluorophore related to macular degeneration, and evidence of singlet oxygen involvement.

The lipofuscin that accumulates in retinal pigment epithelium (RPE) cells may play a role in the deterioration and death of RPE cells which is typical of atrophic age-related macular degeneration (AMD). In human RPE cells, the deposition of this aging pigment is already apparent by age 20,[1] and while it continues to increase until approximately age 70, thereafter it declines.[2±4] The major hydrophobic fluorophores of RPE lipofuscin are the pyridinium bisretinoids A2E (1) (Figure 1, top left) and iso-A2E, its 13-Z photo-isomer.[5±8] A2E is formed by hydrolytic cleavage of A2-PE, a precursor generated from the reaction between two molecules of all-trans-retinal and phosphatidylethanolamine (PE).[9] It has recently been shown that the accumulation of A2E by cultured RPE bestows a sensitivity to light-induced damage.[10, 11] Specifically, the blue region of the spectrum was found to induce the apoptotic death of A2E-containing cells, with a wavelength dependency that reflected the excitation spectrum of A2E.[11, 12] The propensity for A2E-laden RPE cells illuminated by blue light to undergo apoptosis is consistent with the known susceptibility of RPE cells to blue light damage in animal models.[13±15] Moreover, the ability of A2E to serve as an initiator of photodamage may be relevant to studies linking the incidence of advanced atrophic AMD with blue light exposure, particularly in later life.[16] To investigate the blue-light-induced modification of A2E, solutions of it in phosphate-buffered saline (PBS) (200 ; 200 L) containing 0.1% of DMSO for solubility purposes were irradiated with blue light ((430 10) nm) delivered from a 150-W tungsten halogen lamp (radiant energy 0.19 mWmm 2). Irradiation for 10 min generated a series of oxidative derivatives, each of which represented the addition of an oxygen atom at a carbon ± carbon double bond (see Figure 3). Irradiation at longer wavelengths where A2E does not absorb gave no reactions. For further structural studies oxidation withmeta-chloroperoxybenzoic acid (MCPBA) was performed. Purification of the reaction mixture by HPLC yielded 2 as the main component. FAB (fast atom bombardment) high energy collisioninduced dissociation (CID) mass spectra of 2 resulting from the photooxidation and/or MCPBA oxidation showed the same intenseM peak atm/z 624, and product ions atm/z 458 and 488 (Figure 1). Analysis of these ions led to the shown