Accumulating evidences indicate that ceramide is closely involved in apoptotic cell death in neurodegenerative disorders and aging. We examined ceramide levels in the cerebrospinal fluid (CSF) or brain tissues from patients with neurodegenerative disorders and the mechanism of how intra- and extracellular ceramide was regulated during neuronal apoptosis. We screened the ceramide levels in the CSF of patients with neurodegenerative disorders, and found that ceramide was significantly increased in patients with Alzheimer's disease (AD) than in patients with age-matched amyotrophic lateral sclerosis (ALS) and other neurological controls. With immunohistochemistry in AD brains, ceramide was aberrantly expressed in astroglia in the frontal cortices, but not detected in ALS and control brains. To explore for the regulation of ceramide in astroglia in Alzheimer's disease brains, we examined the metabolism of ceramide during neuronal apoptosis. In retinoic acid (RA)-induced neuronal apoptosis, RA slightly increased de novo synthesis of ceramide, but interestingly, RA dramatically inhibited conversion of [14C] ceramide to glucosylceramide (GlcCer), suggesting that the increase of ceramide mass is mainly due to inhibition of the ceramide-metabolizing enzyme GlcCer synthase. In addition, a significant increase of the [14C] ceramide level in the culture medium was detected by chasing and turnover experiments without alteration of extracellular [14C] sphingomyelin levels. A 2.5-fold increase of ceramide mass in the supernatant was also detected after 48 h of treatment with RA. These results suggest a regulatory mechanism of intracellular ceramide through inhibition of GlcCer synthase and a possible role of ceramide as an extracellular/intercellular mediator for neuronal apoptosis. The increased ceramide level in the CSF from AD patients, which may be derived from astroglia, raises a possibility of neuronal apoptosis by the response to intercellular ceramide in AD.

The changes of aroma ingredients during the process of flower opening from Bulgarian rose were monitored by head space method and solvent extraction.W e also analyzed contents of glycosidic alcoholic aroma together with activities of the hydrolytic enzymes throughout the flower development and the opening. At flower petal opening time, the total amount of aromas in the head space gas reached the highest level. The concentration of citronellol was abundant in the head space gas at this stage, whereas the concentration o f 2-phenylethanol became higher than that of citronellol 4 hr after the opening stage. In the volatile extracts, higher accumulation was observed in 2-phenylethanol than those of monoterpenoids at this stage, and the content of the former still increased after flower opening. Glycosidic citronellol, geraniol, and other m onoterpenes started their accumulation ju st before flower opening stage and then reached the maximum level. The amount of these glycosidic compounds were less than those in the volatile extracts. In contrast to the monoterpenes, 2-phenylethyl glycosides accumulated in a higher level than in the volatile extracts starting at least 12 hr before the opening stage. The amount of the glycosidic precursors of 2-phenylethanol detected in the rose petals before flower opening always was higher than the amount of 2-phenylethanol which was released later. The decline of glycosidic 2-phenylethanol at flower opening stage may be due to partial enzymatic hydrol­ysis. Thereafter a drastic decline was observed, indicating that rapid enzymatic hydrolysis occurred during these stages.

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The methanolic extract obtained from rose flowers was subjected to XAD-2 adsorption chromatography. Prefractionation of the methanolic eluate using multilayer coil countercurrent chromatography (MLCCC) yielded five subfractions. From the least polar subfraction V, a major amount of the key odorants of rose oil, that is, isomeric rose oxides 1a/b, was liberated upon heat treatment at pH 2.5. Further chromatographic workup of fraction V led, for the first time, to the identification of the genuine rose oxide precursor (S)-3,7-dimethyl-5-octene-1,7-diol (2). In addition to diol 2, the following monoterpene diols have been identified:  3,7-dimethyl-7-octene-1,6-diol (3), 2,6-dimethyl-1,7-octadiene-3,6-diol (4), (2E,5E)-3,7-dimethyl-2,5-octadiene-1,7-diol (5), (2E)-3,7-dimethyl-2,7-octadiene-1,6-diol (6), (2Z,5E)-3,7-dimethyl-2,5-octadiene-1,7-diol (7), (2Z)-3,7-dimethyl-2,7-octadiene-1,6-diol (8), (Z)-2,6-dimethyl-2-octene-1,8-diol (9), (E)-2,6-dimethyl-2-octene-1,8-diol (10), (Z)-2,6-dimethyl-2,7-octadiene-1,6-diol (11), (E)-2,6-dimethyl-2,7-octadiene-1,6-diol (12), (2E,6E)-2,6-dimethyl-2,6-octadiene-1,8-diol (13), (2E,6Z)-2,6-dimethyl-2,6-octadiene-1,8-diol (14), 2,6-dimethyloctane-1,8-diol (15), 2,6-dimethyl-7-octene-1,6-diol (16), (E)-3,7-dimethyl-2-octene-1,8-diol (17), (Z)-3,7-dimethyl-2-octene-1,8-diol (18), 3,7-dimethyloctane-1,7-diol (19), 2,6-dimethyl-7-octene-2,6-diol (20), 3,7-dimethyl-6-octene-1,3-diol (21) and (2E)-3,7-dimethyl-2,6-octadiene-1,4-diol (22). Keywords: (S)-3,7-Dimethyl-5-octene-1,7-diol; monoterpene diols; rose oxides; aroma precursors; multilayer coil countercurrent chromatography; rose petals; Rosa damascena Mill.

The 9-O-β-d-glucopyranoside of 3-hydroxy-7,8-didehydro-β-ionol (1) has been isolated from a glycosidic XAD-2 extract obtained from rose petals. In addition to the β-damascenone-generating compound 1, the following glycoconjugates have been isolated and characterized as peracetates:  3-hydroxy-7,8-dihydro-β-ionol 9-O-β-d-glucopyranoside (2), 3-hydroxy-7,8-dihydro-β-ionol 3-O-β-d-glucopyranoside (3), 2-phenylethyl-O-β-d-glucopyranoside (4), 2-phenylethyl-O-β-d-galactopyranoside (5), benzyl-O-β-d-glucopyranoside (6), (2E)-2,6-dimethyl-6-hydroxyocta-2,7-dienyl-O-β-d-glucopyranoside (7), (2Z)-2,6-dimethyl-6-hydroxyocta-2,7-dienyl-O-β-d-glucopyranoside (8), and (2E,6E)-2,6-dimethyl-1-hydroxyocta-2,6-dien-8-yl-O-β-d-glucopyranoside (9). Keywords: Rosa damascena; Rosaceae; petals; aroma precursors; glycosides; β-damascenone; 3-hydroxy- 7,8-didehydro-β-ionol 9 -O-β- d - glucopyranoside; 3-hydroxy-7,8-dihydro-β-ionol 3 -O-β- d - glucopyranoside; 3-hydroxy-7,8-dihydro-β-ionol 9 -O-β- d - glucopyranoside; 2-phenylethyl -O-β- d - glucopyranoside; 2-phenylethyl -O-β- d - galactopyranoside; benzyl -O-β- d - glucopyranoside; (2E)-2,6-dimethyl-6-hydroxyocta-2,7-dienyl -O-β- d - glucopyranoside; (2Z)-2,6-dimethyl-6- hydroxyocta-2,7-dienyl -O-β- d - glucopyranoside; (2E,6E)-2,6-dimethyl-1-hydroxyocta-2,6-dien- 8-yl -O-β- d - glucopyranoside

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