Summary(+)-Sesaminol 2-O-triglucoside is the most abundant water-soluble furofuran lignan in sesame seeds (Sesamum indicum) and is considered to be a beneficial compound for human health. The biosyntheses and physiological roles of lignan glycosides, however, remain elusive. Here we report the molecular identification and biochemical characterization of two Sesamum uridine diphosphate (UDP) glucose:lignan glucosyltransferases. Sesamum indicum UGT71A9 preferentially glucosylated at the 2-hydroxyl group of (+)-sesaminol, resulting in (+)-sesaminol 2-O-glucoside. Similarly, two UGT71A9 homologs from Sesamum radiatum (UGT71A10) and Sesamum alatum (UGT71A8) also showed (+)-sesaminol glucosylating activity, evidencing the functional conservation of (+)-sesaminol 2-O-glucosyltransferases in the Sesamum genus. In addition, S. indicum UGT94D1 specifically glucosylated at the 6¢-hydroxyl group of the sugar moiety of (+)-sesaminol 2-O-glucoside but not at that of flavonoid glucosides. The gene expression patterns of UGT71A9 and UGT94D1 during seed development were correlated with the glucosylating activities toward (+)-sesaminol in planta, suggesting that the two lignan UDP-glycosyltransferases participate in the sequential glucosylation steps in the biosynthesis of (+)-sesaminol 2-O-triglucoside.

The photosynthetic reaction center (RC) complex that forms a homodimer of core and cytochrome c subunits was isolated from Chlorobium limicola f. thiosulfatophilum, strain Larsen. The complex showed only two subunit bands at 68 (PscA core) and 21 kDa (cytochrome c551) on SDS-PAGE analysis, indicating the complete deletion of the light-harvesting bacteriochlorophyll a (BChl a) protein as well as the iron-sulfur protein. It contained 27 +/- 3 molecules of BChl a, 7 +/- 1 Chl-670, 3 +/- 1 carotenoids, and 1.6 +/- 0.1 c-type hemes per the primary electron donor P840. The complex showed a light-induced charge separation and recombination between P840 and the acceptor Chl-670 at 77 K as follows: P840*Chl-670-->P840+Chl-670(-)-->P840TChl-670-->P84 0 Chl-670. Pigment compositions and their function in the (PscA/cytochrome c551)2 complex were studied by absorption, circular dichroism, and fluorescence spectroscopy.

BackgroundThe importance of arachidonic acid (ARA) among the elderly has recently gained increased attention. The effects of ARA supplementation in the elderly are not fully understood, although ARA is considered to be associated with various diseases. We investigate whether ARA supplementation to Japanese elderly subjects affects clinical parameters involved in cardiovascular, inflammatory, and allergic diseases. We also examine the levels of ARA metabolites such as prostanoids during intervention.MethodsWe conducted a randomized, double-blind and placebo-controlled parallel group intervention trial. ARA-enriched oil (240 or 720 mg ARA per day) or placebo was administered to Japanese healthy men and women aged 55-70 years for 4 weeks followed by a 4-week washout period. The fatty acid contents of plasma phospholipids, clinical parameters, and ARA metabolites were determined at baseline, 2, 4, and 8 weeks.ResultsThe ARA content in plasma phospholipids in the ARA-administrated groups increased dose-dependently and was almost the same at 2 weeks and at 4 weeks. The elevated ARA content decreased to nearly baseline during a 4-week washout period. During the supplementation and washout periods, no changes were observed in eicosapentaenoic acid and docosahexaenoic acid contents. There were no changes in clinical blood parameters related to cardiovascular, inflammatory and allergic diseases. ARA supplementation did not alter the level of ARA metabolites such as urinary 11-dehydro thromboxane B2, 2,3-dinor-6-keto prostaglandin (PG) F1α and 9,15-dioxo-11α-hydroxy-13,14-dihydro-2,3,4,5-tetranor-prostan-1,20-dioic acid (tetranor-PGEM), and plasma PGE2 and lipoxin A4. ARA in plasma phospholipids was not correlated with ARA metabolite levels in the blood or urine.ConclusionThese results indicate that ARA supplementation, even at a relatively high dose, does not increase ARA metabolites, and suggest that it does not induce cardiovascular, inflammatory or allergic diseases in Japanese elderly individuals.

Dementia has become a major issue that requires urgent measures. The prevention of dementia may be influenced by dietary factors. We focused on green tea and performed a systematic review of observational studies that examined the association between green tea intake and dementia, Alzheimer’s disease, mild cognitive impairment, or cognitive impairment. We searched for articles registered up to 23 August 2018, in the PubMed database and then for references of original articles or reviews that examined tea and cognition. Subsequently, the extracted articles were examined regarding whether they included original data assessing an association of green tea intake and dementia, Alzheimer’s disease, mild cognitive impairment, or cognitive impairment. Finally, we included three cohort studies and five cross-sectional studies. One cohort study and three cross-sectional studies supported the positive effects of green tea intake. One cohort study and one cross-sectional study reported partial positive effects. The remaining one cohort study and one cross-sectional study showed no significant association of green tea intake. These results seem to support the hypothesis that green tea intake might reduce the risk for dementia, Alzheimer’s disease, mild cognitive impairment, or cognitive impairment. Further results from well-designed and well-conducted cohort studies are required to derive robust evidence.

BackgroundAn n-6 essential fatty acid, arachidonic acid (ARA) is converted into prostaglandin E2, which is involved in tumour extension. However, it is unclear whether dietary ARA intake leads to cancer in humans. We thus systematically evaluated available observational studies on the relationship between ARA exposure and the risk of colorectal, skin, breast, prostate, lung, and stomach cancers.MethodsWe searched the PubMed database for articles published up to May 17, 2010. 126 potentially relevant articles from the initial search and 49,670 bibliographies were scrutinised to identify eligible publications by using predefined inclusion criteria. A comprehensive literature search yielded 52 eligible articles, and their reporting quality and methodological quality was assessed. Information on the strength of the association between ARA exposure and cancer risk, the dose-response relationship, and methodological limitations was collected and evaluated with respect to consistency and study design.ResultsFor colorectal, skin, breast, and prostate cancer, 17, 3, 18, and 16 studies, respectively, were identified. We could not obtain eligible reports for lung and stomach cancer. Studies used cohort (n = 4), nested case-control (n = 12), case-control (n = 26), and cross-sectional (n = 12) designs. The number of subjects (n = 15 - 88,795), ARA exposure assessment method (dietary intake or biomarker), cancer diagnosis and patient recruitment procedure (histological diagnosis, cancer registries, or self-reported information) varied among studies. The relationship between ARA exposure and colorectal cancer was inconsistent based on ARA exposure assessment methodology (dietary intake or biomarker). Conversely, there was no strong positive association or dose-response relationship for breast or prostate cancer. There were limited numbers of studies on skin cancer to draw any conclusions from the results.ConclusionsThe available epidemiologic evidence is weak because of the limited number of studies and their methodological limitations, but nonetheless, the results suggest that ARA exposure is not associated with increased breast and prostate cancer risk. Further evidence from well-designed observational studies is required to confirm or refute the association between ARA exposure and risk of cancer.