The identification of biotransformation pathways for removing fishy malodor from Bangia fusco-purpurea using fermentation with Saccharomyces cerevisiae.

The yeast Saccharomyces cerevisiae is effective in reducing the fishy malodor of sea products. However, the biotransformation pathways are still unclear. The seaweed B. fusco-purpurea was taken as an example to investigate the chemical transformation pathways for the deodorization process with S. cerevisiae fermentation. Sensory evaluation, GC-MS, GC-MS-O and odor activity value (OAV) analyses showed the fishy odorants were 1-octen-3-ol, (E)-2-nonenal, 2,4-decadienal, 2-pentylfuran, 2-octen-1-ol and nonanal. The removal of fishy malodor was related to the reactions of reduction, dehydrogenation, deformylation-oxygenation and ester syntheses via catalysis of aldehyde dehydrogenase, alcohol dehydrogenases, epoxide hydrolase, aldehyde deformylating-oxygenase, enone reductase, oxidases, dehydrogenases, aldo-keto reductases, ester synthase and acyltransferase. Interestingly, for the first time, it was found that 3,5-octadien-2-one transformed to 6-octen-2-one; and 2-pentylfuran transformed to o-cymene and hexyl acetate. Our findings enrich the knowledge for the removal of fishy malodor from sea products such as seaweeds.

Survivin regulated by autophagy mediates hyperglycemia-induced vascular endothelial cell dysfunction.

Diabetic vascular complications are often defined by vascular endothelial lesions. However, as a plastic cell type, whether endothelial cells could transit from quiescence to hyper-active status and hamper vascular stability upon hyperglycemia stimulation and whether this process is involved in diabetic vascular complications remain obscure. Survivin has been identified as an anti-apoptotic protein in tumor or epithelial cells by either promoting proliferation or inhibiting apoptosis. Therefore, this study aims at investigating the effects of hyperglycemia on endothelial cell status and the potential involvement of survivin. We found that high glucose (25 mM) did not cause endothelial injuries, instead, it evidently promotes endothelial proliferation and tube formation capacity indicating endothelial cell dysfunction upon hyperglycemia characterized by its preference to hyper-active status. Concomitantly, an upregulation of survivin was detected accompanied by the key component elevations of autophagy pathway including LC3, Beclin1, and p62. YM155, a specific inhibitor of survivin, could abrogate hyperglycemia-induced endothelial hyper-activation. Application of the autophagy inhibitor (3MA) and agonist (rapamycin) supported that survivin could be as a downstream effect or of autophagy. Thus, our results suggested that survivin/autophagy axis a potential therapeutic target in treatment of diabetic vascular complications.

Differential expression and function of survivin during the progress of pterygium.

PURPOSE: To investigate the expression pattern and function of survivin in the development of pterygium. METHODS: Primary pterygia at quiescent or advanced clinical stage and normal human conjunctival tissues were used in this study. Pterygium epithelial cells (PECs) were cultured in keratinocyte serum-free defined medium and harvested at different growth stages. Tissue sections and cultured cells were detected with survivin, phosphorylated survivin (Thr43), p63, p57, and p21 on protein, and/or mRNA level. Cell Counting Kit (CCK)-8 assay was performed to measure proliferation status of primary cultured PECs. Small interfering (si) RNA specific for survivin was transfected on PECs at subconfluence stage. RESULTS: Survivin was highly expressed in all pterygium tissues, but not in normal human conjunctiva, at mRNA and protein levels. It was mainly present in the epithelial cytoplasm of pterygium at quiescent stage, while present in the nucleus of pterygium at advanced stage. Phosphorylated survivin was upregulated in pterygium at advanced stage. Pterygium epithelial cells cultured under subconfluence stage showed higher expression of survivin and p63, but lower expression of p57 and p21, compared with PECs reached confluence. Both total and phosphorylated survivin was mainly expressed in the nuclei of PECs under subconfluence, and there was cytoplasmic translocation of survivin when PECs reached confluence. The knockdown of survivin by siRNA inhibited proliferation of PECs, accompanied by downregulation of p63, and upregulation of p57 and p21. CONCLUSIONS: Higher subcellular expression and phosphorylation of survivin may play roles in the development of pterygium. Survivin could be targeted for the treatment of pterygium.