This study investigated the anaerobic degradation of the polycyclic aromatic hydrocarbons (PAHs) phenanthrene and pyrene in mangrove sediment from Taiwan. The anaerobic degradation of PAH was enhanced by the addition of acetate, lactate, pyruvate, sodium chloride, cellulose, or zero-valent iron. However, it was inhibited by the addition of humic acid, di-(2-ethylhexyl) phthalate (DEHP), nonylphenol, or heavy metals. Of the microorganism strains isolated from the sediment samples, we found that strain MSA3 (Clostridium pascui), expressed the best ability to biodegrade PAH. The inoculation of sediment with the strain MSA3 could enhance PAH degradation.

This study investigated the effects of various factors on the biodegradation of the polycyclic aromatic hydrocarbons (PAHs) phenanthrene and pyrene, and characterized the structure of the microbial community in mangrove sediment from subtropical Taiwan. The degradation of PAH was enhanced by the addition of brij 30, tween 80, yeast extract, hydrogen peroxide, sodium chloride or cellulose. However, PAH degradation was inhibited by the addition of humic acid, di-(2-ethylhexyl), phthalate (DEHP) or nonylphenol. Our results also showed that the addition of various substrates changed the microbial community in mangrove sediment. The strains MS2 (Dyella ginsengisoli) and MS4 (Bacillus pumilus) were the constantly dominant bacteria under various treatments in the mangrove sediment.

Estrogens have been suggested to exhibit neuroprotective activities against several insults including beta-amyloid and glutamate, one of the excitatory neurotransmitters in the central nervous system. In the present study, we showed that exposure to glutamate not only inhibited the cell growth of exponentially growing rat pheochromocytoma PC12 cells in a time- and dose-dependent manner, but also influenced cell adherence capacity. Glutamate-induced growth inhibition was significantly attenuated by the co-administration of estradiol in PC12 cells. Pre-exposure of the PC12 cells to the estradiol was not required for protection against glutamate-induced growth inhibition. Administration of anti-estrogen ICI182,780 efficiently blocked the neuroprotective effects of estradiol. Glutamate-induced changes in cell adherence, on the other hand, were not significantly affected by estradiol. These data indicate that the neuroprotective effects of estradiol against glutamate-induced insults in PC12 cells, at least in part, involve estrogen receptor-dependent pathways.