Construction of an artificial microalgal-bacterial consortium that efficiently degrades crude oil.

Four oil component-degrading bacteria and one oil-tolerant microalgae, Scenedesmus obliquus GH2, were used to construct an artificial microalgal-bacterial consortium for crude-oil degradation. The bacterial strains included Sphingomonas GY2B and Burkholderia cepacia GS3C, along with a mixed culture, named GP3, containing Pseudomonas GP3A and Pandoraea pnomenusa GP3B. GY2B could only degrade polycyclic aromatic hydrocarbons, GS3C was able to degrade aliphatic chain hydrocarbons, and GP3 could utilize both saturated and aromatic hydrocarbons. In combination with unialgal or axenic algae, the bacteria showed different effects on oil degradation. Unialgal GH2 was not suitable for the consortium construction, as it could not cooperate well with GS3C and GP3. The axenic GH2 exhibited no oil-degrading ability; however, it significantly promoted the degradation ability of the oil component-degrading bacteria, especially for degrading biorefractory polycyclic aromatic hydrocarbons. Axenic S. obliquus GH2, combined with the four bacteria mentioned above, formed an optimal algal-bacterial consortium. The artificial consortium demonstrated an elevated efficiency in degrading both aliphatic and aromatic hydrocarbons of crude oil.

Dose-dependent effects of soy phyto-oestrogen genistein on adipocytes: mechanisms of action.

The potential role of genistein in the prevention and treatment of obesity has attracted much attention among public and medical communities. Conversely, increasing evidence indicates that genistein as an endocrine-disrupting substance is likely to play a role in the aetiology of obesity. This review focuses on the role of soy phyto-oestrogen genistein in adipocytes and the underlying mechanisms of action. Genistein dose-dependently inhibits and stimulates adipogenesis in vitro. Increasing evidence shows that genistein dose-dependently influences obesity in both male and female animals. Dose-dependent effects of genistein on adipocytes vary with factors such as age and gender of animals. In addition, the role of developmental exposure of genistein in adult obesity has been discussed. Genistein, different from oestrogen, concurrently activates nuclear receptors, oestrogen receptors and peroxisome proliferator-activated receptors, and it inhibits various enzyme activities. The balance among these pleiotrophic effects of genistein determines its dose-dependent effects on adipocyte differentiation and function. Current data suggest that genistein could regulate adiposity. However, it remains uncertain whether genistein plays a beneficial role in the prevention and treatment of obesity. Additional evidence is required before firm conclusions showing that genistein decreases adiposity.

Metallothionein and cortisol receptor expression in gills of Atlantic salmon, Salmo salar, exposed to dietary cadmium.

Commercial fish feeds may contain significant levels of cadmium (Cd). However, little is known about the effects of dietary cadmium on fish organs, especially gills, the key osmoregulatory organ. We therefore studied the effects of dietary cadmium on metallothionein (MT) and cortisol receptor (GR) immunoreactivity in the branchial epithelium of the Atlantic salmon (Salmo salar). Cadmium was daily administered via food at 0.2mg (control), 5mg (low dose) and 125 mg (high dose) Cd per kilogram dry pellet weight. Fish were sampled after four and eight weeks. After both four and eight weeks, plasma cadmium concentration had increased significantly only in fish fed the high cadmium dose. Plasma calcium, sodium, chloride and cortisol levels were not affected. In the controls, most MT was colocated with the chloride cell marker, Na(+)/K(+)-ATPase, but some MT was present in pavement and respiratory cells. GR expression was found in chloride, pavement, respiratory and undifferentiated cells in all fish groups, but cadmium accumulation and a marked stimulation of MT expression were seen only in the chloride cells in the gills of fish fed the high cadmium dose. Cadmium treatment did not alter GR expression. When the double staining technique for MT and GR was applied, a marked heterogeneity became apparent in the chloride, pavement and respiratory cells of both groups of cadmium-treated fish and in the control fish. Some fish showed double staining, others stained only for one of the antibodies, whereas other cells were negative for both. We conclude that cadmium entering the gut also enters the gills, where it accumulates in chloride cells and stimulates MT expression.

Cortisol increases Na(+)/K(+)-ATPase density in plasma membranes of gill chloride cells in the freshwater tilapia Oreochromis mossambicus.

The effect of cortisol on Na(+)/K(+)-ATPase expression in the gill chloride cells of tilapia Oreochromis mossambicus was studied by immunocytochemistry at the light and electron microscope levels. One of three doses of cortisol (low, 125 mg kg(-1 )food; middle, 375 mg kg(-1 )food; high, 750 mg kg(-1) food) was administered via the food (at a ration of 1.5 % of body mass) and the fish were sampled after 5 days. Plasma osmolality and Na(+) levels were elevated in the middle- and high-dose groups, and plasma cortisol levels in the high-dose groups. Hematocrit values were not affected by the treatments. Opercular membrane chloride cell density increased by 94 % and 286 % in the middle- and high-dose fish, respectively, whereas the gill chloride cell frequency increased by up to 28 % maximally in the high-dose fish. Lamellar gill chloride cells were absent in the control and low-dose groups, but were observed in the middle- and high-dose groups. Cortisol increased the volume of the tubular membrane system in mature gill chloride cells. Quantification of immunogold-labelled Na(+)/K(+)-ATPase antigen (a 104 kDa protein species, as demonstrated by western blot) revealed that the high dose of cortisol increases the Na(+)/K(+)-ATPase density in the tubular system of chloride cells. This is the first direct evidence that cortisol not only increases chloride cell numbers but also Na(+)/K(+)-ATPase density in these cells.