菲律宾蛤仔修复重金属-营养盐-石油烃复合污染的潜在性

为了研究重金属-营养盐-石油烃复合污染下菲律宾蛤仔(Ruditapes philippinarum)的代谢特征及其过氧化物歧化酶(SOD)活性,判断其用于复合污染生态修复的可能性。以海沙模拟菲律宾蛤仔生境,将其暴露于重金属-营养盐-石油烃复合污染,测定其耗氧率、排氨率和SOD活性。结果表明:氨氮和汞对菲律宾蛤仔耗氧有协同增益作用;氨氮促进菲律宾蛤仔氨氮排泄;SOD活性不受重金属、营养盐和石油烃的影响。考虑到菲律宾蛤仔对重金属、营养盐和石油烃的耐受性及富集特性,认为菲律宾蛤仔是修复重金属-营养盐-石油烃复合污染的潜在物种。

Growth and antioxidant status of oriental river prawn Macrobrachium nipponense fed with diets containing vitamin E

A feeding trial was carried out to investigate the dietary vitamin E requirement of the oriental river prawn Macrobrachium nipponense(weight of 0.3–0.4 g) and its effect role on antioxidant activity.Prawns were fed with seven levels of vitamin E(0,25,50,75,100,200,and 400 mg/kg diet) for 60 days.The results show that dietary vitamin E supplementation could significantly increased the prawn weight( P <0.05).The activity of superoxide dismutase(SOD) in the hepatopancreas was significantly higher in prawns fed with diets supplemented with ≤75 mg/kg vitamin E than in those fed with diets supplemented with 100–400 mg/kg vitamin E( P <0.05).The activity of catalase(CAT) in the hepatopancreas decreased significantly as dietary vitamin E supplementation increased( P <0.05),and no significant difference was detected in glutathione peroxidase(GSH-Px) activity between different dietary groups( P >0.05).The contents of vitamin E in the hepatopancreas and in the muscle increased with increasing dietary vitamin E.There was a linear correlation between the vitamin E level in diet and that in muscle,and between the vitamin E level in diet and that in the hepatopancreas.All the above results indicated that dietary vitamin E can be stored in the hepatopancreas and muscle and lower both the activities of SOD and CAT in the hepatopancreas,suggesting that it is a potential antioxidant in M.nipponense.Broken line analysis conducted on the weight gains of prawns in each diet group showed that the dietary vitamin E requirement for maximum growth is 94.10 mg/kg.

Effect of cadmium on the defense response of Pacific oyster Crassostrea gigas to Listonella anguillarum challenge

Heavy metal pollution can affect the immune capability of organisms. We evaluated the effect of cadmium （Cd） on the defense responses of the Pacific oyster Crassostrea gigas to Listonella anguillarum challenge. The activities of several important defensive enzymes, including superoxide dismutase （SOD）, glutathione peroxidase （GPx）, acid phosphatase （ACP）, Na＋, K＋-ATPase in gills and hepatopancreas, and phenoloxidase-like （POL） enzyme in hemolymph were assayed. In addition, the expression levels of several genes, including heat shock protein 90 （IrtSP9~））, metallothionein （MT）, and bactericidal/permeability increasing （BPI） protein were quantified by fluorescent quantitative PCR. The enzyme activities of SOD, ACP, POL, and GPx in hepatopancreas, and the expression of HSP90 were down-regulated, whereas GPx activity in the gill, Na＋, K＋-ATPase activities in both tissues, and MT expression was increased in Cd- exposed oysters post L. anguillarum challenge. However, BPI expression was not significantly altered by co-stress of L. anguillarum infection and cadmium exposure. Our results suggest that cadmium exposure alters the oysters＇ immune responses and energy metabolism following vibrio infection.

miR-210 over-expression enhances mesenchymal stem cell survival in an oxidative stress environment through antioxidation and c-Met pathway activation

microRNA-210(miR-210)has generally been reported to be associated with cell survival under hypoxia.However,there are few data regarding the role of miR-210 in the survival of mesenchymal stem cells(MSCs)under oxidative stress conditions.Thus,we sought to investigate whether miR-210 over-expression could protect MSCs against oxidative stress injury and what the primary mechanisms involved are.The results showed that over-expression of miR-210 significantly reduced the apoptosis of MSCs under oxidative stress,accompanied by obvious increases in cell viability and superoxide dismutase activity and remarkable decreases in malonaldehyde content and reactive oxygen species production,resulting in a noticeable reduction of apoptotic indices when compared with the control.Moreover,the above beneficial effects of miR-210 could be significantly reduced by c-Met pathway repression.Collectively,these results showed that miR-210 over-expression improved MSC survival under oxidative stress through antioxidation and c-Met pathway activation,indicating the potential development of a novel approach to enhance the efficacy of MSC-based therapy for injured myocardium.