石油污染土壤的微生物修复技术

该文介绍了微生物修复技术的最新研究内容和方法、重点对石油污染土壤的微生物原位修复、异位修复研究进展及各自的优点、局限性进行了综述,并就石油对微生物修复的影响因素进行探讨,最后讨论了该技术在我国的研究趋势和前景.     

西北黄土区石油污染土壤原位微生物生态修复试验研究

通过对西北黄土石油开采区石油污染土壤生物强化原位微生物生态修复方法的试验研究,充分利用强化原位微生物菌群辅以物理和化学方法与土壤环境相结合的微生物生态技术,进行了土壤中石油的降解与修复试验研究,试验结果显示,土壤中平均石油含量在2754mg/kg时,经过lld～32d强化原位微生物生态修复技术的修复,土壤中石油含量降解可达40.92%～80.37%,验证了微生物生态修复技术在西北黄土区土壤石油污染修复的有效性,探索了推广应用的可行性.     

污染土壤微生物修复技术

因具处理方式多样、可因地制宜、对环境影响小、处理成本低等特点,目前微生物技术广泛应用于污染土壤修复。本文从原理、技术及处理工艺三方面综述了污染土壤微生物修复研究进展和发展现状,指出其存在的局限性及土壤微生物修复再今后发展方向和趋势,为污染土壤微生物修复技术的理论研究和利用提供参考。     

低温微生物修复石油烃类污染土壤研究进展

耐冷菌、嗜冷菌等低温微生物广泛存在于极地、高山以及高纬度等土壤环境中,是石油烃类污染物在低温条件下降解与转化的重要微生物资源.利用低温微生物的独特优势,石油污染土壤的低温生物修复技术的研究成为当前热点领域.本文系统综述了低温石油烃降解菌的分类及冷适机制,低温微生物对不同类型石油烃组分的降解特征和降解机理,低温环境中接种降解菌、添加营养物质和表面活性剂等强化技术在石油污染土壤中生物修复的应用.以及微生物分子生物学技术在低温微生物降解石油烃的研究现状,为拓展我国石油污染土壤生物修复技术提供参考.     

石油污染微生物修复技术研究进展

石油污染是我国目前陆地和海洋面临的主要污染问题之一,尽管以微生物为主体的原位修复技术在以往的实践中取得了良好的效果,但随着石油污染形式的严峻,微生物修复技术依然面临着巨大的挑战。随着石油降解微生物资源库的不断累积和研究手段的发展,人们对微生物石油降解机制有了更加深入的研究,为提高微生物修复技术的应用范围和应用效果奠定了良好的基础。从石油污染与技术应用趋势、石油降解微生物聚类分析、石油微生物降解的分子机制、石油污染的微生物修复技术几方面总结和梳理了国内外近期的研究进展,以其为迎接新的挑战提供抓手。     

溶磷微生物在钝化和植物修复重金属污染土壤中的作用

钝化和植物修复是重金属污染土壤修复的重要技术手段,而溶磷微生物可进一步增强钝化和植物修复重金属污染土壤的作用。介绍了钝化和植物修复重金属污染土壤的基本原理,总结了溶磷微生物对土壤中难溶性磷酸盐的溶解、利用磷酸盐钝化修复重金属污染土壤、溶磷微生物对磷酸盐钝化修复的强化以及溶磷微生物强化植物修复重金属污染土壤的研究进展,探讨了溶磷微生物对重金属的抗性及其溶磷机理、溶磷微生物对磷酸盐钝化修复重金属污染土壤的强化作用机理以及溶磷微生物强化植物修复重金属污染土壤的作用机理。旨在为生物修复重金属污染土壤研究提供一定的理论依据和技术支撑。     

固定化微生物技术修复多氯联苯污染土壤的应用前景

多氯联苯(PCBs)是一类持久性有机污染物,生物危害性极大,流入环境后易被土壤颗粒吸附而长期蓄积在土壤中.运用生物技术修复PCBs污染土壤一直是国内外学者研究的热点.其中固定化微生物技术因其独特的优势而具备了较高的开发与应用价值.本文简要评述了当前PCBs污染土壤的主要修复技术,并通过分析固定化微生物技术的特点及其在有机污染土壤修复方面的研究进展,论述了运用该技术修复PCBs污染土壤的可行性以及所面临的关键科学问题.     

石油污染土壤植物-微生物修复研究进展

依据国内外近10年来有关石油污染土壤生物修复研究的成果,综合阐述了石油污染土壤的植物修复、微生物修复及植物-微生物联合修复方法研究,重点讨论植物-微生物联合作用,主要包括植物根际微生物、根分泌物以及菌根对石油污染物降解的影响,提出了污染土壤原位修复中需要重视的问题.     

重金属污染农田微生物修复机理研究进展

土壤重金属污染严重,而修复技术纷繁多样,物理化学修复技术应用较为常见,但存在一定程度的弊端。微生物修复技术因高效、经济、绿色受到环境学者的广泛关注。文章阐述了重金属污染的现状、微生物与重金属之间的作用机理,总结了植物与微生物之间的协同修复机制。为微生物修复技术在重金属污染土壤修复领域广泛应用提供参考。     

多环芳烃污染土壤微生物修复研究进展

多环芳烃是我国土壤环境质量标准中要求严格管控的一类持久性有机污染物,利用微生物技术修复有机污染土壤具有绿色、经济等突出特点,应用前景广泛。目前多学科的协同发展和新技术的研究应用,为多环芳烃土壤微生物转化机制与污染生态过程等方面带来了新的认识,同时对修复技术的实际应用与调控提供了新的思考方向。本文以多环芳烃污染土壤微生物修复为主体,从污染土壤微生物修复应用技术、多环芳烃微生物降解特征、土壤体系污染物归趋规律与微生物作用及土壤污染微生物群落响应与研究技术等方面进行综合评述,并针对现存应用技术瓶颈和理论空白作进一步思考和展望。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.