海洋石油污染物的微生物降解与生物修复

石油是海洋环境的主要污染物 ,已经对海洋及近岸环境造成了严重的危害。微生物降解是海洋石油污染去除的主要途径。海洋石油污染物的微生物降解受石油组分与理化性质、环境条件以及微生物群落组成等多方面因素的制约 ,N和P营养的缺乏是海洋石油污染物生物降解的主要限制因子。在生物降解研究基础上发展起来的生物修复技术在海洋石油污染治理中发展潜力巨大 ,并且取得了一系列成果。介绍了海洋中石油污染物的来源、转化过程、降解机理、影响生物降解因素及生物修复技术等方面内容 ,强调了生物修复技术在治理海洋石油污染环境中的优势和重要性 ,指出目前生物修复技术存在的问题。     

海洋石油污染及其微生物修复研究进展

海洋石油污染严重影响了海洋生态系统平衡和人类健康,海洋石油污染的微生物修复技术因其自身的优势越来越受到人们的重视。介绍了海洋石油污染的现状和治理方法,并着重介绍了海洋中石油污染微生物修复中降解微生物的种类、降解机理和生物修复的研究进展,并指出了生物修复存在并需要克服的问题,以期为海洋石油污染环境修复研究提供参考。     

石油污染生态系统中细菌群落结构及其代谢机制研究进展

石油化工产品的不合理处置与泄漏导致石油及其衍生物大量释放到环境中,由此造成的环境污染问题日益严重,石油污染已成为全球性公害之一。微生物修复技术凭借其成本低、环境友好等优势,广泛应用于石油污染的治理。大量研究表明功能微生物群落在石油污染生态系统的修复体系中发挥了重要的作用。其中,细菌是最主要、最活跃的石油降解微生物。然而,在原位/异位生物修复过程中,存在功能菌群在污染体系中难维持、易失调及石油烃降解途径不明晰等问题。因此,本文总结了石油污染自然生态系统和微宇宙实验体系中的细菌群落结构、石油烃代谢机制及相关功能基因,并对微生物法处理石油污染的未来研究方向提出展望,为石油污染场地生物修复方案的制定提供理论参考。     

石油污染环境中固氮和寡氮营养细菌的分离鉴定及其特性

[背景]石油污染治理中的生物修复因无二次污染、处理成本低等优点受到人们的广泛关注,但由于石油烃向环境中大量输入,导致环境中氮源的相对不足成为制约生物修复效率的关键因素之一,因此筛选能够适应寡氮环境的微生物具有重要的生态意义.[目的]从辽河油田油藏水中筛选在不添加氮源培养基中生长的微生物,为石油污染环境生物修复提供候选菌...     

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.     

石油污染对土壤细菌结构特征的影响

[目的]探究准东油田地区石油污染对土壤细菌结构特征的影响。[方法]提取准东油田的背景土和油污土中的细菌DNA并进行PCR扩增,利用Miseq平台对其16S r DNA进行测序统计。[结果]总共得到93 033个细菌16S rRNA有效序列,划分为371个OTU单元;样品中优势菌群是放线菌门(Actinobacteria)、厚壁菌门(Firmicutes)及变形菌门(Proteobacteria),厚壁菌门在背景样本中总数为29 732个,污染样本中为8 097个,数量剧减;变形菌门和放线菌门在石油污染土样中数目分别增长70%和47%;污染样品中多样性shannon指数平均为3.77,高于背景样品的2.77。[结论]证明了石油污染物对环境中的细菌结构影响显著,石油污染土壤中细菌结构多样性高于背景土壤,环境中能降解利用石油烃的菌种可能属于放线菌门和变形菌门。     

微生物降解石油污染物机制研究进展

石油污染是当前紧迫的水环境问题,研究石油污染物降解机制有助于探索石油污染修复技术路径。重点介绍了微生物降解石油污染物过程中的微生物种类、降解机制和反应机理,即具有代表性的细菌、真菌和藻类,石油烃的有氧降解(链烷烃、环烷烃和芳香烃)和厌氧降解(脱氢羟基化、延胡索酸盐加成)。并对微生物降解石油组分的影响因素进行了讨论,具体包括:烃类结构(支链多结构越复杂,越难降解)、微生物种类(混合菌的生化降解能力更强)、环境因子(pH、温度、盐度、含氧量和营养物质),进一步指出了生物修复技术应用于石油污染修复治理研究中的优缺点。此外,还对现有微生物降解技术的应用做了简要概述,归纳总结现有研究中存在的问题,尝试性的提出了今后生物降解石油污染物的研究重点,即生物降解石油的机制还需进一步明确,并重点分析了生物电化学方法在降解去除石油污染物方面可行性。综述石油烃生物降解机制和反应机理,以期为生物修复水体石油污染提供参考和借鉴作用。     

石油污染对鸟类的影响及石油污染清洁修复技术的研究进展

石油污染物通过自然泄漏和各种人类活动进入生态环境,对鸟类的生存产生影响。本文综述了国内外有关石油污染物对鸟类所产生的影响、受污染鸟类及其栖息地的清洁修复技术的研究现状以及发展趋势。现有研究发现,石油的毒性和石油对羽毛结构与功能的破坏是石油污染影响鸟类的主要原因。石油污染不仅对鸟类有直接的致死作用,而且能产生许多慢性危害,包括引起鸟类溶血性贫血、使其免疫能力下降、降低羽毛的保温和防水能力等。对鸟类栖息地中的石油污染进行及时清理并开展对受污染鸟类的清洁修复工作,是减轻石油污染对鸟类影响的重要手段。我国作为石油消费大国,关于石油污染对鸟类影响的研究与国外相比滞后,亟需在石油污染对鸟类的短期和长期影响、受污染鸟类及其栖息地的清洁修复技术等方面开展更多的研究。     

石油污染土壤自然衰减过程多环芳烃降解基因动态特征

新疆石油污染土壤中微生物多环芳烃(polycyclic aromatic hydrocarbons,PAHs)降解功能基因研究甚少,且环境因子和功能基因之间相关性仍不清楚。【目的】揭示新疆石油污染砂质土壤自然衰减过程中多环芳烃降解关键基因结构和变化规律。【方法】以新疆准东油田为研究区,分析同一采油区不同石油污染年限土壤理化因子和多环芳烃含量变化,采用扩增子测序研究石油自然衰减过程中多环芳烃降解酶基因结构变化规律,利用Mental检验探讨其环境驱动因子。【结果】石油污染时间1年和3年的土壤中有多项理化指标与背景土存在显著性差异,而污染5年土壤与背景土之间仅2项指标具有显著性差异,随石油自然衰减逐渐恢复至正常。石油污染1年的土壤中16种多环芳烃除苊烯和?以外,其余14种多环芳烃均高于石油污染3年和5年土壤,多环芳烃总量和含油率污染1年土壤均显著高于污染3年和5年的土壤,多环芳烃会在污染后短时间内迅速被降解。扩增子测序结果显示,萘双加氧酶基因分类操作单元(operational taxonomic units,OTUs)序列随污染年限延长逐渐增多;芳环羟化双加氧酶基因OTUs序列BLAST(...     

石油烃类的微生物降解

石油作为重要能源之一已被世界各国广泛使用,由于在石油的开采、储存、运输、加工和石化产品生产等过程中的漏油以及突发性泄油事故致使大量的石油进入环境造成污染。石油污染的危害主要表现在对土壤生态系统的结构和功能的破坏,严重影响土壤的透气性和渗水性,导致土壤板结、肥力下降;在水体表面形成油膜,致使水中溶氧量急剧下降,造成水生生物的大量死亡,破坏水生生态环境和渔业资源;还可进入地下水系,直接污染地下水源,影响居民用水和农田灌溉;石油中的一些致畸致癌物质还可通过食物链的生物富集作用而直接危害人类健康。随着人们对环境问题的日益关注,石油烃类的微生物降解研究工作也不断得以深入。近十年来这一领域又有许多研究和相关报道,本文对相关工作进行了综述。     

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.