A kinetic model for surfactant inhibition of pentachlorophenol biodegradation

A kinetic model is used to describe the effect of the nonionic surfactant Tergitol NP-10 (TNP10) on pentachlorophenol (PCP) biodegradation by Sphingomonas chlorophenolica sp. strain RA2. Different initial biomass to initial substrate ratios ranging from 13 to 418 were tested with 23 TNP10 concentrations ranging from 0 to 1500 mg/L. Tests were also conducted at 10 degrees C and 20 degrees C. No PCP biodegradation inhibition was observed at concentrations below the critical micelle concentration (CMC) of 50 mg/L. TNP10 concentrations above 100 to 200 mg/L were increasingly inhibitory to PCP biodegradation rates. This inhibition was best described by the Monod kinetic equation wherein the effect of TNP10 inhibition is reflected in the half-saturation constant (Ks). The value of the Ks increased from between 1.5 and 13.5 mg/L with no surfactant present to 44 to 131 mg/L at 1000 mg/L TNP10. Using a standard competitive inhibition approach, the inhibition constant for TNP10 was approximately 100 mg/L at both 10 degrees C and 20 degrees C.     

Nonradioactive analysis of phosphatidylinositides and other anionic phospholipids by anion-exchange high-performance liquid chromatography with suppressed conductivity detection

Phosphatidylinositol 4,5-biphosphate (PIP(2)) modulates the function of numerous ion transporters and channels, as well as cell signaling and cytoskeletal proteins. To study PIP(2) levels of cells without radiolabeling, we have developed a new method to quantify anionic phospholipid species. Phospholipids are extracted and deacylated to glycero-head groups, which are then separated by anion-exchange HPLC and detected by suppressed conductivity measurements. The major anionic head groups can be quantified in single runs with practical detection limits of about 100 pmol, and the D3 isoforms of phosphatidylinositol phosphate (PIP) and PIP(2) are detected as shoulder peaks. In HeLa, Hek 293 and COS cells, as well as intact heart, PIP(2) amounts to 0.5 to 1.5% of total anionic phospholipid (10 to 30 micromol/liter cell water or 0.15 to 0.45 nmol/mg protein). In cell cultures, overexpression of Type I PIP5-kinase specifically increases PIP(2), whereas overexpression of Type II PI4-kinase can increase both PIP and PIP(2). Phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) and the D3 isomers of PIP(2) are detected after treatment of cells with pervanadate; in yeast, overexpression of a phosphatidylinositol 3-kinase (VPS34) specifically increases phosphatidylinositol 3-phosphate (PI3P). Using isolated cardiac membranes, lipid kinase and lipid phosphatase activities can be monitored with the same methods. Upon addition of ATP, PIP increases while PIP(2) remains low; exogenous PIP(2) is rapidly degraded to PIP and phosphatidylinositol (PI). In summary, the HPLC methods described here can be used to probe multiple aspects of phosphatidylinositide (Ptide) metabolism without radiolabeling.     

Conservation of Surfactant Protein A: Evidence for a Single Origin for Vertebrate Pulmonary Surfactant

Surface tension is reduced at the air–liquid interface in the lung by a mixture of lipids and proteins termed pulmonary surfactant. This study is the first to provide evidence for the presence of a surfactant-specific protein (Surfactant Protein A—SP-A) in the gas-holding structures of representatives of all the major vertebrate groups. Western blot analysis demonstrated cross-reactivity between an antihuman SP-A antibody and material lavaged from lungs or swimbladders of members from all vertebrate groups. Immunocytochemistry localized this SP-A–like protein to the air spaces of lungs from the actinopterygiian fish and lungfish. Northern blot analysis indicated that regions of the mouse SP-A cDNA sequence are complementary to lung mRNA from all species examined. The presence of an SP-A–like protein and SP-A mRNA in members of all the major vertebrate groups implies that the surfactant system had a single evolutionary origin in the vertebrates. Moreover, the evolution of the surfactant system must have been a prerequisite for the evolution of airbreathing. The presence of SP-A in the goldfish swimbladder demonstrates a role for the surfactant system in an organ that is no longer used for airbreathing. Received: 5 March 1997 / Accepted: 14 June 1997     

Environmental and biological factors influence the relationship between a predator fish,Gambusia holbrooki,and its main prey in rice fields of the Lower Mondego River Valley (Portugal)

We studied the relationships between a predator fish, Gambusia holbrooki, and its main food prey, within the content of a rice field food web. The influence of some environmental and biological factors on these trophic interactions, in combination with existent quantitative information, allowed us to evaluate the ecological viability of using a non-ionic surfactant, Genapol OXD-080, to control a plague caused by crayfish (Procambarus clarkii) populations in the rice fields. In the Lower Mondego River Valley, Portugal, G. holbrooki is abundant in rice fields. It feeds mainly on copepods, cladocerans and rotifers. Surface insects, such as aphids, collembolans, adult (imago) chironomids and other dipterans, are additional food. Large G. holbrooki consumed greater amounts of cladocerans and adult chironomids than other smaller size groups, while small fish prefered rotifers. Gravid females ate copepods, cladocerans, and adult chironomids and other dipterans in significantly greater amounts than immatures, males, and non-gravid females. Non-gravid females ate collembolans in significantly greater quantities than any other fish group. The population density of copepods, cladocerans, adult chironomids, and other dipterans, the area covered by aquatic vegetation, and water temperature all had significant effects on the total number of prey caught by G. holbrooki. In contrast, a negative correlation was found with rotifers, collembolans, aphids in higher densities, and of increased water volume, dissolved oxygen and pH. G. holbrooki holds a key intermediate position in the rice field food chain, feeding in large amounts of aquatic invertebrates and being eaten, in turn, by piscivores. With regard to the toxicity of Genapol OXD-080 on non-target organisms, LC₅₀ values for G. holbrooki and some of its main prey were several times lower than the concentration necessary to decrease the activity of crayfish populations in the rice fields. Thus, Genapol OXD-080 could potentially cause greater damage to the local populations of non-target species and should not be used without taking precautions not to contaminate other important biological reservoirs, such as the rice field irrigation channels. This revised version was published online in July 2006 with corrections to the Cover Date.     

Sorption isotherms and kinetics in the primary biodegradation of anionic surfactants by immobilized bacteria:: II. Comamonas terrigena N3H

Comamonas terrigena N3H was immobilized by covalent linking on silanized inorganic supports and by physical entrapment of cells within calcium alginate beads and reticulated polyurethane foam. Both entrapped cells were efficient for the primary biodegradation of the anionic surfactants dihexyl sulphosuccinate (DHSS) and dioctyl sulphosuccinate (DOSS), furthermore, exhibiting, in the case of polyurethane immobilized cells, a positive fractionating effect of the substrate by adsorption onto the polymer matrix. The overall kinetics for the surfactant removal from water were well-fitted to a biphasic process, a rapid passive sorption step of the surfactant onto the cell-loaded support and the intrinsic primary biodegradation slower step, both acting synergically.     

雌二醇对成年大鼠肺表面活性物质分泌的影响

采用离体非灌流肺模型,观察了雌二醇(E_2)对成年大鼠肺表面活性物质(PS)分泌的影响,并探讨了前列腺素(PG)在其中的作用。结果显示:E_2(10~(-6)mol/L)可使肺磷脂释放指数和肺磷脂释放量增多,分别为对照组的150.0％(P<0.05)及160.7％(P<0.01),表明E_2可促进成年大鼠PS的分泌;PG合成抑制剂消炎痛(10~(-5)mol/L)可以抑制E_2促进肺磷脂释放的效应,表明PG在E_2促进PS分泌中起介导作用。以上结果提示E_2可能参与成年动物PS分泌的调控。     

肺泡巨噬细胞对肺表面活性物质分泌的调控

为了观察肺泡巨噬细胞(AM)对肺表面活性物质(PS)分泌的影响,本实验以激活的AM培养上清液对离体非灌流肺进行持续灌洗,观察肺内PS含量的变化。结果表明,由调理酵母多糖(OPZ)激活的AM上清液,能使肺磷脂释放量(PL)和肺磷脂释放指数(b)增大,与激活物(OPZ)对照组及细胞对照组比较,有显著差异,P<0.01。用消炎痛预处理AM 30min后,再用OPZ激活AM,PL值和b值减少;而用细胞松弛素B预处理AM30min后,再用OPZ激活AM,则PL值和b值增大。以上两组与对照组比较,P<0.01。这表明激活AM增强肺PS分泌的作用能被消炎痛所抑制,而被细胞松弛素所增强,提示激活AM增强肺PS分泌可能是以前列腺素为中介的。激活AM能使PS分泌增加,这对于在生理和病理情况下稳定肺泡表面张力和增强肺的防御机能有重要意义。     

肺表面活性物质治疗新生儿呼吸窘迫综合征前给予nCPAP呼吸支持最佳时间窗的临床研究

摘要 目的：探讨肺表面活性物质（PS）治疗新生儿呼吸窘迫综合征（NRDS）前给予经鼻持续气道正压通气（nCPAP）呼吸支持的最佳时间窗。方法：选择2017年1月至2019年12月期间我院收治的NRDS患儿100例。根据随机数字表法分为A组（给予PS前预先进行小于2 h的nCPAP,n=33）、B组（给予PS前预先进行2-4 h的nCPAP,n=33）和C组（立即给予PS,n=34）。对比三组患儿的血气分析指标、肺功能指标、临床指标和并发症发生率。结果：A组、B组给予PS后4h、给予PS后24 h动脉血氧分压（PaO₂）、pH值高于C组,且B组高于A组（P<0.05）,而动脉二氧化碳分压（PaCO₂）低于C组,且B组低于A组（P<0.05）。A组、B组给予PS后4 h、给予PS后24 h潮气量（VT）、肺动态顺应性（CD）高于C组,且B组高于A组（P<0.05）,而吸气阻力（Raw）低于C组,且B组低于A组（P<0.05）。B组用药后3天内需气管插管行机械通气例数少于A组和C组,住院时间短于A组和C组（P<0.05）,A组、C组的用药后3天内需气管插管行机械通气例数、住院时间对比无明显差异（P>0.05）。三组患儿并发症发生率未见统计学差异（P>0.05）。结论：给予PS前预先进行2-4h的nCPAP,可较好地改善患儿血气分析指标和肺功能,有助于改善患儿预后。