Anthropogenic effects on the biota: towards a new system of principles and criteria for analysis of ecological hazards.

The currently accepted system of criteria for evaluating environmental and ecological hazards of man-made chemicals (pollutants) is vulnerable to criticism. In this paper, a new concept of the system of approaches towards criteria for evaluating the ecological hazard from man-made impact is proposed. It is suggested to assess the man-made impacts (including effects of pollutants and xenobiotics) on the biota according to the following four levels of disturbance in biological and ecological systems: (1) the level of individual responses; (2) the level of aggregated responses of groups of organisms; (3) the level of stability and integrity of the ecosystem; (4) the level of contributions of the ecosystem to biospheric processes. On the basis of the author's experimental studies, an example is given of how to apply the proposed approach and the system of criteria to the analysis of concrete experimental data. To exemplify the efficiency of the proposed approach, it is shown how to use it to analyze new data on effects of a synthetic surfactant on water filtering by bivalves. It is concluded that the proposed approach will be helpful in better assessing environmental and ecological hazards from anthropogenic effects on biota, including effects of man-made chemicals polluting ecosystems.     

模拟水生态系统及其在环境研究中的应用

随着70年代污染生态毒理学的发展,微宇宙作为评价化学品的环境影响的有力工具日益受到重视。由于从点源和非点源释放的化学物质可经直接或间接途径进入水生态系统,水生微宇宙在环境研究中的应用发展很快。早期的研究工作侧重于化学污染物在水环境的归宿。自70年代末以来,研究注意力逐渐集中于有毒物质在水生态系统内不同生物学组织水平上的生态学效应。本文分下列4个方面进行述评:(1)关于模拟生态系统的若干基本概念;(2)应用于环境研究的不同类型水生微宇宙;(3)尚有争议的若干问题;(4)水生微宇宙技术应用的新动向和展望。     

Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships

Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits, including cancer, asthma, metabolic disorders, and various reproductive conditions. It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition, tobacco smoke, air pollutants, metals, organic chemicals, other sources of oxidative stress, and the microbiome, particularly if the exposure occurs during key periods of development. Thus, epigenetic changes could represent an important pathway by which environmental factors influence disease risks, both within individuals and across generations. We discuss some of the challenges in studying epigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.     

Studies on the effects of copper deficiency on rat liver mitochondria. II. Effects on oxidative phosphorylation

Effects of dietary copper deficiency in rats on respiratory enzymes of isolated rat liver mitochondria have been studied. After 2 weeks of Cu-depletion, cytochrome c oxidase (EC 1.9.3.1) activity had declined by 42% and between 4 and 8 weeks exhibited between 20 and 25% of the activity of control mitochondria. Activities of NADH cytochrome c reductase (EC 1.6.99.3) and succinate cytochrome c reductase (EC 1.3.99.1), were unaffected initially but declined by 32 and 46%, respectively, after 8 weeks of Cu-depletion. After 4 weeks there was a significant (34%) decline in succinate supported state 3 respiration with only a modest (18%) decline in state 4 respiration. The ADP:O ratio was unaffected by Cu-depletion after 6 and 8 weeks of dietary Cu-restriction. State 3 respiration was significantly reduced after 6 weeks when glutamate/malate or beta-hydroxybutyrate were used as substrates, whereas state 4 respiration and ADP:O ratios were unaffected. The fall in state 3 respiration was of sufficient magnitude at 8 weeks to cause a significant decline in the respiratory control ratio with all substrates. Comparisons between the relative activities of cytochrome c oxidase and reductase activities in Cu-deficient preparations, the relatively specific effect of the deficiency on state 3 respiration with all substrates tested and the ability to increase significantly oxygen consumption in excess of maximal state 3 respiration by the uncoupler 2,4-dinitrophenol suggest that the defect in Cu-deficient mitochondria cannot be attributed solely to the decreased activity of cytochrome c oxidase.     

Embryos as targets of endocrine disrupting contaminants in wildlife

Environmental contaminants are now a ubiquitous part of the ecological landscape, and a growing literature describes the ability of many of these chemicals to alter the developmental trajectory of the embryo. Because many environmental pollutants readily bioaccumulate in lipid rich tissues, wildlife can attain considerable body burdens. Embryos are often exposed to these pollutants through maternal transfer, and a growing number of studies report long-term or permanent developmental consequences. Many biological mechanisms are reportedly affected by environmental contaminants in the developing embryo and fetus, including neurodevelopment, steroidogenesis, gonadal differentiation, and liver function. Embryos are not exposed to one chemical at a time, but are chronically exposed to many chemicals simultaneously. Mixture studies show that for some developmental disorders, mixtures of chemicals cause a more deleterious response than would be predicted from their individual toxicities. Synergistic responses to low dose mixtures make it difficult to estimate developmental outcomes, and as such, traditional toxicity testing often results in an underestimate of exposure risks. In addition, the knowledge that biological systems do not necessarily respond in a dose-dependent fashion, and that very low doses of a chemical can prove more harmful than higher doses, has created a paradigm shift in studies of environmental contaminant-induced dysfunction. Although laboratory studies are critical for providing dose-response relationships and determining specific mechanisms involved in disease etiology, wildlife sentinels more accurately reflect the genetic diversity of real world exposure conditions, and continue to alert scientists and health professionals alike of the consequences of developmental exposures to environmental pollutants.     

Top-down control analysis of the effect of temperature on ectotherm oxidative phosphorylation

Top-down control and elasticity analysis was conducted on mitochondria isolated from the midgut of the tobacco hornworm (Manduca sexta) to assess how temperature affects oxidative phosphorylation in a eurythermic ectotherm. Oxygen consumption and protonmotive force (measured as membrane potential in the presence of nigericin) were monitored at 15, 25, and 35 degrees C. State 4 respiration displayed a Q(10) of 2.4-2.7 when measured over two temperature ranges (15-25 degrees C and 25-35 degrees C). In state 3, the Q(10)s for respiration were 2.0 and 1.7 for the lower and higher temperature ranges, respectively. The kinetic responses (oxygen consumption) of the substrate oxidation system, proton leak, and phosphorylation system increased as temperature rose, although the proton leak and substrate oxidation system showed the greatest thermal sensitivity. Whereas there were temperature-induced changes in the activities of the oxidative phosphorylation subsystems, there was no change in the state 4 membrane potential and little change in the state 3 membrane potential. Top-down control analysis revealed that control over respiration did not change with temperature. In state 4, control of respiration was shared nearly equally by the proton leak and the substrate oxidation system, whereas in state 3 the substrate oxidation system exerted over 90% of the control over respiration. The proton leak and phosphorylation system account for <10% of the temperature-induced change in the state 3 respiration rate. Therefore, when the temperature is changed, the state 3 respiration rate is altered primarily because of temperature's effect on the substrate oxidation system.     

Removing environmental organic pollutants with bioremediation and phytoremediation

Hazardous organic pollutants represent a threat to human, animal, and environmental health. If left unmanaged, these pollutants could cause concern. Many researchers have stepped up efforts to find more sustainable and cost-effective alternatives to using hazardous chemicals and treatments to remove existing harmful pollutants. Environmental biotechnology, such as bioremediation and phytoremediation, is a promising field that utilizes natural resources including microbes and plants to eliminate toxic organic contaminants. This technology offers an attractive alternative to other conventional remediation processes because of its relatively low cost and environmentally-friendly method. This review discusses current biological technologies for the removal of organic contaminants, including chlorinated hydrocarbons, focusing on their limitation and recent efforts to correct the drawbacks.     

Bacterial anaerobic respiration and electron transfer relevant to the biotransformation of pollutants

Bacterial anaerobic respiration is one of the most ancient and essential metabolism processes, possessing the characteristics of both flexibility and high diversity, and a very close relationship with the physiological function in the ecological environment. Under anaerobic conditions, bacteria and anthropogenic substances can form coupling process facilitating terminal electron transfer. Several forms of bacterial anaerobic respiration and electron transfer related to the biotransformation of pollutants, including respiration with humics, sulfonates, halogenated chemicals, azo compounds, TNTs, metallic and non-metallic elements, are reviewed in this paper. These respirations and electron transfers on diverse electron acceptors in the environment have important biotechnological implications because these biochemical reactions have their roles on the transformation/degradation of toxic substances and the cycling of organic carbon as well as many inorganic elements. Furthermore, remediation of sites contaminated with toxic pollutants based on bacterial anaerobic respirations is being recognized widely.     

Controversial role of intracellular iron in the mechanisms of chemically-induced hepatotoxicity

Hepatotoxicity induced by various therapeutic agents, industrial chemicals and environmental pollutants is a well-recognized phenomenon. These chemicals are known to cause liver damage that is localized to either periportal or centrilobular regions of the liver lobule (1–3). Depending on dose, duration, and route of exposure, the resultant liver injury may regress or progress and becomes irreversible (1). Mechanisms involved in this selective, localized toxicity have been the target of extensive research efforts, and many Studies produced conflicting results. As depicted in Figure 1, although many investigators implicate iron and lipid peroxidation in this process (4-9), others dispute such assertions (10–12).     

微生物厌氧呼吸与有机污染水体沉积物修复

水体沉积物有机污染是当前全球关注的重要环境问题。微生物具有呼吸和代谢多样性,能以多种污染物作为厌氧呼吸的电子供体或受体,与周围环境中的生物和非生物因素组成代谢网络耦合有机污染物降解转化,是有机污染水体沉积物修复的重要驱动者。本文重点综述了微生物厌氧呼吸、电子传递网络及其对有机污染水体沉积物的修复机制研究进展,并对有机污染水体沉积物微生物修复理论和技术研究的问题和挑战进行了探讨。     

Effects of Picoxystrobin and 4-n-Nonylphenol on Soil Microbial Community Structure and Respiration Activity

There is widespread use of chemical amendments to meet the demands for increased productivity in agriculture. Potentially toxic compounds, single or in mixtures, are added to the soil medium on a regular basis, while the ecotoxicological risk assessment procedures mainly follow a chemical by chemical approach. Picoxystrobin is a fungicide that has caused concern due to studies showing potentially detrimental effects to soil fauna (earthworms), while negative effects on soil microbial activities (nitrification, respiration) are shown to be transient. Potential mixture situations with nonylphenol, a chemical frequently occurring as a contaminant in sewage sludge used for land application, infer a need to explore whether these chemicals in mixture could alter the potential effects of picoxystrobin on the soil microflora. The main objective of this study was to assess the effects of picoxystrobin and nonylphenol, as single chemicals and mixtures, on soil microbial community structure and respiration activity in an agricultural sandy loam. Effects of the chemicals were assessed through measurements of soil microbial respiration activity and soil bacterial and fungal community structure fingerprints, together with a degradation study of the chemicals, through a 70 d incubation period. Picoxystrobin caused a decrease in the respiration activity, while 4-n-nonylphenol caused an increase in respiration activity concurring with a rapid degradation of the substance. Community structure fingerprints were also affected, but these results could not be directly interpreted in terms of positive or negative effects, and were indicated to be transient. Treatment with the chemicals in mixture caused less evident changes and indicated antagonistic effects between the chemicals in soil. In conclusion, the results imply that the application of the fungicide picoxystrobin and nonylphenol from sewage sludge application to agricultural soil in environmentally relevant concentrations, as single chemicals or in mixture, will not cause irreversible effects on soil microbial respiration and community structure.     

Role of UCP3 in state 4 respiration during contractile activity-induced mitochondrial biogenesis.

In an effort to better characterize uncoupling protein-3 (UCP3) function in skeletal muscle, we assessed basal UCP3 protein content in rat intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondrial subfractions in conjunction with measurements of state 4 respiration. UCP3 content was 1.3-fold (P < 0.05) greater in IMF compared with SS mitochondria. State 4 respiration was 2.6-fold greater (P < 0.05) in the IMF subfraction than in SS mitochondria. GDP attenuated state 4 respiration by approximately 40% (P < 0.05) in both subfractions. The UCP3 activator oleic acid (OA) significantly increased state 4 respiration in IMF mitochondria only. We used chronic electrical stimulation (3 h/day for 7 days) to investigate the relationship between changes in UCP3 protein expression and alterations in state 4 respiration during contractile activity-induced mitochondrial biogenesis. UCP3 content was increased by 1.9- and 2.3-fold in IMF and SS mitochondria, respectively, which exceeded the concurrent 40% (P < 0.05) increase in cytochrome-c oxidase activity. Chronic contractile activity increased state 4 respiration by 1.4-fold (P < 0.05) in IMF mitochondria, but no effect was observed in the SS subfraction. The uncoupling function of UCP3 accounted for 50-57% of the OA-induced increase in state 4 respiration in IMF mitochondria, which was independent of the induced twofold difference in UCP3 content due to chronic contractile activity. Thus modifications in UCP3 function are more important than changes in UCP3 expression in modifying state 4 respiration. This effect is evident in IMF but not SS mitochondria. We conclude that UCP3 at physiological concentrations accounts for a significant portion of state 4 respiration in both IMF and SS mitochondria, with the contribution being greater in the IMF subfraction. In addition, the contradiction between human and rat training studies with respect to UCP3 protein expression may partly be explained by the greater than twofold difference in mitochondrial UCP3 content between rat and human skeletal muscle.     

Appearance and Disappearance of Cyanide-Resistant Respiration in Vigna mungo Cotyledons during and following Germination of the Axis

Mitochondrial preparations isolated from black gram (Vigna mungo L.) cotyledons exhibited cyanide-resistant respiration which was of mitochondrial origin. The appearance and the disappearance of this alternative respiration took place during and following imbibition. During the first 6 hours of imbibition, the respiration was completely inhibited by cyanide, but after this time the alternative respiration markedly developed, reaching a maximal cyanide-resistance 12 to 16 hours after the start of imbibition. Subsequently, the alternative respiration gradually disappeared. The actions of cycloheximide and chloramphenicol indicated that the appearance was dependent on cytoplasmic protein synthesis and that the disappearance depended on both cytoplasmic and mitochondrial protein synthesis. The alternative pathway contributed to state 4 respiration, but not to state 3 respiration, in mitochondria from 1-day-old cotyledons. On day 3, it contributed to neither state 3 nor state 4.     

Influence of menhaden oil on mitochondrial respiration in BHE rats

The effects of corn or menhaden oil and thyroxine treatment on hepatic mitochondrial respiration was studied. BHE rats were fed a 64% sucrose, 6% corn, or menhaden oil diet until they were 60-70 days of age. Succinate-supported mitochondrial respiration was studied at 3 degrees C intervals from 4 to 40 degrees C. Upper and lower activation energies and transition temperatures were determined through the calculation of Arrhenius plot. Menhaden oil plus daily thyroxine injection resulted in higher and lower activation energies than the other treatments. This combined treatment also resulted in lower state 3 and higher state 4 respiration rates and tighter coupling of respiration to ATP synthesis. These effects were thought to be due to the effect this treatment combination had on membrane fluidity.     

Effect of the polycationic antibiotic polymyxin B on the respiratory activity of rat liver mitochondria

the mechanism of the effect of the peptide antibiotic polymixin B on respiration of rat liver mitochondria was studied. It was shown that polymixin B at concentrations of (1,6--2,0) . 10(-3) M inhibits mitochondrial respiration in state 3 and 3u irrespective of the oxidation substrate used and activates oxygen consumption in state 4 at lower concentrations. It is assumed that the antibiotic affects mitochondrial respiration by changing the ionic permeability of the membranes.     

Effect of Peroxide, Sodium, and Calcium on Brain Mitochondrial Respiration In Vitro: Potential Role in Cerebral Ischemia and Reperfusion

Mitochondrial pyruvate-supported respiration was studied in vitro under conditions known to exist following ischemia, i.e., elevated extramitochondrial Ca2+, Na+, and peroxide. Ca2+ alone (7-10 nmol/mg) decreased state 3 and increased state 4 respiration to 81 and 141% of control values, respectively. Sodium (15 mM) and/or tert-butyl hydroperoxide (tBOOH; up to 2,000 nmol/mg protein) alone had no effect on respiration; however, Na+ or tBOOH in combination with Ca2+ dramatically altered respiration. Respiratory inhibition induced by Ca2+ and tBOOH does not involve pyruvate dehydrogenase (PDH) inhibition since PDH flux increased linearly with tBOOH concentration (R = 0.96). Calcium potentiated tBOOH-induced mitochondrial NAD(P)H oxidation and shifted the redox state of cytochrome b from 67 to 47% reduced. Calcium (5.5 nmol/mg) plus Na+ (15 mM) decreased state 3 and increased state 4 respiratory rates to 55 and 202% of control values, respectively. Sodium- as well as tBOOH-induced state 3 inhibition required mitochondrial Ca2+ uptake because ruthenium red addition before Ca2+ addition negated the effect. The increase in state 4 respiration involved Ca2+ cycling since ruthenium red immediately returned state 4 rates back to control values. The mechanisms for the observed Ca2(+)-, Na(+)-, and tBOOH-induced alterations in pyruvate-supported respiration in vitro are discussed and a multifactorial etiology for mitochondrial respiratory dysfunction following cerebral ischemia in vivo is proposed.     

The Effect of the Lipid Peroxidation Product 4-Hydroxynonenal and of its Metabolite 4-Hydroxynonenoic Acid on Respiration of Rat Kidney Cortex Mitochondria

In rat kidney cortex mitochondria, 4-hydroxynonenal inhibits state 3 respiration as well as uncoupled respiration at micromolar concentrations. The inhibition is more distinct for NAD-linked than for FAD-linked respiration. 4-Hydroxynonenal increases the state 4 respiration. It is assumed that 4-hydroxynonenal behaves like a decoupling agent. 4-Hydroxynonenal augments the inhibitory effect of 2, 4-dinitrophenol observed at superoptimal concentrations. 4-Hydroxynonenal is metabolised by renal mitochondria, and 4-hydroxynonenoic acid is one of the metabolites generated. This metabolite is without effect on respiration at concentrations up to 50 μM. Therefore, the effect of 4-hydroxynonenal on respiration is not mediated by this fatty acid derivative formed during respiratory measurements.     

Effects of Cd2+ and two cadmium organic complexes on isolated rat liver mitochondria

Effects of Cd2+ and two complexes of bivalent cadmium with 1,3-bis(4-chlorbenzylidenamino)-guanidine and anabasine on ion permeability of the inner membrane and respiration of isolated rat liver mitochondria were studied. Starting from 5 microM, Cd2+ decreased state 3 and DNP-stimulated respiration of mitochondria and increased their state 4 respiration. At 30 microM, Cd2+ decreased state 4 respiration. The complexes, particularly complex of Cd2+ with 1,3-bis(4-chlorbenzylidenamino)-guanidine, inhibited the mitochondrial respiration at lower concentration of Cd2+. Nonenergized mitochondria incubated in media containing 125 mM of NH4NO3 or KNO3 showed more pronounced swelling in experiments with 10 microM of the complexes than with Cd2+. The complexes produced swelling of the mitochondria energized by 5 mM of succinate and incubated in medium containing 25 mM K-acetate and 100 mM sucrose. Uptake of 137-Cs by succinate-energized mitochondria in the presence of 10(-8) M of valinomycin was substantially decreased in experiments with 10 microM of the complexes than with Cd2+. Ruthenium red (7.5 microM) prevented this effect with 10 microM of complex of Cd2+ with 1,3-bis(4-chlorbenzylidenamino)-guanidine and especially complex of Cd2+ with anabasine and Cd2+. These results indicate that the cadmium organic complexes affect respiration and perturb ion permeability significantly stronger than Cd2+.     

Zooplankters as indicators of ecosystem health: past findings and future directions

Both acute (ingestion, respiration) and chronic bioassays (reproduction, survival) have been used to identify sources of pollutants. A mass-balance analysis suggests that acute tests be paired, using important indicator species asDaphnia, Ceriodaphnia and potentially others, to estimate the impact of contaminants upon the zooplankton community. Eventually groups of community bioassays may be combined to approximate an ecosystem bioassay. Hormesis or the stimulation of a physiological process by a compound which is toxic at high concentrations is characteristic of several bioassays; in this paper the ecotoxicology community is challenged to keep detailed records of the species, toxic compound, and physiological response involving hormesis in order to understand it; and ultimately to use it to simplify interpretation of bioassays. Life history characteristics of the cladoceran zooplankton, including early reproduction, high net reproductive rates, and the potential for many parthenogenetic generations with constant genotypes and low mutation rates make good choices for environmental bioassays. In contrast, high mutation rates of rotifers make them questionable choices. Five innovations, one or more of which may improve our ability to detect and identify pollutants, are suggested for ecotoxicologists using zooplankton. These include (a) the use of strains of known genotype; (b) determination of the genetic adaptation of clones to common toxins; (c) the use of common behaviors, including responses to light in detection of non-lethal chemicals at ambient levels; (d) record keeping on occurrence of cladoceran tumors; and (e) the determination of precise toxins responsible for the inhibition of zooplankton function and behavior.     

细菌对环境污染物的趋化性及其在生物修复中的作用

细菌对有机化合物的降解能力是一种利用碳源和能源的优势,这种能力可以用来设计安全、有效和无二次污染的污染物的生物修复系统。趋化性是细菌适应外界化学环境变化而作出的行为反应,是一种寻找碳源和能源的优势。细菌的趋化性能够增强细菌在自然环境中的降解污染物的效果,细菌的趋化性与降解性之间的关系研究已经成为热点。介绍了细菌的趋化性的基本概念和趋化信号转导的机制,重点讨论了细菌对环境污染化合物的趋化性,从基因水平揭示了趋化性与降解性之间的紧密联系,认为趋化性可以有效地促进降解性细菌对污染物的生物修复作用。