Growth inhibitory activity of Daphne gnidium L. (Thymelaeaceae) extracts on the elm leaf beetle (Col., Chrysomelidae)

Abstract:  An investigation has been performed on the activity of spurge flax ( Daphne gnidium L., Thymelaeaceae), a typical component of the Mediterranean vegetation, on the development of the elm leaf beetle ( Xanthogaleruca luteola Muller; Col., Chrysomelidae), one of the most serious defoliators of urban forests. Different concentrations of ethanolic extracts of D. gnidium leaves were added to the natural diet (elm leaf discs) of X. luteola , starting with L2 larvae, and the effects induced on the vitality, growth and phase duration of the different stages have been evaluated. A significant reduction of larval survival and adult emergence, together with an increased length of the larval period, heavy reduction of weight gain and appearance of malformations in emerged imagines were observed in presence of spurge flax extracts. These findings agree to ascribe to D. gnidium leaf extracts a growth inhibitory activity and allowed identifying what should be the optimal concentration to be applied on elm leaves to prevent heavy damages by X. luteola .     

Assessment of Carcinogenic Risk and Non-Carcinogenic Health Hazard from Exposure to Toxicants in Water from the Southwestern Coastal River System in Ghana

This study evaluated cancer risk and non-cancer human health hazard from exposure to the toxicants such as As, Cu, Pb, Zn, Mn, and CN in water from a southwestern river system in Ghana that drains through gold mining areas, using 108 water samples collected with random sampling techniques and analyzed in accordance with standard methods of chemical analysis outlined by the U.S. Environmental Protection Agency (USEPA). The concentrations of Cu and Zn were within World Health Organization and USEPA guideline values; Mn, free cyanide, As, and Pb values in most cases either exceeded USEPA and WHO values or both. The concentrations of the toxicants were used as input parameters in the cancer and non-cancer study that was conducted in line with USEPA risk assessment guidelines. The results of As cancer health risk revealed higher risk cases in two locations (Potroase and Dominase); non-cancer health risk for As was higher in 10 of the 14 locations, with other metals being of health concern at few locations in the study area. In conclusion, the findings of this study hold several policy implications as residents of mining communities still depend on these water bodies as their source of drinking water.     

Altered predator/prey behavior in polluted environments: implications for fish conservation

Predator/prey behavior has important consequences for individual survival and recruitment into fish populations, both of which can be affected by stressors such as environmental contaminants. The degree to which prey capture or predator avoidance abilities of a predator or prey species are affected will determine the direction in which the balance will be shifted. In a contaminated estuary we have studied, prey capure and predator avoidance of resident mummichogs, Fundulus heteroclitus, are impaired, which may account for individuals in that estuary having reduced growth and longevity compared with those from uncontaminated sites. Exposure to sediments, water, and grass shrimp from the contaminated site can impair the predatory abilities of mummichogs from a clean site. An important prey species, the grass shrimp, Palaemonetes pugio, has a greater population density and a greater proportion of large individuals at the polluted site, apparently because of reduced predation pressure. Mummichog larvae at the polluted site are initially more active and better at prey capture and predator avoidance than larvae from clean sites, but later they become poorer at both. Differences in predator vulnerability among larvae appear to be due to population differences in behavior, which may be due in part to both genetic and environmentally-caused factors. Conservation of fish populations should consider fish behavior and its interaction with contaminants.     

免疫传感器用于堆肥复杂系统监测的研究进展

随着免疫测定技术与传感技术的发展以及堆肥法在固体废物处理中的日益受重视,将免疫传感器从环境监测中细化到堆肥化过程中的监测,实时、在线测定,具有现实意义.本文将堆肥复杂系统组分按其物理性质,分为固相、液相、气相三类,着重介绍免疫传感器在其中的应用和发展状况, 综述了近年来用于痕量有害物质检测的免疫传感器的最新研究成果,并探讨了免疫传感器在环境监测中的应用和发展方向。     

Extrapolating toxic effects on individuals to the population level: the role of dynamic energy budgets

The interest of environmental management is in the long-term health of populations and ecosystems. However, toxicity is usually assessed in short-term experiments with individuals. Modelling based on dynamic energy budget (DEB) theory aids the extraction of mechanistic information from the data, which in turn supports educated extrapolation to the population level. To illustrate the use of DEB models in this extrapolation, we analyse a dataset for life cycle toxicity of copper in the earthworm Dendrobaena octaedra. We compare four approaches for the analysis of the toxicity data: no model, a simple DEB model without reserves and maturation (the Kooijman-Metz formulation), a more complex one with static reserves and simplified maturation (as used in the DEBtox software) and a full-scale DEB model (DEB3) with explicit calculation of reserves and maturation. For the population prediction, we compare two simple demographic approaches (discrete time matrix model and continuous time Euler-Lotka equation). In our case, the difference between DEB approaches and population models turned out to be small. However, differences between DEB models increased when extrapolating to more field-relevant conditions. The DEB3 model allows for a completely consistent assessment of toxic effects and therefore greater confidence in extrapolating, but poses greater demands on the available data.     

A Critical Review of Procedures and Approaches Used for Assessing Pollution-Induced Community Tolerance (PICT) in Biotic Communities

Pollution-induced community tolerance (PICT) is used for the detection of minor effects of toxicants in biotic communities. Organisms survive in toxic environments only if they are tolerant to the chemicals present in their habitat. In the selection phase, toxicants hinder the success of sensitive individuals and species and replace them by more tolerant ones. The resulting increase in community tolerance is quantified in the detection phase by short-term toxicity tests. In this way PICT can establish causal linkages between contaminants and effects. An increase in community tolerance compared to the baseline tolerance at reference sites suggests that the community has been adversely affected by toxicants. PICT has been used in aquatic and terrestrial environments with communities of periphyton, phytoplankton, bacteria, nematodes and insects. A variety of methods have been used for quantification of community tolerance including photosynthesis, sulfolipid synthesis, respiration, thymidine and leucine incorporation, survival, and substrate utilisation patterns. PICT has been observed for copper, zinc, nickel, mercury, cadmium, arsenate, monomethylarsonic acid, diuron, tributyl tin, 4,5,6-trichloroguaiacol, irgarol 1051, seanine 211, atrazine, and trinitrotoluene. It is necessary to validate PICT, at least by showing that it is related to the preexposure concentration of the toxicants and that it is coupled to a toxicant-induced succession (TIS) in the community. Care must also be taken to ascertain that PICT interpretation is not confounded by co-tolerance or bioavailability differences. Co-tolerance patterns, which are indicative of the specificity of PICT, have only been investigated for arsenate, diuron and a few metals. For the further improvement of PICT methodology special attention should be given to co-tolerance patterns and development of new integrating short-term tests for quantification of tolerance. It is also important to broaden the scope of organisms and toxicants used. Properly validated, PICT is a powerful tool for detection of community effects and its use in monitoring and site-specific risk assessment should be encouraged.     

Ecotoxicology of ozone: bioactivation of extracellular ascorbate

The ascorbate pools of the extracellular respiratory lining fluids and the plant apoplast are currently considered as part of the first line of defence against ambient ozone. Ozone is in fact rapidly decomposed by ascorbate, but the only product identified so far (singlet oxygen) is toxic. Peroxy-l-threonic and peroxy-oxalic acids are now derived as further decomposition products on the basis of Criegee-type ozone chemistry. These secondary toxicants may resemble known ozone induced transmitter molecules by participating in signalling events affecting plant and animal innate immunity.     

Utilization of juvenile animal studies to determine the human effects and risks of environmental toxicants during postnatal developmental stages

BACKGROUND: Toxicology studies utilizing animals and in vitro cellular or tissue preparations have been used to study the toxic effects and mechanism of action of drugs and chemicals and to determine the effective and safe dose of drugs in humans and the risk of toxicity from chemical exposures. Testing in animals could be improved if animal dosing using the mg/kg basis was abandoned and drugs and chemicals were administered to compare the effects of pharmacokinetically and toxicokinetically equivalent serum levels in the animal model and human. Because alert physicians or epidemiology studies, not animal studies, have discovered most human teratogens and toxicities in children, animal studies play a minor role in discovering teratogens and agents that are deleterious to infants and children. In vitro studies play even a less important role, although they are helpful in describing the cellular or tissue effects of the drugs or chemicals and their mechanism of action. One cannot determine the magnitude of human risks from in vitro studies when they are the only source of toxicology data. METHODS: Toxicology studies on adult animals is carried out by pharmaceutical companies, chemical companies, the Food and Drug Administration (FDA), many laboratories at the National Institutes of Health, and scientific investigators in laboratories throughout the world. Although there is a vast amount of animal toxicology studies carried out on pregnant animals and adult animals, there is a paucity of animal studies utilizing newborn, infant, and juvenile animals. This deficiency is compounded by the fact that there are very few toxicology studies carried out in children. That is one reason why pregnant women and children are referred to as "therapeutic orphans." RESULTS: When animal studies are carried out with newborn and developing animals, the results demonstrate that generalizations are less applicable and less predictable than the toxicology studies in pregnant animals. Although many studies show that infants and developing animals may have difficulty in metabolizing drugs and are more vulnerable to the toxic effects of environmental chemicals, there are exceptions that indicate that infants and developing animals may be less vulnerable and more resilient to some drugs and chemicals. In other words, the generalization indicating that developing animals are always more sensitive to environmental toxicants is not valid. For animal toxicology studies to be useful, animal studies have to utilize modern concepts of pharmacokinetics and toxicokinetics, as well as "mechanism of action" (MOA) studies to determine whether animal data can be utilized for determining human risk. One example is the inability to determine carcinogenic risks in humans for some drugs and chemicals that produce tumors in rodents, When the oncogenesis is the result of peroxisome proliferation, a reaction that is of diminished importance in humans. CONCLUSIONS: Scientists can utilize animal studies to study the toxicokinetic and toxicodynamic aspects of drugs and environmental toxicants. But they have to be carried out with the most modern techniques and interpreted with the highest level of scholarship and objectivity. Threshold exposures, no-adverse-effect level (NOAEL) exposures, and toxic effects can be determined in animals, but have to be interpreted with caution when applying them to the human. Adult problems in growth, endocrine dysfunction, neurobehavioral abnormalities, and oncogenesis may be related to exposures to drugs, chemicals, and physical agents during development and may be fruitful areas for investigation. Maximum permissible exposures have to be based on data, not on generalizations that are applied to all drugs and chemicals. Epidemiology studies are still the best methodology for determining the human risk and the effects of environmental toxicants. Carrying out these focused studies in developing humans will be difficult. Animal studies may be our only alternative for answering many questions with regard to specific postnatal developmental vulnerabilities.     

Toxic action/toxicity

Some six or so physiological systems, essential to normal mammalian life, are involved in poisoning; an intoxication that causes severe injury to any one of them could be life threatening. Reversible chemical reactions showing Scatchard-type binding are exemplified by CO, CN- and cyclodiene neurotoxin insecticide intoxications, and by antigen-antibody complex formation. Haemoglobin (Hb) molecular biology accounts for the allosteric co-operativity and other characteristics of CO poisoning, CN- acts as a powerful cytochrome oxidase inhibitor, and antigen binding in a deep antibody cleft between two domains equipped with epitopes for antigen-binding groups explains hapten-specific immune reactions. Covalent chemical reactions with second-order (SN2) kinetics characterize Hg and Cd poisonings, the reactions of organophosphates and phosphonates with acetylcholinesterase and neurotoxic esterase and the reaction sequence whereby Paraquat accepts electrons and generates superoxide under aerobic conditions. Indirect carcinogens require cytochrome P450 activation to form DNA adducts in target-organ DNA and cause cancer, but a battery of detoxifying enzymes clustered with the P450 system must be overcome. Thus, S-metabolism competes ineffectively with target DNA for reactive vinyl chloride (VC) metabolites, epoxide hydrolase is important to the metabolism and carcinogenicity of alfatoxins and polycyclic aromatic hydrocarbons (benzo[a]pyrene, etc.), and the non-toxic 2-naphthylhydroxylamine N-glucuronide acts as a transport form in 2-naphthylamine bladder cancer. VC liver-cancer pathogenesis is explicable in terms of the presence of the glutathione S-transferase detoxifying system in hepatocytes and its absence from the fibroblastic elements, and of the VC concentrations reaching the liver by different administrative routes. In VC carcinogenicity, chemical reactions give imidazo-cyclization products with nucleoside residues of target DNA, and in benzene leukaemia, Z,Z-muconaldehyde forms cyclic products containing a pyrrole residue linked to purine. Increased HbCO concentrations reduce the O2-carrying capacity of the blood, and the changed shape of the O2-Hb dissociation curve parallels disturbance in O2 unloading. CN- acts on electron transport and paralyses respiration. In telodrin poisoning, preconvulsive glutamine formation abstracts tricarboxylic acid intermediates incommensurately with normal cerebral respiration. Antigen-antibody complexing depletes the antibody titre, available against infection. At high doses of Cd, Cd-thionein filtered through the kidneys is reabsorbed and tubular lesions produced. Some organophosphate insecticides promote irreversible acetylcholinesterase phosphorylation and blockade nerve function, and others react with neurotoxic esterase to cause delayed neuropathy. The evidence for Paraquat pulmonary poisoning suggests a radical mechanism involving three interrelated cyclic reaction stages. The action of N- and O8 (O substituent in 6-position of the purine) demethylases explains deletion mechanisms for DNA-alkyl adducts. DNA-directed synthesis in the presence of ultimate carcinogens provides for an estimation of misincorporations, which implicate the same transversions as those found by direct mutagenicity testing. Chemical carcinogens recognize tissue-sensitive cells and modify their heritable genetic complement. Oncoproteins encoded by activated oncogenes signal the transformation of normal cells into cancer cells. The importance of the H-ras oncogene and p53 tumour-suppressor gene is stressed. Antidotal action is analysed; for example, parenteral glutamine administration to telodrin-intoxicated rats restores the depleted cerebral glutamate level and prevents seizures. Glutamate acts as anticonvulsant in petit mal epilepsy. In general, therefore, the reaction of the toxicant-related substance with the relevant target-tissue macromolecule accounts for the biochemical/biological events at a cellular level a     

Effects of copper sulphate on Tisbe holothuriae Humes (Copepoda) and development of tolerance to copper

A study was made of the toxicity of copper to the marine copepod Tisbe holothuriae Humes and the development of increased tolerance due to acclimation. In sublethal concentrations, copper causes a prolongation of maturation time and a reduction in offspring production. These effects increased proportionally to the copper concentration used, while the respiratory rate (measured at the highest concentration used: 0.008 mg l^–1 Cu) increased. A tendency for higher tolerance due to acclimation was also observed. The copper induced delay in maturation time observed in the F₂ generation, became less pronounced from F₃ onwards. In animals exposed at 0.008 mg l^–1 Cu the maturation time of F₃ was not statistically different from that of untreated animals. The LC50 48 h also presented an increase due to acclimation in animals exposed at 0.004 (F₅) and 0.008 mg l^–1 Cu (F₃ and F₅ generations), but this increase was not statistically significant.