Towards an ecological modelling approach for assessing ionizing radiation impact on wildlife populations.

The emphasis of the international system of radiological protection of the environment is to protect populations of flora and fauna. Throughout the MODARIA programmes, the United Nations' International Atomic Energy Agency (IAEA) has facilitated knowledge sharing, data gathering and model development on the effect of radiation on wildlife. We present a summary of the achievements of MODARIA I and II on wildlife dose effect modelling, extending to a new sensitivity analysis and model development to incorporate other stressors. We reviewed evidence on historical doses and transgenerational effects on wildlife from radioactively contaminated areas. We also evaluated chemical population modelling approaches, discussing similarities and differences between chemical and radiological impact assessment in wildlife. We developed population modelling methodologies by sourcing life history and radiosensitivity data and evaluating the available models, leading to the formulation of an ecosystem-based mathematical approach. This resulted in an ecologically relevant conceptual population model, which we used to produce advice on the evaluation of risk criteria used in the radiological protection of the environment and a proposed modelling extension for chemicals. This work seeks to inform stakeholder dialogue on factors influencing wildlife population responses to radiation, including discussions on the ecological relevance of current environmental protection criteria. The area of assessment of radiation effects in wildlife is still developing with underlying data and models continuing to be improved. IAEA's ongoing support to facilitate the sharing of new knowledge, models and approaches to Member States is highlighted, and we give suggestions for future developments in this regard.

The functional role of the photosynthetic apparatus in the recovery of Brassica napus plants from pre-emergent metazachlor exposure.

Metazachlor is a chloroacetamide herbicide, frequently used in Brassica napus cultivations around the world. Its primary target is the inhibition of very long chain fatty acid biosynthesis. This study included a morphological and physiological screening of hydroponically grown B. napus, exposed to a concentration range of 0, 0.25, 0.50, 0.75 and 1.0kg metazachlor per hectare. The results indicate that within a month after application, growth and development of B. napus are severely affected by low metazachlor doses. At intermediate metazachlor concentrations, loss of phosphorous and potassium from the plant tissues suggests destabilisation of cellular membranes, which may be a direct consequence of metazachlor application. This membrane instability could be indirectly linked with alterations of electron transport and a reduction of carbon assimilation. At increased metazachlor doses of 0.75kga.i.ha(-1), pigment concentrations are strongly reduced. However, chlorophyll fluorescence parameters seem to remain unaffected at metazachlor doses up to 0.75kga.i.ha(-1). At a metazachlor concentration of 1.0kga.i.ha(-1), negative effects are observed on all tested parameters, resulting in limited survival. The results indicate photosynthesis is assured at intermediate metazachlor concentrations for the cost of growth and development. It is clear that photosynthesis plays a key role in the survival strategy of young plants to overcome initially induced chemical stress.

Effect of external K on the block of the inward rectifier during hyperpolarization in guinea-pig ventricular myocytes by external Na.

The effect of changes of the external K concentration on the block of the inward-rectifying K current during hyperpolarization in guinea-pig ventricular myocytes by external Na was investigated. The voltage-dependent block of iK1 by external Na ions is decreased when the external K concentration is lowered between 5.4 and 0.54 mM, but is not influenced when Ko is increased from 5.4 to 27 mM. The effect of lowering Ko can be described as a decrease of the rate of entry of blocking Na ions at lower external K.

The effect of inhibition of mitochondrial energy metabolism on the transient inward current of isolated guinea-pig ventricular myocytes.

Delayed afterdepolarizations (DADs) might underlie ischemic or reperfusion arrhythmias (Ferrier et al., 1985; Coetzee and Opie, 1987). These DADs are the result of a transient inward current iti, which is caused by instability of the intracellular level of free Ca2+ (Cai) due to an oscillatory release of Ca from the sarcoplasmic reticulum (Kass et al., 1978). DADs are known to be abolished by hypoxia and by metabolic inhibition (Di Gennaro et al., 1987; Coetzee and Opie, 1987), which could be caused by a number of different mechanisms: (1) The large increase of potassium conductance associated with metabolic inhibition (Vleugels et al., 1980; Isenberg et al., 1983) could prevent iti from causing a marked depolarization, and would thus "mask" the DADS. (2) Although metabolic inhibition will eventually result in an increase of Cai, a temporary decrease could initially take place, thereby minimizing the Ca instability. Two mechanisms are known which might produce such an effect: Firstly, the shortening of the action potential which occurs during metabolic inhibition will markedly reduce the time during which Ca channels remain open, thereby causing a diminished total Ca influx during the action potential (Isenberg et al., 1983; Noma and Shibasaki, 1985; Kakei et al., 1985). Secondly, a direct reduction of iCa by a decrease in ATP concentration, described by Irisawa and Kokubun (1983), could also contribute to a decreased Ca load. (3) Metabolic inhibitors could possibly interfere with the cycling of Ca between different compartments within the cell, thereby altering the temporal variation in Cai, and thus influencing iti.(ABSTRACT TRUNCATED AT 250 WORDS)

Potassium currents in cardiac cells.

The kinetic properties of the inwardly rectifying K current and the transient outward current in cardiac cells were investigated. In sheep Purkinje fibers superfused with Na-free K-free solution, time-dependent changes in the conductance of the inward rectifier are described. In patch clamp experiments the inward rectifier inactivates during hyperpolarization, as can be seen by a decrease in the open state probability. Using whole cell clamp on ventricular myocytes it is demonstrated that the inactivation during hyperpolarization is due to blocking of the channel by external Na, Mg and Ca. The channels responsible for the transient outward current in cow, sheep and rabbit Purkinje fibers are identified using single channel recording. It is demonstrated that in all three preparations the channels are K-selective. The channel in cow Purkinje cells has a large conductance and is regulated by voltage and internal Ca concentration. The channels identified in the sheep and rabbit cells have a much smaller conductance.

The mechanism of the inactivation of the inward-rectifying K current during hyperpolarizing steps in guinea-pig ventricular myocytes.

The time course of the inward-rectifying K current during hyperpolarizing clamp steps was investigated in single myocytes isolated from guinea-pig ventricles. The experiments were done using a two-electrode voltage-clamp technique with two patch pipettes in the whole-cell configuration. Hyperpolarizations to potentials negative to -100 mV, induced large inward-rectifying K currents (iK1), which showed a marked decay. The current-voltage relation of the peak inward current was almost linear, but the steady-state current-voltage relation had a region of negative slope at potentials negative to -140 mV. These findings indicate that the channel inactivates during hyperpolarizing steps. When Na ions in the extracellular solution were replaced by choline, Tris, TMA or sucrose, the decay of the inward currents was largely reduced, and the negative slope in the steady-state current-voltage relation was absent. When divalent ions were removed from the Na-free bathing solution, a marked increase in iK1 was found, and the currents became time-independent. These experiments demonstrate that the inactivation during hyperpolarization is largely due to a block of the channel by external Na ions. The block by Na is most pronounced at very negative potentials, and is strongly voltage-dependent. External Ca and Mg ions also cause a marked block of the channel. The block by these divalent ions is however much less voltage-dependent than the one by Na, but is already present at the cell's resting potential.