Narcosis Due to Environmental Pollutants in Aquatic Organisms: Residue-Based Toxicity, Mechanisms, and Membrane Burdens

Abstract

The well-known correlation between the hydrophobicity of narcotic chemicals and the exposure concentration needed to produce an effect indicates that a lipid phase in the aquatic organism is the most likely target. The molar concentration in aquatic organisms at death is found to be approximately constant for different narcotic chemicals, varying from 2 to 8 mmol/kg organism. Because the proportion of lipid is known, the lethal in vivo membrane burden can be calculated to be 40 to 160 mmol/kg lipid. The exact mechanism underlying narcosis is still unknown. However, disturbance by narcotic chemicals in model membrane systems has been investigated, attention having been paid to disturbance of phospholipids and proteins, and of the interaction between the two groups. Model membrane burdens of different chemicals have been shown to be approximately constant for a particular effect. Different effects are found at different membrane concentrations. In the present review, the toxicity of narcotic chemicals to aquatic organisms is discussed, the possible mechanisms underlying narcosis are reviewed, and a comparison is made between membrane burdens that are lethal in vivo and membrane burdens that cause an effect in in vitro systems.

Uptake and toxicity of polycyclic aromatic hydrocarbons in terrestrial springtails—studying bioconcentration kinetics and linking toxicity to chemical activity

“…Springtail lethality was then fitted as a function of this lipid-based exposure parameter (C lipid , Fig. 3D), and the acute effective lethal concentrations (LC lipid 50s) were 101 and 104 mmol kg À1 lipid for naphthalene and phenanthrene, respectively (Table 3), well within the expected range of lethal membrane burden for baseline toxicity (40-160 mmol kg À1 lipid [17]). Pyrene toxicity was initiated at a higher equilibrium lipid concentration and had an LC lipid 50 value of 343 mmol kg À1 lipid, likely because the equilibrium estimate exceeded the actual concentrations in the lipid membranes due to underequilibration.…”

“…This might be explained by chemical activity not only controlling the uptake in the organism but also the internal distribution of the contaminant to the site of toxic action. Naphthalene, phenanthrene, and pyrene are believed to be baseline toxicants and, thus, to have the same mode of action, that is, perturbation of the cell membrane integrity [17]. Baseline toxicity is expected to initiate in the chemical activity range 0.01 to 0.1 [2,11,34], and springtail lethality values of all three PAHs were within this range (Fig.…”

“…Since the lipid membranes are considered the site of toxic action for baseline toxicity [17], the chemical activities of the PAHs were converted into equilibrium partitioning concentrations in lipid using compound-specific activity coefficients in lipid (Eqn. 6).…”

“…Chemical activity and equilibrium partitioning PAH concentrations in lipid were selected as exposure parameters since chemical activity drives diffusion and partitioning of HOCs into small soil organisms and membrane lipid is the site of toxic action for these compounds. The working hypothesis was that the toxicity of PAHs is initiated in the chemical activity range for baseline toxicity of 0.01 to 0.1 [2,11] and, when expressed on a lipid basis, in the range of lethal membrane burden for baseline toxicity of 40 to 160 mmol kg À1 lipid [17].…”

Developing Methods to Predict Chemical Fate and Effect Endpoints for Use Within REACH

“…Inside the organisms they accumulate preferentially in storage lipids and in membrane lipids. Membrane lipids are target sites for toxic effects, with baseline toxicity being a nonspecific disturbance of structure and functioning of the lipid bilayer of membranes [48]. Baseline toxicity, also called narcosis, constitutes the minimum toxicity of any compound.…”