Improving pollutants environmental risk assessment using a multi model toxicity determination with in vitro, bacterial, animal and plant model systems: The case of the herbicide alachlor.

Several environmental pollutants, including pesticides, herbicides and persistent organic pollutants play an important role in the development of chronic diseases. However, most studies have examined environmental pollutants toxicity in target organisms or using a specific toxicological test, losing the real effect throughout the ecosystem. In this sense an integrative environmental risk of pollutants assessment, using different model organisms is necessary to predict the real impact in the ecosystem and implications for target and non-target organisms. The objective of this study was to use alachlor, a chloroacetanilide herbicide responsible for chronic toxicity, to understand its impact in target and non-target organisms and at different levels of biological organization by using several model organisms, including membranes of dipalmitoylphosphatidylcholine (DPPC), rat liver mitochondria, bacterial (Bacillus stearothermophilus), plant (Lemna gibba) and mammalian cell lines (HeLa and neuro2a). Our results demonstrated that alachlor strongly interacted with membranes of DPPC and interfered with mitochondrial bioenergetics by reducing the respiratory control ratio and the transmembrane potential. Moreover, alachlor also decreased the growth of B. stearothermophilus and its respiratory activity, as well as decreased the viability of both mammalian cell lines. The values of TC50 increased in the following order: Lemna gibba < neuro2a < HeLa cells < Bacillus stearothermophilus. Together, the results suggest that biological membranes constitute a putative target for the toxic action of this lipophilic herbicide and point out the risks of its dissemination on environment, compromising ecosystem equilibrium and human health.

Toxicity of the herbicide linuron as assessed by bacterial and mitochondrial model systems.

Linuron is one of the most intensively used herbicides with predictable effects on the environment and non-target organisms. In the present study, two in vitro biological models (a Bacillus sp. and rat liver mitochondria) were used to evaluate linuron toxicity at a cell/subcellular level. Linuron inhibited bacterial growth and NADH-supported respiration, similar IC50 values being estimated for both toxic responses (74 and 98 µM, respectively). At concentrations up to 120 µM, linuron perturbed the respiration and phosphorylation efficiency of rat liver mitochondria, reflected by an increase of state 4 respiration and a decrease of the transmembrane potential, state 3 and FCCP-uncoupled respiration, when malate/glutamate or succinate were used as respiratory substrates. Consequently, a decrease of the respiratory control and ADP/O ratio was observed. This study suggests that linuron membrane interactions with adverse repercussions in the activity of membrane enzymatic complexes, such as those which constitute the prokaryotic and mitochondrial respiratory systems, may underlie the toxic effects exerted by that herbicide on non-target organisms. Moreover, this work contributes to the establishment of our bacterial model system as a good tool for chemical toxicity screening.

Studies on the toxicity of an aqueous suspension of C60 nanoparticles using a bacterium (gen. Bacillus) and an aquatic plant (Lemna gibba) as in vitro model systems.

The increasing use of C60 nanoparticles and the diversity of their applications in industry and medicine has led to their production in a large scale. C60 release into wastewaters and the possible accumulation in the environment has raised concerns about their ecotoxicological impact. In the present study, an aqueous suspension of C60 nanoparticles was prepared and its potential toxicity studied in laboratory, using a bacterium (Bacillus stearothermophilus) and an aquatic plant (Lemna gibba) as model systems. C60 nanoparticles inhibited the growth of L. gibba, in contrast to that of the bacterium. Consistently, the ultrastructure and respiratory activity of bacterial cells were not affected by C60, but the contents of chlorophylls a and b and chloroplast oxygen production decreased considerably in L. gibba. Altogether, our results suggest that C60 aqueous dispersions must be viewed as an environmental pollutant, potentially endangering the equilibrium of aquatic ecosystems.