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

- Linuron inhibited growth and respiratory activity of B. stearothermophilus.
- Linuron perturbed respiration and oxidative phosphorylation of rat liver mitochondria.
- Linuron impaired bacterial and mitochondrial systems at similar concentrations.
- A membrane-mediated mechanism was proposed as underlying linuron adverse effects.

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.