We aimed to evaluate the bioherbicide potential of Eucalyptus saligna leaf litter essential oil, its fractions and major compounds. Six essential oil fractions were obtained by preparative thin‐layer chromatography and analyzed by gas chromatography/mass spectrometry. Effects of the oil, its fractions and major compounds (1,8‐cineole and/or α‐pinene) diluted in aqueous solution were assessed on germination and seedling growth. Recipient species were Lactuca sativa (model), Amaranthus viridis (weed), Eragrostis plana (weed), and Paspalum notatum (forage). The essential oil was more phytotoxic on A. viridis and L. sativa, followed by E. plana, and caused no effects on P. notatum. Amaranthus viridis was inhibited by all treatments, mainly the essential oil, α‐pinene and fraction 6, whereas E. plana was more affected by the oil fractions. Results revealed the species‐specific phytotoxic effects of E. saligna essential oil, indicating its potential use for controlling A. viridis and E. plana. Phytotoxic effects of essential oils or their components should not be generalized, as effects may change according to recipient species.

Schinus essential oils were tentatively identified by GC×GC/TOFMS, which revealed a greater number of compounds than previously reported. Eighty‐six, seventy‐two, and eighty‐eight components were identified in Schinus lentiscifolius, Schinus molle and Schinus terebinthifolius essential oils, respectively. Compound separation due to 2D selectivity was observed. Phytotoxic effects of Schinus essential oils were assessed on germination and initial growth of Arabidopsis thaliana. All essential oils in all tested quantities (5 μL, 10 μL, 15 μL, 20 μL, and 25 μL) affected germination rate, speed of accumulated germination, and root and shoot length of A. thaliana. Considering the mode of action of the essential oils, no differences were observed on expression of the genes ANP1 and CDK B1;1 in A. thaliana, which was analyzed by RT‐qPCR. Results suggest that phytotoxic effects of Schinus essential oils seem to be explained by cellular damage rather than by induction of stress‐inducible genes.