Staphylococcus aureus is one of the most commonly isolated microbes in chronic rhinosinusitis (CRS) that can be complicated due to the formation of a staphylococcal biofilm. In this study, we investigated antimicrobial efficacy of single mupirocin and three types of monoterpenes (thymol, menthol and 1,8-cineole) as well as mupirocin-monoterpene combinations against S. aureus ATCC 29213 and 5 methicilin-resistant S. aureus strains (MRSA) grown in planktonic and biofilm form. MIC against planktonic bacteria as well as minimum biofilm-eliminating concentrations (MBECs) and minimum biofilm inhibitory concentrations (MBICs) were determined by TTC and MTT reduction assay, respectively. The MICs of mupirocin (0.125-0.156 μg ml(-1)) were three orders of magnitude lower than the MICs of monoterpenes, which were as follows: thymol (0.250-0.375 mg ml(-1)) > menthol (1 mg ml(-1)) > 1,8-cineole (4-8 mg ml(-1)). Mupirocin-monoterpene combinations showed indifferent effect as compared with MICs of single substances. Mupirocin (0.016-2 mg ml(-1)) failed to destroy the biofilm. The MBECs of thymol and menthol were two- to sixfold higher than their MICs, while 1,8-cineole exerted a weak antibiofilm effect with MBECs 16- to 64-fold higher than MICs. Mixture of mupirocin and 1,8 cineole exerted a potentiated biofilm-eliminating effect, mupirocin-menthol showed antagonism, while effect of thymol-mupirocin mixture was inconclusive. MBICs of antimicrobials were close to their MICs, except 1,8-cineole, MBIC was about three- to fivefold higher. Dominant synergy was observed for mixtures of mupirocin and menthol or thymol, whereas mupirocin-1,8-cineol exerted an indifferent or additive biofilm inhibitory effect. Particular combinations of mupirocin and the monoterpenes could be applied in CRS therapy in order to eliminate or prevent bacterial biofilm growth.

Humans have used insecticides since ancient times. The spectrum and potency of available insecticidal substances has greatly expanded since the industrial revolution, resulting in widespread use and unforeseen levels of synthetic chemicals in the environment. Concerns about the toxic effects of these new chemicals on non-target species became public soon after their appearance, which eventually led to the restrictions of use. At the same time, new, more environmentally-friendly insecticides have been developed, based on naturally occurring chemicals, such as pyrethroids (derivatives of pyrethrin), neonicotinoids (derivatives of nicotine), and insecticides based on the neem tree vegetable oil (Azadirachta indica), predominantly azadirachtin. Although these new substances are more selective toward pest insects, they can still target other organisms. Neonicotinoids, for example, have been implicated in the decline of the bee population worldwide. This review summarises recent literature published on non-target toxicity of neonicotinoids, pyrethroids, and neem-based insecticidal substances, with a special emphasis on neonicotinoid toxicity in honeybees. We also touch upon the effects of pesticide combinations and documented human exposure to these substances.

Chlorpyrifos, imidacloprid, and α‐cypermethrin are some of the most widely used insecticides in contemporary agriculture. However, their low‐dose, nontarget genotoxic effects have not been extensively assayed. As one of the most relevant cancer biomarkers, we aimed to assess the aneuploidy due to chromosome missegregation during mitosis. To aim it we treated human lymphocytes in vitro with three concentrations of insecticides equivalents relevant for real scenario exposure assessed by regulatory agencies. We focused on chlorpyrifos as conventional and imidacloprid and α‐cypermethrin as sustainable use insecticides. Cytokinesis‐blocked micronucleus assay was performed coupled with fluorescence in situ hybridization (FISH) with directly labeled pancentromeric probes for chromosomes 9, 18, X and Y. None of the insecticides induced significant secondary DNA damage in terms of micronuclei (MN), nuclear buds (NB), or nucleoplasmic bridges (NPB). However, significant disbalances in chromosomes 9, 18, X and Y, and in insecticide‐treated cells has been observed. According to recent studies, these disbalances in chromosome numbers may be atributted to defect sister chromatid cohesion which contribute to the increase of chromosome missegregation but not to micronuclei incidence. We conclude that tested insecticidal active substances exert chromosome missegregation effects at low concentrations, possibly by mechanism of sister chromatid cohesion. These findings may contribute to future risk assesments and understanding of insecticide mode of action on human genome. Environ. Mol. Mutagen. 60:72–84, 2019. © 2018 Wiley Periodicals, Inc.

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