Gedunin is an important limonoid present in several genera of the Meliaceae family, mainly in seeds. Several biological activities have been attributed to gedunin, including antibacterial, insecticidal, antimalarial, antiallergic, anti-inflammatory, anticancer, and neuroprotective effects. The discovery of gedunin as a heat shock protein (Hsp) inhibitor represented a very important landmark for its application as a biological therapeutic agent. The current study is a critical literature review based on the several biological activities so far described for gedunin, its therapeutic effect on some human diseases, and future directions of research for this natural compound.

β-Cyclodextrin (βCD) inclusion compounds of chloramphenicol in the solid-state were prepared via two different procedures, co-crystallisation from aqueous solution and the solvent-free method of co-grinding. Chloramphenicol inclusion into permethylated βCD (TRIMEB) was also performed by co-dissolution in ethanol. The co-crystallisation procedure was the best for preparing chloramphenicol·βCD in 1 : 1 stoichiometry in high purity, while with the co-grinding treatment and the same starting proportion, a complete inclusion was not achieved. Microcrystals of chloramphenicol·βCD inclusion compound presented polymorphism, crystallising simultaneously in the triclinic P1 or monoclinic C2 space groups. Only crystals of the latter were suitable for single-crystal diffraction and data for the guest atoms was comprised of a smeared-out electron cloud, so theoretical calculations were used to propose their plausible geometry and location inside the host molecules. The co-grinding procedure curbed polymorphism and allowed the preparation of chloramphenicol·βCD in the amorphous state; chloramphenicol·TRIMEB prepared by co-dissolution of the components in a 1 : 1 proportion was also an amorphous material. The influence of inclusion with βCD and TRIMEB on the antimicrobial performance of chloramphenicol was evaluated, and both inclusion compounds demonstrated selective action against Enterococcus faecalis strains ATCC 29212 and A33562 and Listeria monocytogenes ATCC 7644. Chloramphenicol·TRIMEB also had higher activity against the E. faecalis strains A35906, 9308 and E4856 and against Listeria inocua.

The Neem tree, Azadirachta indica A. Juss., is known for its large spectrum of compounds with biological and pharmacological interest. These include, among others, activities that are anticancer, antibacterial, antiviral, and anti-inflammatory. Some neem compounds are also used as insecticides, herbicides, and/or antifeedants. The safety of these compounds is not always taken into consideration and few in vivo toxicity studies have been performed. The current study is a literature review of the latest in vivo toxicity of A. indica. It is divided in two major sections—aquatic animals toxicity and mammalian toxicity—each related to neem’s application as a pesticide or a potential new therapeutic drug, respectively.

To investigate the role of a putative small multidrug resistance transporter, annotated in Enterococcus faecalis V583 genome as EFA0010 (we will refer to this gene as qacZ), in decreased susceptibility to biocides. A derivative strain of V583, susceptible to erythromycin (V583ErmS), was complemented with pORI23 carrying the qacZ gene (strain EF-SAVE1). MICs of benzalkonium chloride, chlorhexidine and ethidium bromide were determined for the complemented strain and wild-type. RT–PCR and ethidium bromide efflux assays were performed in order to fully understand the role and specificity of the qacZ gene. The presence of qacZ in 73 enterococcal strains from different origins was investigated by PCR, and MICs of benzalkonium chloride and chlorhexidine were determined for the same strains. The complemented strain, EF-SAVE1, presented a higher MIC of benzalkonium chloride (8 mg/L) than V583ErmS (4 mg/L); the MICs of chlorhexidine and ethidium bromide were the same for both strains, 4 mg/L and 16 mg/L, respectively. Expression of qacZ was found to be higher in EF-SAVE1 and constitutive, i.e. not inducible by any of the three tested biocides. Overexpression of qacZ was not responsible for changes in ethidium bromide efflux. This gene was present in 52% of the enterococcal isolates studied and the MICs of benzalkonium chloride and chlorhexidine ranged between 2 and 8 mg/L. We demonstrate the involvement of the qacZ gene in tolerance to the quaternary ammonium compound benzalkonium chloride, but not ethidium bromide. This work constitutes the first report of a biocide resistance mechanism in E. faecalis, and reveals its dissemination amongst the genus Enterococcus.