Chemical composition and antimicrobial activities of the essential oil from the seeds of Enterolobium contortisiliquum (leguminosae)

Seeds of Enterolobium contortisiliquum were subjected to steam distillation to obtain a light yellow essential oil in a yield of 3 ml/kg of seeds. The major components of the oil were identified using gas chromatography/mass spectrometry (GC-MS) and were furfural, limonene, linalool, estragole, carvone, and apiole with carvone representing more than 50% of the total composition. Antimicrobial activities of the essential oil were determined against four species of gram positive bacteria (Bacillus subtilis, Bacillus cereus, Staphylococcus aureus, Micrococcus luteus) and two gram negative bacteria (Klebsiella pneumoniae, Serratia Marcescencs). The essential oil inhibited the growth of all tested bacteria but was most effective against the gram positive bacteria. Chemicals that are responsible for the antibacterial effect of the essential oil were determined using the bio-autography thin layer chromatography (TLC) technique. The active compounds responsible for the activity were found to be carvone and estragole.     

Propetamphos enhances chlorpyrifos-induced organophosphate-induced delayed neurotoxicity (OPIDN) in Hens: a role for plasma butyrylcholinesterase

This study examined dose-response effects of chlorpyrifos (CPF) and propetamphos (PRO) on producing organophosphorus-induced delayed neurotoxicity (OPIDN) in hens. A single oral dose of 1, 3, 30, or 100 mg/kg of each compound was administered individually, or in combination to groups of 10 hens. Plasma butyrylcholinesterase (BChE) activity was inhibited by all doses of each individual compound. Chlorpyrifos alone or in combination with PRO resulted in decreased acetylcholinesterase (AChE) activity. No dose of CPF or PRO alone resulted in the inhibition of neuropathy target esterase (NTE) or produced OPIDN. In contrast, combined exposure to high doses of CPF and PRO produced diminished NTE activity and produced OPIDN. Brain NTE activity was decreased by 67% and 71% by combined treatment of 100 mg/kg CPF with 30 mg/kg and 100 mg/kg PRO, respectively, consistent with the development of ataxia and paralysis, characteristic of OPIDN. Only the highest dose of CPF 100 mg/kg interacted with the two highest doses of PRO to block NTE and induce OPIDN, whereas no marked interaction occurred at lower doses. Data indicate that PRO enhances the ability of high doses of CPF to produce OPIDN by binding to plasma BChE that appears to act as a buffering system to modulate the toxicity of CPF. In effect, the ability of BChE to bind to CPF is diminished by PRO, resulting in more CPF delivery to the brain, and subsequent development of OPIDN at a dose that does not initiate this effect by itself.