Isolation and LC-QToF Characterization of Secondary Metabolites from an Endemic Plant Artemisia heptapotamica Poljak.

Phytochemical investigation of the aerial parts of Artemisia heptapotamica Poljak led to the isolation of ten known compounds, including four alkyl p-coumarates: octadecyl trans-p-coumarate (1), icosy trans-p-coumarate (2), docosyl trans-p-coumarate (3), and tetracosyl trans-p-coumarate (4), one sesquiterpene lactone: santonin (5), four flavonoids; axillarin (6), quercetin 3-O-methyl ether (7), luteolin (8), and quercetin (9), and one phenolic acid derivative: p-coumaric acid (10). The structures of the isolated compounds were identified by various spectroscopic analyses. Additionally, the antimicrobial activity of the total extract and different fractions was screened, and they exhibited no inhibition of the growth of Candida albicans, C. neoformans, Aspergillus fumigatus, methicillin-resistant Staphylococcus aureus (MRS), E. coli, Pseudomonas aeruginosa, Klebsiella pneumonia, and Vancomycin-resistant Enterococci (VRE) at the tested concentrations ranging from 8 to 200 µg/mL. The identification and tentative characterization of the secondary metabolites were conducted using LC-QToF analysis. This method helps in the putative characterization of sesquiterpene lactones, flavonoids, coumarate derivatives, and aliphatic compounds. The developed method identified 43 compounds, of which the majority were sesquiterpene lactones, such as eudesmanolides, germacranolides, and guaianolide derivatives, followed by flavonoids. The proposed LC-QToF method helps develop dereplication strategies and understand the major class of chemicals before proceeding with the isolation of compounds.

Oral lead exposure induces dysbacteriosis in rats.

OBJECTIVES: Lead's (Pb(II)) possible role in intestinal pathologies of microbial etiology remains mostly unknown. The aim of this study was to examine the effects of lead on the gut microbial community and its interactions with rat intestinal epithelium. METHODS: The lead-induced changes in different intestinal microbial groups (lactose-positive lac(+) and -negative lac(-) E.coli strains, lactobacilli and yeasts) were followed separately by the colony-forming unit (CFU) method. Samples were taken from outbred white rats subjected to different exposure schedules. Additionally, the impact of different lead doses on microbial adhesion to cultured intestinal cells (IEC-6) was investigated. Finally, the lead accumulation and distribution were measured by means of atomic absorption spectrometry. RESULTS: For the first time it was shown that oral lead exposure causes drastic changes in the gut microbial community. Proportional to the lead dose received, the relative number of lactose-negative E.coli cells increased dramatically (up to 1,000-fold) in comparison to the other microbial groups during 2 wk of exposure. Considering the number of microbes in the intestine, such a shift in intestinal microflora (dysbacteriosis) is very significant. Adhesion studies showed certain stimulating effects of lead on E. coli attachment to rat intestinal epithelium as compared to Lactobacillus attachment. CONCLUSIONS: The mechanisms providing the apparent competitive success of the lac(-) group are unclear but could be related to changes in surface interactions between microbial and host cells. This study may provide important clues for understanding the pathological effects of metal dietary toxins in human beings.