In:
Journal of Occupational Health, Wiley, Vol. 51, No. 1 ( 2009-01), p. 64-73
Kurzfassung:
Oral Lead Exposure Induces Dysbacteriosis in Rats: Rustam S adykov , et al . Laboratory of Cellular Biophysics, Aachen University of Applied Sciences, Germany 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.
Materialart:
Online-Ressource
ISSN:
1341-9145
,
1348-9585
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2009
ZDB Id:
1340985-2
ZDB Id:
2075956-3
