4 research outputs found
Biotransformation of the UV-Filter Sulisobenzone: Challenges for the Identification of Transformation Products
The
UV-filter substance Sulisobenzone (BP-4) is widely employed
in sunscreens and other personal care products. In the current study,
its behavior during biological wastewater treatment was investigated.
In contact with activated sludge BP-4 was degraded in aerobic batch
experiments forming at least nine transformation products (TPs). The
mass balance in the batch experiments was closed, as measurements
with LC-UV underlined that the quantity of the TPs was comparable
to the BP-4 quantity transformed. The chemical structures of the nine
TPs could be proposed based on accurate mass measurements by high
resolution mass spectrometry (LTQ-Orbitrap-MS), several fragmentation
experiments up to MS<sup>6</sup> and synthesis of one TP. NMR analyses
of the main TP confirmed its proposed chemical structure. At the beginning
of the biotransformation of BP-4, a benzhydrol analogue was formed
due to the reduction of the keto moiety. Further reactions (e.g.,
oxidation, demethylation, decarboxylation) led to the formation of
extremely polar TPs. A biodegradation pathway was proposed based on
the TP structures identified and the sequence of the TP formation.
The isolated TPs exhibited higher toxic effects on <i>Vibrio
fischeri</i> than BP-4. The results contribute to a better general
understanding and prediction of the biotransformation of aromatic
sulfonic acids in WWTPs
Loss or Inhibition of Stromal-Derived PlGF Prolongs Survival of Mice with Imatinib-Resistant Bcr-Abl1(+) Leukemia (vol 19, pg 740, 2011)
status: publishe
Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1<sup>+</sup>leukemia
Imatinib has revolutionized the treatment of Bcr-Abl1<sup>+</sup> chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PlGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of Bcr-Abl1 signaling. Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib. These results may warrant further investigation of the therapeutic potential of PlGF inhibition for (imatinib-resistant) CML