We have evaluated the toxicity of four glyphosate (G)-based herbicides in
Roundup (R) formulations, from 105 times dilutions, on three different
human cell types. This dilution level is far below agricultural recommendations
and corresponds to low levels of residues in food or feed. The formulations
have been compared to G alone and with its main metabolite AMPA or with one
known adjuvant of R formulations, POEA. HUVEC primary neonate umbilical cord
vein cells have been tested with 293 embryonic kidney and JEG3 placental cell lines.
All R formulations cause total cell death within 24 h, through an
inhibition of the mitochondrial succinate dehydrogenase activity, and
necrosis, by release of cytosolic adenylate kinase measuring membrane damage.
They also induce apoptosis via activation of enzymatic caspases 3/7 activity.
This is confirmed by characteristic DNA fragmentation, nuclear shrinkage
(pyknosis), and nuclear fragmentation (karyorrhexis), which is demonstrated
by DAPI in apoptotic round cells. G provokes only apoptosis, and
HUVEC are 100 times more sensitive overall at this level. The deleterious
effects are not proportional to G concentrations but rather depend on the nature of
the adjuvants. AMPA and POEA separately and synergistically damage cell membranes
like R but at different concentrations. Their mixtures are generally even more harmful
with G. In conclusion, the R adjuvants like POEA change human cell permeability
and amplify toxicity induced already by G, through apoptosis and necrosis.
The real threshold of G toxicity must take into account the presence of adjuvants but
also G metabolism and time-amplified effects or bioaccumulation. This should be
discussed when analyzing the in vivo toxic actions of R. This work clearly confirms
that the adjuvants in Roundup formulations are not inert. Moreover, the
proprietary mixtures available on the market could cause cell damage and
even death around residual levels to be expected, especially in food and feed
derived from R formulation-treated crops.
Roundup (R) formulations, from 105 times dilutions, on three different
human cell types. This dilution level is far below agricultural recommendations
and corresponds to low levels of residues in food or feed. The formulations
have been compared to G alone and with its main metabolite AMPA or with one
known adjuvant of R formulations, POEA. HUVEC primary neonate umbilical cord
vein cells have been tested with 293 embryonic kidney and JEG3 placental cell lines.
All R formulations cause total cell death within 24 h, through an
inhibition of the mitochondrial succinate dehydrogenase activity, and
necrosis, by release of cytosolic adenylate kinase measuring membrane damage.
They also induce apoptosis via activation of enzymatic caspases 3/7 activity.
This is confirmed by characteristic DNA fragmentation, nuclear shrinkage
(pyknosis), and nuclear fragmentation (karyorrhexis), which is demonstrated
by DAPI in apoptotic round cells. G provokes only apoptosis, and
HUVEC are 100 times more sensitive overall at this level. The deleterious
effects are not proportional to G concentrations but rather depend on the nature of
the adjuvants. AMPA and POEA separately and synergistically damage cell membranes
like R but at different concentrations. Their mixtures are generally even more harmful
with G. In conclusion, the R adjuvants like POEA change human cell permeability
and amplify toxicity induced already by G, through apoptosis and necrosis.
The real threshold of G toxicity must take into account the presence of adjuvants but
also G metabolism and time-amplified effects or bioaccumulation. This should be
discussed when analyzing the in vivo toxic actions of R. This work clearly confirms
that the adjuvants in Roundup formulations are not inert. Moreover, the
proprietary mixtures available on the market could cause cell damage and
even death around residual levels to be expected, especially in food and feed
derived from R formulation-treated crops.
Source:
Glyphosate Formulations Induce Apoptosis and Necrosis in Human Umbilical, Embryonic, and Placental Cells
Nora Benachour and Gilles-Eric S
ralini*
University of Caen, Laboratory Estrogens and Reproduction, UPRES EA 2608, Institute of Biology, Caen 14032, France
Chem. Res. Toxicol., 2009, 22 (1), pp 97–105
DOI: 10.1021/tx800218n
Publication Date (Web): December 23, 2008
Copyright © 2008 American Chemical Society
* To whom correspondence should be addressed. Tel: 33(0)2-31-56-56-84. Fax: 33(0)2-31-56-53-20. E-mail:criigen@unicaen.fr.
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