Subject: glufosinate and birth defects
Here are abstracts of a number of scientific articles, forwarded by Joe Cummins, Professor Emeritus of Genetics at the University of Western Ontario about the toxic effects of glufosinate. Several genetically engineered crops are engineered to be resistant to this herbicide - the Munlochy oilseed rape is one).
The glufosinate aluminium herbicide to be used at Munlochy is sold by Aventis under the brand name "Liberty".
"arbeit macht frei"
Dr. Cummins comments:
The herbicide glufosinate (Basta) is being used in conjunction with sugar beets or canola which have been genetically engineered. This use may be extensive in Europe. I am enclosing abstracts of articles showing that glufosinate causes birth defects by killing brain cells in the embryo.
Glufosinate acts by causing the premature death
of brain cells in the embryo by a process called apoptosis (greek for petals
falling from a flower). A teratogen is an agent that causes birth defects.
Glufosinate tolerant canola has been grown in Canada and sold in the United
States since 1995. Currently not only canola but soybeans, corn and other
crops are being grown with glufosinate resistance.
Approval of the teratogenic herbicide and its
genetically engineered crops on a massive scale seems to have relied on
the judgement and human experimentation undertaken by the Canadian government.
However, the public is not generally aware that the Canadian government
agencies are merely the paid public relations voice of the multinational
companies that market genetically engineered crops and toxic herbicides.
For a number of years the Canadian government bureaucracy has been taking
millions from the companies to support their operations through a "cooperative"
research program. The government bureaucrats serve their rich patrons very
well. Our worst nightmare, government approved harmful genetic combinations
is coming forward.
In the articles, the technical term used for birth
defects is 'teratogenicity'
1. Glufosinate caused teratogenicity in vitro in mouse embryos.
Title: Developmental effects of glufosinate ammonium on mammalian embryos in vitro.
by Watanabe T, Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Yamagata, Japan.
Journal: Teratology 1995 Oct;52(4):25B-26B
Abstract
Glufosinate ammonium, which is a component of the herbicide BASTA®, is a phosphinic analog of glutamic acid. Its activity is related to the inhibition of glutamine synthetase. Previous studies demonstrated that glufosinate has no teratogenic potential in rats and rabbits in vivo. In the present study, we determined whether glufosinate could affect embryonic development in mice and rats using whole embryo and micromass cultures. In day 8 mouse embryos cultured for 48 hours, glufosinate (10 ug/mL) caused significant overall embryonic growth retardation which was especially prevalent in the craniofacial region. Approximately one third of the embryos exhibited specific defects including hypoplasia of prosencephalon and visceral arches. These findings were similar to those observed in day 9 rat embryos. The glufosinate treatment (more than 10 ug/mL) greatly reduced the size of crown-rump length and produced 100% malformed embryos. In day 10 mouse embryos cultured for 24 hours, glufosinate produced a high percentage of embryos with morphological defects (84.6%) and caused dead embryos (7.1%) at 60 ug/mL. These embryos were characterized by hypoplasia of prosencephalon and edema of lateral face and visceral arches.
For histological evaluation, much pyknotic debris was present throughout
the neuroepithelium in the brain vesicle and neural tube, but did not involve
the underlying mesenchyme. In addition, glufosinate inhibited the proliferation
of mouse embryonic midbrain cells on day 12 with 50%inhibition occurring
at 3.4 ug/mL. The ratio of IP50/ID50 (50% inhibition concentration for
cell profileration/differentiation) in limb bud cells was 0.76 and 1.52
on days 11 and 12 mouse embryos, respectively. These findings indicated
that glufosinate caused teratogenicity in vitro, which may be related to
the cell growth inhibition of neuroepithelium in mouse embryos.
2. Glufosinate causes toxicity in mice
Title: Chronotoxicity of glufosinate ammonium in mice.
Authors: Yoshiyama Y; Kobayashi T; Kondo R; Tomonaga F; Ohwada T
Address: School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.
Source: Vet Hum Toxicol; VOL 37, ISS 1, 1995, P22-3
Secondary Source ID TOXBIB/95/224928;
Abstract
The effect of a circadian-stage dependent dosing schedule on the toxicity
of glufosinate was studied in mice. Male ICR mice were housed in a standardized
12:12 light:dark cycle for 3 w. Each animal was given 1500 or 3000 mg glufosinate/kg
po. A highly significant circadian rhythm occurred in the resulting mortality,
with the highest mortality from doses given during the light phase and
the lowest from doses administered during the dark phase. The circadian-stage
dependent dosing schedule had a marked influence on the pattern of acute
glufosinate toxicity in mice.
3. Women experience toxic poisoning from glufosinate
Title : Delayed and severe toxicities of a herbicide containing glufosinate and a surfactant.
Authors: Koyama K; Andou Y; Saruki K; Matsuo H
Address: Department of Emergency Medicine, Hidaka Hospital, Gumma, Japan.
Source: Vet Hum Toxicol; VOL 36, ISS 1, 1994, P17-8
Secondary Source ID TOXBIB/94/205172;
Abstract
We report a case of a 59-y-old woman who ingested a herbicide containing
glufosinate. Though suffering from severe toxicity of this herbicide, she
did not develop convulsions, which experimentally occurs in rats treated
with glufosinate. The mechanisms of convulsions are not clear. Several
clinical findings in poisoning by this herbicide are suspected to be caused
by the surfactant components.
4. Glufosinate damages brain cell development in rats
Title: Alteration in the response to kainic acid in rats exposed to glufosinate ammonium during infantile period or fetal life.
Author: FuJii T; Ohata T
Address: Department of Pharmacology, Teikyo University School of Medicine, Tokyo, Japan.
Source ; J Toxicol Sci 1994 Nov;19(4):328
Secondary Source ID DART/T/95000859;
Abstract
Glufosinate ammonium (GLA), a herbicide, has been reported to inhibit
glutamine synthetase. Reported oral LD50 value for GLA is approx. 1.5 g/kg
in the rat. We examined the response to kainic acid of rats exposed to
GLA during an infantile period or fetal life. Wistar-Imamichi rats were
used. In the first experiment, female rats were injected s.c. with 1, 2
or 5 mg/kg of GLA from 7 to 13 days of age. In the second experiment, pregnant
rats were injected s.c. with 2 mg/kg GLA from 13-20 days of pregnancy.
The litter size was adJusted to 12 pups and the pups were crossfostered.
All rats were weaned at 21 days of age and fed ad libitum. GLA (Reidel-de
Haen)was dissolved in distilled water. Control rats were treated with saline.
At 5 or 6 weeks of age, the rats were tested for the response to the s.c.
injection of 9 mg/kg kainic acid. Rats exposed to GLA during infantile
period showed a significant decrease in the frequency of wet-dog shakes
and a less frequent limbic seizures were noted. The GLA-F1 rats also exhibited
a decreased manifestation of wet-dog shakes and limbic seizures after kainic
acid as compared with that in the saline-F1 rats. The results indicate
that GLA exposure in immature or fetal rats affects the development of
glutamate receptors in the brain.
5. Glufosinate ammonium causes toxic effects and birth
defects in rats
Title: INITIAL SUBMISSION:
LETTER FROM HOECHST CELANESE CORP SUBMITTING
INFORMATION ON AN ORAL STUDY OF
THE EMBRYOTOXIC EFFECT WITH A FORMULATION OF GLUFOSINATE NH4 IN WISTAR
RATS
Source: EPA/OTS; Doc #88-920006596
Secondary Source ID TSCATS/432471
Abstract
Glufosinate ammonium (77182-82-2) was evaluated for developmental toxicity. Twenty pregnant Wistar rats per group were administered the test material by oral gavage at 0, 10, 50, or 250 mg/kg/day on days 7- 16 of gestation. Dose-dependent maternal toxicity was observed at all treatment levels including motorial unrest, hyperactivity (50-150 mg/kg/day), drowsiness, vaginal hemorrhages, weight loss, and at 250 mg/kg/day only, intrauterine death and one mortality. Ureter and kidney dilation were observed in fetuses of all treatment groups. A slight retardation of skeletal ossification was observed at 250 mg/kg/day. This study was briefly summarized. No further information was reported.
6. Glufosinate ammonium causes birth defects and toxic
effects in Rabbits
Title :INITIAL SUBMISSION: LETTER FROM HOECHST
CELANESE CORP DESCRIBING A STUDY
ENTITLED: HOE 39866: TESTING FOR EMBRYOTOXICITY
IN HIMALAYAN RABBITS FOLLOWING ORAL ADMINISTRATION
Source: EPA/OTS; Doc #88-920003678
Secondary Source IDTSCATS/427382
Abstract
Glufosinate ammonium (77182-82-2) was evaluated for developmental toxicity.
Fifteen Himalayan rabbits per group were exposed to the test material
by gavage at 0, 2, 6.3, or 20 mg/kg/day on days 7-19 of gestation Decreased
maternal food consumption at 6.3 mg/kg/day and decreased food/water consumption
at 20 mg/kg/day were observed. An increase in the number of premature births
and abortions was observed at 20 mg/kg/day. This study was briefly summarized.
No further information was reported.
7. Glufosinate ammonium causes
birth defects and toxic effects in mice
Title: Developmental and dysmorphogenic effects of glufosinate ammonium on mouse embryos in culture.
Author: Watanabe T; Iwase T
Address: Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan. twatanab@med.id.yamagata-u.ac.jp
Source: Teratog Carcinog Mutagen, 16(6):287-99 1996
Abstract
The effects of glufosinate ammonium on embryonic development in mice were examined using whole embryo and micromass cultures of midbrain and limb bud cells. In day 8 embryos cultured for 48 hr, glufosinate caused significant overall embryonic growth retardation and increased embryolethality to 37.5% at 10 micrograms/ml (5.0 x 10(-5) M). All embryos in the treated groups exhibited specific morphological defects including hypoplasia of the prosencephalon (forebrain) (100%) and visceral arches (100%). In day 10 embryos cultured for 24 hr, glufosinate significantly reduced the crown-rump length and the number of somite pairs, and produced a high incidence of morphological defects (84.6%) at 10 micrograms/ml. These embryos were characterized by blister in the lateral head (100%), hypoplasia of prosencephalon (57.1%), and cleft lips (42.9%) at 20 micrograms/ml (10.0 x 10(-5) M). Histological examination of the treated embryos showed numerous cell death (pyknotic debris) present throughout the neuroepithelium in the brain vesicle and neural tube, but did not involve the underlying mesenchyme. In micromass culture, glufosinate inhibited the differentiation of midbrain cells in day 12 embryos with 50% inhibition occurring at 0.55 microgram/ml (2.8 x 10(-6) M). The ratios of 50% inhibition concentration for cell proliferation to cell differentiation in limb bud cells were 0.76 and 1.52 in day 11 and 12 embryos, respectively. These findings indicate that glufosinate ammonium is embryotoxic in vitro. In addition to causing growth retardation, glufosinate specifically affected the neuroepithelium of the brain vesicle and neural tube, leading to neuroepithelial cell death.
8. Glufosinate ammoniu causes birth defects and toxic effects in mice
Title: Apoptosis induced by glufosinate ammonium in the neuroepithelium of developing mouse embryos in culture.
Author: Watanabe T
Address: Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan. twatanab@medid.yamagata_u.ac.jp
Source: Neurosci Lett, 222(1):17-20 1997 Jan 24
Abstract
Glufosinate ammonium structurally resembles glutamate and blocks glutamine
synthetase. Glufosinate was recently found to be dysmorphogenic in mammals
in vitro. The present study examined the cell death induced specifically
by glufosinate in the neuroepithelium of mouse embryos. Electron micrograph
revealed characteristic chromatin condensation and segregation, extracellular
apoptotic bodies, and cell fragments phagocytosed in macrophages in the
neuroepithelium of the brain vesicle and neural tube. Moreover neuroepithelial
cells undergoing DNA fragmentation were histochemically identified. DNA
gel electrophoresis of the neuroepithelial layer revealed a DNA ladder.
These observations demonstrate that glufosinate specifically induced apoptosis
in the neuroepithelium of embryos.