Scientific Abstracts Related to Genetically-Manipulated Crop Herbicides That Cause Birth Defects
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In the articles, the technical term used for birth defects is 'teratogenicity'
1. The first article shows that glufosinate caused teratogenicity in vitro
in mouse embryos.
Title: Developmental effects of glufosinate ammonium on mammaliam 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=AE, 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.
Language
Eng
2. glufosinate causes toxicity in mice
Title
Chronotoxicity of glufosinate ammonium in mice.
Author
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.
Language
Eng
3. women experiences toxic poisoning from glufosinate
Title
Delayed and severe toxicities of a herbicide containing glufosinate and a
surfactant.
Author
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.
Language
Eng
4. glutamate 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.
Language
Eng
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 ammoniu 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 ID
TSCATS/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 ammoniu 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.
Language
Eng
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.
Language
Eng
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