glufosinate and birth defects

Daniel D. Worley (dan.worley@icepr.com)
Mon, 16 Feb 1998 10:12:53 -0400

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>Errors-To: <rwolfson@concentric.net>
>X-Sender: rwolfson@pop3.concentric.net
>Date: Sun, 15 Feb 1998 12:05:05 -0500
>To: info@natural-law.ca
>From: Richard Wolfson <rwolfson@concentric.net>
>Subject: glufosinate and birth defects
>X-MIME-Autoconverted: from quoted-printable to 8bit by ice.icepr.com id
NAA26163
>X-UIDL: da88598381ac16a9fccb11e1dcceb7f4
>
>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.
>
>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. 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 BASTAŽ, 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
>
>_________________________________________________________
>Richard Wolfson, PhD
>Consumer Right to Know Campaign,
>for Mandatory Labelling and Long-term
>Testing of all Genetically Engineered Foods,
>500 Wilbrod Street
>Ottawa, ON Canada K1N 6N2
>email: rwolfson@concentric.net
>
>Our website, http://www.natural-law.ca/genetic/geindex.html
>contains more information on genetic engineering as well as
>previous genetic engineering news items
>Subscription fee to genetic engineering news is $35 for 12 months
>See website for details.
>__________________________________________________________
>__________________________________________________________
>
>
>
>

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