Basta (Glufosinate)

Thank you to Richard Wolfson, PhD. for helping to compile this information:

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 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.
    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.

  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.

  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
    Jii 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 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. =46ifteen 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.

  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.


    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

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