Click for articles
Glyphosate is one of the most widely used herbicides worldwide and is the active ingredient of the product Roundup. Worldwide, glyphosate is used in more than 750 different herbicide products and has been detected in the air during spraying, in water, and in food. It has been used by U.S. farmers for more than 40 years to kill weeds and grasses that compete with crops such as corn, wheat, oats, and barley, as well as certain edible beans. More recently glyphosate is being used by farmers growing ‘Roundup-Ready’ GMO crops, which are engineered to tolerate applications of glyphosate herbicide. The first glyphosate-tolerant (Roundup Ready) crop was soybean, introduced in the U.S in 1996; and soybean remains the crop with the highest use of glyphosate in U.S. at nearly double the amount used of the next largest crop, corn. It is also used to control vegetation around transmission towers, pipelines, water drainage channels, public squares, and streets throughout the world. Consumers also use glyphosate on their lawns and gardens.
Glyphosate is an organophosphorus compound, specifically a phosphonate, which acts an herbicide by inhibiting the plant enzyme 5-enolpyruvylshikimate-3-phosphate synthase responsible for the biosynthesis of the important amino acids phenylalanine, tyrosine, and tryptophan. Thus, glyphosate inhibits plant growth through interference with the production of these essential aromatic amino acids. This reduction in protein synthesis causes termination of growth and eventually, cellular disruption and death of the plant. Glyphosate works against all plant species, even killing large trees. No other herbicide is so non-selective, and no other herbicide costs so little to buy. Hence, it is easy to destroy wild or semi-natural habitats, and easy to overdo weed control, as is increasingly happening. Glyphosate, being a phosphoric amino derivative of glycine, tends to behave like the inorganic phosphates naturally present in the soil and as such is generally persistent.
Glyphosate is applied by a wide range of methods, including aerial spraying, backpack sprayers, ground broadcast sprayers of various types, shielded and hooded sprayers, wiper applications, sponge bars, injection systems, and controlled droplet applicators.
Glyphosate was first synthesized in 1950 by Swiss chemist Henry Martin, who worked for the Swiss pharmaceutical company Cilag, a subsidiary of American pharmaceutical giant Johnson and Johnson. Glyphosate is a phosphonic acid resulting from the formal oxidative coupling of the methyl group of methylphosphonic acid with the amino group of glycine. Stauffer Chemical Co. first patented glyphosate as a mineral chelator in 1964 as it binds and removes minerals such
as calcium, magnesium, manganese,
copper, and zinc. Thus, glyphosate potentially depletes the soil of these important nutrient minerals. Then in 1974, Monsanto introduced this chelator as the herbicide Roundup. Since then Americans have applied 1.8 million tons of glyphosate to crops. Worldwide, 9.4 million tons of the chemical has been sprayed on fields – enough to spray nearly half a pound of Roundup on every cultivated acre of land in the world. The pharmaceutical giant Bayer acquired Round-Up from Monsanto in 2018.
Aggressive public relations and marketing by its developer, Monsanto and now Bayer, has resulted in the widespread belief that glyphosate is ‘safe’. However, as far back as 2009, France’s Supreme Court upheld judgements by two previous courts that glyphosate was harmful to human biochemistry. Registration processes continue to allow the use of the herbicide without raising concerns about safety even as new data identifying adverse effects emerges. However, the 2015 classification by the International Agency for Research on Cancer (IARC) of glyphosate as a ‘probable human carcinogen’ is resulting in massive widespread concern about its continued use, especially preharvest and in public places. The most appropriate and scientifically based evaluation of the cancers reported in humans and laboratory animals as well as supportive mechanistic data is that glyphosate is a probable human carcinogen. Based on IARC’s conclusion and in the absence of evidence to the contrary, it is reasonable to conclude that glyphosate formulations should also be considered likely human carcinogens.
Additionally, independent scientific studies and widespread poisonings in Latin America (resulting from aerial application) have begun to reveal numerous acute and chronic effects of glyphosate-based herbicides.
Both the nature and severity of human health impacts following long-term chronic exposures to glyphosate herbicides are quickly becoming known. Numerous studies now demonstrate that glyphosate exposure is associated with oxidative free radical damage, genotoxicity and mutagenicity, neurotoxicity, and endocrine disruption. Ataxia, breathing difficulties and occasionally convulsions, preceded death in rats receiving lethal doses of glyphosate. After ingestion in humans, mild poisoning symptoms may include stomach cramps, vomiting, nausea and diarrhea, and mouth and throat pain. Moderate poisoning is associated with gastrointestinal tract ulceration, hypotension, and hepatic and renal damage. Severe poisoning is characterized by respiratory and renal failure, seizures, coma and eventually death.
Glyphosate and metabolite residues bioaccumulate and concentrate in the liver and kidney and both animal studies and human investigations have highlighted liver and kidney problems. The recent classification by International Agency for Research on Cancer (IARC) of glyphosate as a probable human carcinogen has generated litigation. At the time of this writing there are 42,000 plaintiffs suing Bayer over claiming glyphosate caused cancer – particularly non-Hodgkin lymphoma.
The following are selected articles on the detrimental effects of glyphosate on humans and the environment.
Genotoxicity / Mutagenicity
A pesticide is genotoxic if it causes damage to a gene that could result in cell death or result in a change in the structure or function of the gene. The damage can be mutagenic (heritable) or non-mutagenic. Mutagenic means causing a change in the genetic structure, usually through base-pair substitution (change in amino acid sequence), deletion, or addition of gene fragments, or some other mechanism which include disruptions or breaks in chromosomes that result in the gain, loss, or rearrangements of chromosomal segments (clastogenicity). It also includes “sister chromatid exchanges”, interchanges and re-attachments of strands in the chromosome during DNA replication, and induction (increase) in the frequency of micronuclei (small fragments formed when chromosomes break). Besides causing inheritable damage (germ cell mutagenicity) one of the main health implications of genotoxicity in somatic cells is the induction of cancer.
The International Agency for Research on Cancer (IARC) performed a thorough review of numerous publications and came to the conclusion that “(t)here is strong evidence that exposure to glyphosate or glyphosate-based formulations is genotoxic based on studies in humans in vitro and studies in experimental animals” (IARC 2015, p. 78).
Alvarez-Moya, Carlos, Mónica Reynoso Silva, Carlos Valdez Ramírez, David Gómez Gallardo, Rafael León Sánchez, Alejandro Canales Aguirre, and Alfredo Feria Velasco. "Comparison of the in vivo and in vitro genotoxicity of glyphosate isopropylamine salt in three different organisms." Genetics and molecular biology 37, no. 1 (2014): 105-110.
In this study glyphosate isopropylamine was tested at 0.7, 7 and 700 µM concentrations in a comet assay with human lymphocytes. A dose dependent, statistically significant increase in glyphosate-exposed cells was observed for all concentrations. They concluded, “These results indicate that glyphosate is genotoxic in the cells and organisms studied at concentrations of 0.7-7 µM.”
Bolognesi, Claudia, Stefania Bonatti, Paolo Degan, Elena Gallerani, Marco Peluso, Roberta Rabboni, Paola Roggieri, and Angelo Abbondandolo. "Genotoxic activity of glyphosate and its technical formulation Roundup." Journal of Agricultural and food chemistry 45, no. 5 (1997): 1957-1962.
In this study glyphosate Roundup caused dose dependent increases in sister chromatid exchange in human lymphocytes; roundup had a greater effect.
Gasnier, Céline, Coralie Dumont, Nora Benachour, Emilie Clair, Marie-Christine Chagnon, and Gilles-Eric Séralini. "Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines." Toxicology 262, no. 3 (2009): 184-191.
RoundUp caused dose-dependent DNA damage in human liver cells, with 50% DNA strand breaks at 5 mg/kg, described by the authors as “residual levels corresponding to 120 nM of glyphosate.”
IARC. 2015. Glyphosate. In: Some Organophosphate Insecticides and Herbicides: Diazinon, Glyphosate, Malathion, Parathion, and Tetrachlorvinphos. IARC Monograph No. 112. International Agency for Research on Cancer, World Health Organization.
Koller, Verena J., Maria Fürhacker, Armen Nersesyan, Miroslav Mišík, Maria Eisenbauer, and Siegfried Knasmueller. "Cytotoxic and DNA-damaging properties of glyphosate and Roundup in human-derived buccal epithelial cells." Archives of toxicology 86, no. 5 (2012): 805-813.
In this study both glyphosate and RoundUp caused DNA damage in human buccal (mouth) epithelial cells with short-term (20 mins) exposure to concentrations corresponding to a 450-fold dilution of concentrations normally used in agriculture, prompting the authors of the study to warn that inhalation may cause DNA damage in mouth and respiratory tissues of exposed individuals. Even a 1,350-fold dilution of a spraying solution of Roundup caused acute and genotoxic effects on human cells in this study. They concluded, “Comparisons with results of earlier studies with lymphocytes and cells from internal organs indicate that epithelial cells are more susceptible to the cytotoxic and DNA-damaging properties of the herbicide and its formulation. Since we found genotoxic effects after short exposure to concentrations that correspond to a 450-fold dilution of spraying used in agriculture, our findings indicate that inhalation may cause DNA damage in exposed individuals.”
Lioi, Maria B., Maria R. Scarfi, Antonietta Santoro, Rocchina Barbieri, Olga Zeni, Francesca Salvemini, Dino Di Berardino, and Matilde V. Ursini. "Cytogenetic damage and induction of pro‐oxidant state in human lymphocytes exposed in vitro to gliphosate, vinclozolin, atrazine, and DPX‐E9636."
Environmental and Molecular Mutagenesis 32, no. 1 (1998): 39-46.
In this study glyphosate caused a dose-dependent increase in chromosomal aberrations and an increase in sister chromatid exchange in human lymphocytes.
Mañas, Fernando, Laura Peralta, José Raviolo, Hugo García Ovando, Alicia Weyers, Laura Ugnia, Marcela Gonzalez Cid, Irene Larripa, and Nora Gorla. "Genotoxicity of glyphosate assessed by the comet assay and cytogenetic tests."
Environmental toxicology and pharmacology 28, no. 1 (2009): 37-41.
In this study they researchers concluded, “In the present study glyphosate was genotoxic in the comet assay in Hep-2 cells and in the MNT test at 400 mg/kg in mice. Thiobarbituric acid reactive substances (TBARs) levels, superoxide dismutase (SOD) and catalase (CAT) activities were quantified in their organs. The results showed an increase in these enzyme activities.”
Paz-y-Miño, César, María Eugenia Sánchez, Melissa Arévalo, María José Muñoz, Tania Witte, Gabriela Oleas De-la-Carrera, and Paola E. Leone. "Evaluation of DNA damage in an Ecuadorian population exposed to glyphosate." Genetics and Molecular Biology 30, no. 2 (2007): 456-460.
Abstract: “We analyzed the consequences of aerial spraying with glyphosate added to a surfactant solution in the northern part of Ecuador. A total of 24 exposed and 21 unexposed control individuals were investigated using the comet assay. The results showed a higher degree of DNA damage in the exposed group (comet length = 35.5 µm) compared to the control group (comet length = 25.94 µm). These results suggest that in the formulation used during aerial spraying glyphosate had a genotoxic effect on the exposed individuals.”
Vigfusson, N. V., and E. R. Vyse. "The effect of the pesticides, Dexon, Captan and Roundup, on sister-chromatid exchanges in human lymphocytes in vitro." Mutation Research/Genetic Toxicology 79, no. 1 (1980): 53-57.
In this study Roundup at high concentrations caused an increase in sister chromatid exchange in human lymphocytes.
Endocrine Disruption
The US EPA Endocrine Disruptor Screening Program (US EPA 2015) reported that “glyphosate demonstrates no convincing evidence of potential interaction with the estrogen, androgen or thyroid pathways in mammals or wildlife”. This conclusion was drawn from a battery of Tier-1 tests, composed of in vitro and short-term in vivo tests, on glyphosate alone. No further long-term studies were carried out, and not all endocrine relevant endpoints were examined in each assay (for example estrogen receptor (ER) binding or ER activation each was measured just in one assay). Furthermore, US EPA did not take into consideration any of the findings from studies that tested the formulations of glyphosate-based herbicides, which is what people and the environment are exposed to.
However, several studies since then have demonstrated that both glyphosate and the Roundup formulation do disrupt estrogen, androgen, and other steroidogenic pathways. The following studies indicate that glyphosate has the potential to elicit endocrine-disrupting effects in cell lines, and the effects in comparison to glyphosate are either significant or more pronounced in studies where Roundup (glyphosate and its adjuvants) is used.
Richard, Sophie, Safa Moslemi, Herbert Sipahutar, Nora Benachour, and Gilles-Eric Seralini. "Differential effects of glyphosate and roundup on human placental cells and aromatase." Environmental health perspectives 113, no. 6 (2005): 716-720.
Romano, Marco Aurelio, Renata Marino Romano, Luciana Dalazen Santos, Patricia Wisniewski, Daniele Antonelo Campos, Paula Bargi de Souza, Priscila Viau, Maria Martha Bernardi, Maria Tereza Nunes, and Claudio Alvarenga de Oliveira. "Glyphosate impairs male offspring reproductive development by disrupting gonadotropin expression." Archives of toxicology 86, no. 4 (2012): 663-673.
Romano, Renata Marino, Marco Aurélio Romano, Maria Martha Bernardi, P. V. Furtado, and Cláudio Alvarenga de Oliveira. "Prepubertal exposure to commercial formulation of the herbicide glyphosate alters testosterone levels and testicular morphology." Archives of toxicology 84, no. 4 (2010): 309-317.
Thongprakaisang, Siriporn, Apinya Thiantanawat, Nuchanart Rangkadilok, Tawit Suriyo, and Jutamaad Satayavivad. "Glyphosate induces human breast cancer cells growth via estrogen receptors." Food and Chemical Toxicology 59 (2013): 129-136.
Walsh, Lance P., Chad McCormick, Clyde Martin, and Douglas M. Stocco. "Roundup inhibits steroidogenesis by disrupting steroidogenic acute regulatory (StAR) protein expression." Environmental health perspectives 108, no. 8 (2000): 769-776.
In this cell line or in vitro study Walsh et al demonstrated that Roundup, but not glyphosate, significantly inhibited the production of the hormone progesterone in mouse cells, by disrupting the expression of the steroidogenic acute regulatory (StAR) protein. The authors concluded that, as the StAR protein is also indispensable for steroidogenesis in the adrenal glands, a disruption in StAR protein expression may potentially affect carbohydrate metabolism, immune system function, and water balance, as well as fertility. It may have an impact on reproduction in humans, other mammals, birds, and amphibians.
Immune Function
Several studies indicate that glyphosate formulations may interfere with the immune system resulting in adverse respiratory effects including asthma, rheumatoid arthritis, and autoimmune skin and mucous membrane effects.
Kumar, Sudhir, Marat Khodoun, Eric M. Kettleson, Christopher McKnight, Tiina Reponen, Sergey A. Grinshpun, and Atin Adhikari. "Glyphosate-rich air samples induce IL-33, TSLP and generate IL-13 dependent airway inflammation."
Toxicology 325 (2014): 42-51.
This study designed to explore the ability of glyphosate to cause airway asthma-like pathology and occupational lung disease, found exposure to glyphosate to result in airway barrier damage and to modulate the immune system in mice. Glyphosate-rich air samples from farms, and pure glyphosate, induced substantial type 2 airway inflammation in mice, over both short and longer time periods. They increased eosinophil and neutrophil counts, mast cell degranulation, and production of asthma-related cytokines (IL5, IL-10, IL-13, IL-33, TSLP). The rates used were 100 ng and 1 µg glyphosate per air sample; increasing the dose of glyphosate 100-fold up to 100 µg did not substantially change the degree or character of inflammation, however, a longer exposure to glyphosate did significantly worsen histological pathology. Additionally, co-exposure with an allergen led to a profound inflammatory and antigen-specific innate and adaptive immune response.
Parks, Christine G., Jane A. Hoppin, Anneclaire J. De Roos, Karen H. Costenbader, Michael C. Alavanja, and Dale P. Sandler. "Rheumatoid arthritis in agricultural health study spouses: associations with pesticides and other farm exposures." Environmental health perspectives 124, no. 11 (2016): 1728-1734.
In a case-control study on the systemic autoimmune disease rheumatoid arthritis amongst female partners of pesticide applicators in USA, (275 cases, 24,081 non-cases), women with RA were more likely to have used glyphosate.
Neurological Toxicity
Several studies have shown that glyphosate can adversely affect neuronal development and nerve cells, including those in the brain’s dopaminergic system. There are indications it may have a role in Parkinson’s disease, and in autism and Attention Deficit Hyperactivity Disorder (ADD/ADHD) in children. US EPA (2006) stated that they did not require neurotoxicity or developmental neurotoxicity studies and
found no evidence of neurotoxicity.
Anadón, A., M. R. Martinez-Larranaga, M. A. Martinez, V. J. Castellano, M. Martínez, M. T. Martin, M. J. Nozal, and J. L. Bernal. "Toxicokinetics of glyphosate and its metabolite aminomethyl phosphonic acid in rats." Toxicology letters 190, no. 1 (2009): 91-95.
Benachour, Nora, H. Sipahutar, S. Moslemi, C. Gasnier, C. Travert, and G. E. Séralini. "Time-and dose-dependent effects of roundup on human embryonic and placental cells."
Archives of environmental contamination and toxicology 53, no. 1 (2007): 126-133.
Benachour, Nora, and Gilles-Eric Séralini. "Glyphosate formulations induce apoptosis and necrosis in human umbilical, embryonic, and placental cells." Chemical research in toxicology 22, no. 1 (2009): 97-105.
Clair, Émilie, Robin Mesnage, Carine Travert, and Gilles-Éric Séralini. "A glyphosate-based herbicide induces necrosis and apoptosis in mature rat testicular cells in vitro, and testosterone decrease at lower levels." Toxicology in vitro 26, no. 2 (2012): 269-279.
Coullery, Romina P., María E. Ferrari, and Silvana B. Rosso. "Neuronal development and axon growth are altered by glyphosate through a WNT non-canonical signaling pathway."
Neurotoxicology 52 (2016): 150-161.
In this study Coullery et al demonstrated that the exposure of neuronal cells to glyphosate (4mg/mL, 23mM) induces a delay in neuronal development and differentiation. The study did not show evidence of any lethal effect in cultured neurons, nonetheless the total axonal length and the number of branches were irreversibly reduced by the treatment with the herbicide.
Gasnier, Céline, Coralie Dumont, Nora Benachour, Emilie Clair, Marie-Christine Chagnon, and Gilles-Eric Séralini. "Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines." Toxicology 262, no. 3 (2009): 184-191.
Gui, Ya-xing, Xiao-ning Fan, Hong-mei Wang, and Gang Wang. "Glyphosate induced cell death through apoptotic and autophagic mechanisms." Neurotoxicology and teratology 34, no. 3 (2012): 344-349.
Hernández-Plata, Isela, Magda Giordano, Mauricio Díaz-Muñoz, and Verónica M. Rodríguez. "The herbicide glyphosate causes behavioral changes and alterations in dopaminergic markers in male Sprague-Dawley rat." Neurotoxicology 46 (2015): 79-91.
In this study Hernández-Plata et al showed that repeated intraperitoneal injections of glyphosate (50 to 150 mg/kg bw) caused decreased exploratory behavior and spontaneous locomotor activity in rats immediately after each injection, showing an acute effect. The effect was also apparent 2 days after the last injection, but not after 16 days suggesting that these alterations occur while a critical concentration of glyphosate is present in the system. However, the study also found that the D1 dopamine receptor binding was reduced in the nucleus accumbens in the brain and that acute glyphosate administration immediately decreases extracellular levels of basal striatal dopamine. These results suggest that glyphosate affects the dopaminergic system.
Planche, Vincent, Sylvain Vergnet, Nicolas Auzou, Marie Bonnet, Thomas Tourdias, and François Tison. "Acute toxic limbic encephalopathy following glyphosate intoxication."
Neurology 92, no. 11 (2019): 534-536.
Malhotra, R. C., D. K. Ghia, D. J. Cordato, and R. G. Beran. "Glyphosate–surfactant herbicide-induced reversible encephalopathy." Journal of Clinical Neuroscience 17, no. 11 (2010): 1472-1473.
Richard, Sophie, Safa Moslemi, Herbert Sipahutar, Nora Benachour, and Gilles-Eric Seralini. "Differential effects of glyphosate and roundup on human placental cells and aromatase." Environmental health perspectives 113, no. 6 (2005): 716-720.
Parkinson’s Disease
Anadón, A., M. R. Martinez-Larranaga, M. A. Martinez, V. J. Castellano, M. Martínez, M. T. Martin, M. J. Nozal, and J. L. Bernal. "Toxicokinetics of glyphosate and its metabolite aminomethyl phosphonic acid in rats." Toxicology letters 190, no. 1 (2009): 91-95.
In this study Anadón et al identified the possible role of glyphosate in neurodegenerative diseases, especially Parkinson’s disease. Glyphosate produced a significant dose-dependent depletion of serotonin and dopamine, also increasing the metabolites of these 2 neurotransmitters in male rats.
Eriguchi, Makoto, Kotaro Iida, Shuhei Ikeda, Manabu Osoegawa, Kenya Nishioka, Nobutaka Hattori, Hiroshi Nagayama, and Hideo Hara. "Parkinsonism relating to intoxication with glyphosate: A case report." Internal Medicine (2019): 2028-18.
Wang, Gang, Xiao-Ning Fan, Yu-Yan Tan, Qi Cheng, and Sheng-Di Chen. "Parkinsonism after chronic occupational exposure to glyphosate." Parkinsonism & related disorders 17, no. 6 (2011): 486-487.
Zheng, Qian, Jianhong Yin, Lina Zhu, Ling Jiao, and Zhu Xu. "Reversible Parkinsonism induced by acute exposure glyphosate." Parkinsonism & related disorders 50 (2018): 121.
Oxidative Free Radical Pathology (Oxidative Stress)
Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and an organism’s capacity to detoxify them and/or repair the resulting damage. Damage to DNA and other subcellular structures can occur when this capacity to detoxify or repair is saturated. Hence, oxidative stress may be a causative factor in cancer as well as neurodegenerative and other diseases. Oxidative stress can be assessed by measuring lipid peroxidation (ROS-generation) using thiobarbituric acid-reactive substances (TBARS), by determining the activity of specific enzymes (e.g. superoxide dismutase, catalase, glutathione-S-transferase) or by other, less frequently used methods. In numerous studies glyphosates was shown to produce ROS generation in human cell lines and animal studies.
Astiz, Mariana, María JT de Alaniz, and Carlos Alberto Marra. "Effect of pesticides on cell survival in liver and brain rat tissues." Ecotoxicology and environmental safety 72, no. 7 (2009): 2025-2032.
In this study rodents revealed a glyphosate-associated ROS-increase in blood plasma, liver and kidney of rats after repeated intraperitoneal injection of 10 mg/kg body weight.
Bolognesi, Claudia, Stefania Bonatti, Paolo Degan, Elena Gallerani, Marco Peluso, Roberta Rabboni, Paola Roggieri, and Angelo Abbondandolo. "Genotoxic activity of glyphosate and its technical formulation Roundup." Journal of Agricultural and food chemistry 45, no. 5 (1997): 1957-1962.
This study demonstrated oxidative DNA damage in liver and kidney of CD-1 mice after a single intraperitoneal injection of 300 mg/kg body weight.
Beuret, Cecilia Judith, Fanny Zirulnik, and María Sofía Giménez. "Effect of the herbicide glyphosate on liver lipoperoxidation in pregnant rats and their fetuses." Reproductive toxicology 19, no. 4 (2005): 501-504.
Beuret et al gave a glyphosate-based formulation via drinking water containing 1% glyphosate to pregnant rats during the entire gestation. At the end of pregnancy, a significant ROS-increase was detected in the livers of dams as well as fetuses.
Cattani, Daiane, Vera Lúcia de Liz Oliveira Cavalli, Carla Elise Heinz Rieg, Juliana Tonietto Domingues, Tharine Dal-Cim, Carla Inês Tasca, Fátima Regina Mena Barreto Silva, and Ariane Zamoner. "Mechanisms underlying the neurotoxicity induced by glyphosate-based herbicide in immature rat hippocampus: involvement of glutamate excitotoxicity."
Toxicology 320 (2014): 34-45.
In this in vitro study, hippocampal slices from 15-day-old rats exhibited oxidative stress after 30 minutes of incubation with a 0.01% “Roundup Original” solution, corresponding to a glyphosate concentration of 36 mg/L. The authors hypothesized that oxidative stress was resulting from the activation of NMDA receptors (N-methyl-D-aspartate receptor is a glutamate receptor and ion channel protein found in nerve cells), and voltage-dependent calcium channels.
Çavuşoğlu, Kültiğin, Emine Yalçın, Zafer Türkmen, Kürşad Yapar, Kürşat Çavuşoğlu, and Figen Çiçek. "Investigation of toxic effects of the glyphosate on Allium cepa." Tarım Bilimleri Dergisi (2011).
This study showed administration of glyphosate-based formulations to Swiss albino mice caused oxidative stress in liver and/ or kidney at a single intraperitoneal injection dose of 50 mg/kg.
Chaufan, Gabriela, Isis Coalova, and María del Carmen Ríos de Molina. "Glyphosate commercial formulation causes cytotoxicity, oxidative effects, and apoptosis on human cells: differences with its active ingredient." International journal of toxicology 33, no. 1 (2014): 29-38.
Coalova, Isis, María del Carmen Ríos de Molina, and Gabriela Chaufan. "Influence of the spray adjuvant on the toxicity effects of a glyphosate formulation." Toxicology in Vitro 28, no. 7 (2014): 1306-1311.
Elie-Caille, Celine, Celine Heu, Catherine Guyon, and Laurence Nicod. "Morphological damages of a glyphosate-treated human keratinocyte cell line revealed by a micro-to nanoscale microscopic investigation." Cell biology and toxicology 26, no. 4 (2010): 331-339.
Gehin, Audrey, Catherine Guyon, and Laurence Nicod. "Glyphosate-induced antioxidant imbalance in HaCaT: The protective effect of Vitamins C and E." Environmental Toxicology and Pharmacology 22, no. 1 (2006): 27-34.
Gehin, Audrey, Yves Claude Guillaume, Joëlle Millet, Catherine Guyon, and Laurence Nicod. "Vitamins C and E reverse effect of herbicide-induced toxicity on human epidermal cells HaCaT: a biochemometric approach." International journal of pharmaceutics 288, no. 2 (2005): 219-226.
Jasper, Raquel, Gabriel Olivo Locatelli, Celso Pilati, and Claudriana Locatelli. "Evaluation of biochemical, hematological and oxidative parameters in mice exposed to the herbicide glyphosate-Roundup®." Interdisciplinary toxicology 5, no. 3 (2012): 133-140.
Kwiatkowska, Marta, Bogumiła Huras, and Bożena Bukowska. "The effect of metabolites and impurities of glyphosate on human erythrocytes (in vitro)." Pesticide biochemistry and physiology 109 (2014): 34-43.
Martini, Claudia N., Matías Gabrielli, María Magdalena Codesido, and María C. Del Vila. "Glyphosate-based herbicides with different adjuvants are more potent inhibitors of 3T3-L1 fibroblast proliferation and differentiation to adipocytes than glyphosate alone." Comparative Clinical Pathology 25, no. 3 (2016): 607-613.
Martini et al described a ROS increase in 3T3-L1 fibroblasts (a cell line derived from mouse adipose tissue) after exposure to a glyphosate-based formulation.
Mladinic, Marin, Suzana Berend, Ana Lucic Vrdoljak, Nevenka Kopjar, Bozica Radic, and Davor Zeljezic. "Evaluation of genome damage and its relation to oxidative stress induced by glyphosate in human lymphocytes in vitro." Environmental and molecular mutagenesis 50, no. 9 (2009): 800-807.
Intestinal Microbiome Disruption
Glyphosate is toxic to many microbes as well as to most plants, and one likely effect of chronic low-dose oral exposure to glyphosate is a disruption of the balance among gut microbes towards an over-representation of pathogens. This leads to a chronic inflammatory state in the gut, as well as an impaired gut barrier and many other sequelae.
Aitbali, Yassine, Saadia Ba-M'hamed, Najoua Elhidar, Ahmed Nafis, Nabila Soraa, and Mohamed Bennis. "Glyphosate based-herbicide exposure affects gut microbiota, anxiety and depression-like behaviors in mice." Neurotoxicology and teratology 67 (2018): 44-49.
Lozano, Veronica L., Nicolas Defarge, Louis-Marie Rocque, Robin Mesnage, Didier Hennequin, Renaud Cassier, Joël Spiroux de Vendômois, Jean-Michel Panoff, Gilles-Eric Séralini, and Caroline Amiel. "Sex-dependent impact of Roundup on the rat gut microbiome." Toxicology reports 5 (2018): 96-107.
Mao, Qixing, Fabiana Manservisi, Simona Panzacchi, Daniele Mandrioli, Ilaria Menghetti, Andrea Vornoli, Luciano Bua et al. "The Ramazzini Institute 13-week pilot study on glyphosate and Roundup administered at human-equivalent dose to Sprague Dawley rats: effects on the microbiome." Environmental Health 17, no. 1 (2018): 50.
Samsel, Anthony, and Stephanie Seneff. "Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance." Interdisciplinary toxicology 6, no. 4 (2013): 159-184. (Google Revoved)
NCBI, READ MORE AT. "Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance."
Glyphosate Protection
Rebai, Olfa, Manel Belkhir, Adnen Boujelben, Sami Fattouch, and Mohamed Amri. "Morus alba leaf extract mediates neuroprotection against glyphosate-induced toxicity and biochemical alterations in the brain." Environmental Science and Pollution Research 24, no. 10 (2017): 9605-9613.