Glyphosate - HH-RA.org

Bibliography Tag: glyphosate

Milesi et al., 2018

Milesi, Maria M, Lorenz, Virginia, Pacini, Guillermina, Repetti, Maria R, Demonte, Luisina D, Varayoud, Jorgelina, & Luque, Enrique H, “Perinatal exposure to a glyphosate-based herbicide impairs female reproductive outcomes and induces second-generation adverse effects in Wistar rats,” Archives of Toxicology, 2018, 92(8), 2629-2643. DOI: 10.1007/s00204-018-2236-6.

ABSTRACT:

Glyphosate-based herbicides (GBHs) are the most globally used herbicides raising the risk of environmental exposition. Here, we investigated whether perinatal exposure to low doses of a GBH alters the female reproductive performance, and/or induced second-generation effects related to congenital anomalies or growth alterations. Pregnant rats (F0) received a GBH through food, in a dose of 2 mg (GBH-LD: GBH-low dose group) or 200 mg (GBH-HD: GBH-high dose group) of glyphosate/kg bw/day from gestational day (GD) 9 until weaning. Body weight gain and vaginal canal-opening of F1 females were recorded. Sexually mature F1 females were mated to evaluate their reproductive performance by assessing the pregnancy rate, and on GD19, the number of corpora lutea, the implantation sites (IS) and resorption sites. To analyze second-generation effects on F2 offspring, we analyzed the fetal morphology on GD19, and assessed the fetal length and weight, and the placental weight. GBH exposure neither altered the body weight gain of F1 females, nor vaginal opening onset. Although all GBH-exposed F1 rats became pregnant, a lower number of IS was detected. F2 offspring from both GBH groups showed delayed growth, evidenced by lower fetal weight and length, associated with a higher incidence of small for gestational age fetuses. In addition, higher placental weight and placental index were found in F2 offspring from GBH-HD dams. Surprisingly, structural congenital anomalies (conjoined fetuses and abnormally developed limbs) were detected in the F2 offspring from GBH-HD group. In conclusion, perinatal exposure to low doses of a GBH impaired female reproductive performance and induced fetal growth retardation and structural congenital anomalies in F2 offspring. FULL TEXT

Martinez et al., 2018

Martinez, Daisy A, Loening, Ulrich E, & Graham, Margaret C, “Impacts of glyphosate-based herbicides on disease resistance and health of crops: a review,” Environmental Sciences Europe, 2018, 30(1), 2. DOI: 10.1186/s12302-018-0131-7.

ABSTRACT:

Based on experimental data from laboratory and field, numerous authors have raised concern that exposure to glyphosate-based herbicides (GBHs) may pre-dispose crops to damage by microbial pathogens. In this review, we distinguish and evaluate two principal pathways by which GBHs may affect the susceptibility of crops to disease: pathway 1-via disruptions to rhizosphere microbial ecology, and pathway 2-via restriction of nutrients to crops. We conclude that GBHs have the potential to undermine crop health in a number of ways, including: (i) impairment of the innate physiological defences of glyphosate-sensitive (GS) cultivars by interruption of the shikimic acid pathway; (ii) impairment of physiological disease defences has also been shown to occur in some glyphosate-resistant (GR) cultivars, despite their engineered resistance to glyphosate’s primary mode of action; (iii) interference with rhizosphere microbial ecology (in particular, GBHs have the potential to enhance the population and/or virulence of some phytopathogenic microbial species in the crop rhizosphere); and finally, (iv) the as yet incompletely elucidated reduction in the uptake and utilisation of nutrient metals by crops. Future progress will best be achieved when growers, regulators and industry collaborate to develop products, practices and policies that minimise the use of herbicides as far as possible and maximise their effectiveness when used, while facilitating optimised food production and security. FULL TEXT

Luo et al., 2017

Luo, Lei, Wang, Fei, Zhang, Yiyuan, Zeng, Ming, Zhong, Caigao, & Xiao, Fang, “In vitro cytotoxicity assessment of Roundup (glyphosate) in L-02 hepatocytes,” Journal of Environmental Science and Health, Part B, 2017, 52(6), 410-417. DOI: 10.1080/03601234.2017.1293449.

ABSTRACT:

The goal of the present study was to elucidate the in vitro cytotoxicity of Roundup and to reveal the possible related mechanisms in L-02 hepatocytes. By detecting reactive oxygen species (ROS) production, glutathione (GSH)/superoxide dismutase (SOD) levels, mitochondrial permeability transition pore (PTP) open rate, apoptosis-inducing factor (AIF) release, intracellular Ca2+ concentration, and alanine aminotransferease (ALT)/aspartate aminotransferase (AST) leakage, we determined that Roundup induced anti-oxidant system inhibition, mitochondria damage, DNA damage, membrane integrity and permeability changes, and apoptosis in L-02 hepatocytes. By revealing the mechanistic insights of Roundup-induced cytotoxicity, our results are valuable for the design of preventive and therapeutic strategies for the occupational population exposed to Roundup and other pesticides.

Kniss, 2016

Kniss, A. R., “Long-term trends in the intensity and relative toxicity of herbicide use,” Nature Communications, 2017, 8, 14865. DOI: 10.1038/ncomms14865.

ABSTRACT:

Herbicide use is among the most criticized aspects of modern farming, especially as it relates to genetically engineered (GE) crops. Many previous analyses have used flawed metrics to evaluate herbicide intensity and toxicity trends. Here, I show that herbicide use intensity increased over the last 25 years in maize, cotton, rice and wheat. Although GE crops have been previously implicated in increasing herbicide use, herbicide increases were more rapid in non-GE crops. Even as herbicide use increased, chronic toxicity associated with herbicide use decreased in two out of six crops, while acute toxicity decreased in four out of six crops. In the final year for which data were available (2014 or 2015), glyphosate accounted for 26% of maize, 43% of soybean and 45% of cotton herbicide applications. However, due to relatively low chronic toxicity, glyphosate contributed only 0.1, 0.3 and 3.5% of the chronic toxicity hazard in those crops, respectively. FULL TEXT

Kwiatkowska et al., 2017

Kwiatkowska, Marta, Reszka, Edyta, Wozniak, Katarzyna, Jablonska, Ewa, Michalowicz, Jaromir, & Bukowska, Bozena, “DNA damage and methylation induced by glyphosate in human peripheral blood mononuclear cells (in vitro study),” Food and Chemical Toxicology, 2017, 105, 93-98. DOI: 10.1016/j.fct.2017.03.051.

ABSTRACT:

Glyphosate is a very important herbicide that is widely used in the agriculture, and thus the exposure of humans to this substance and its metabolites has been noted. The purpose of this study was to assess DNA damage (determination of single and double strand-breaks by the comet assay) as well as to evaluate DNA methylation (global DNA methylation and methylation of p16 (CDKN2A) and p53 (TP53) promoter regions) in human peripheral blood mononuclear cells (PBMCs) exposed to glyphosate. PBMCs were incubated with the compound studied at concentrations ranging from 0.1 to 10 mM for 24 h. The study has shown that glyphosate induced DNA lesions, which were effectively repaired. However, PBMCs were unable to repair completely DNA damage induced by glyphosate. We also observed a decrease in global DNA methylation level at 0.25 mM of glyphosate. Glyphosate at 0.25 mM and 0.5 mM increased p53 promoter methylation, while it did not induce statistically significant changes in methylation of p16 promoter. To sum up, we have shown for the first time that glyphosate (at high concentrations from 0.5 to 10 mM) may induce DNA damage in leucocytes such as PBMCs and cause DNA methylation in human cells. FULL TEXT

Krimsky and Gillam, 2018

Krimsky, Sheldon, & Gillam, Carey, “Roundup litigation discovery documents: implications for public health and journal ethics,” Journal of Public Health Policy, 2018, 39(3), 318-326. DOI: 10.1057/s41271-018-0134-z.

ABSTRACT:

This paper reviews the court-released discovery documents obtained from litigation against Monsanto over its herbicide Roundup and through Freedom of Information Act requests (requests to regulatory agencies and public universities in the United States). We sought evidence of corporate malfeasance and undisclosed conflicts of interest with respect to issues of scientific integrity. The findings include evidence of ghostwriting, interference in journal publication, and undue influence of a federal regulatory agency.

Koo et al., 2018

Koo, Dal-Hoe, Molin, William T, Saski, Christopher A, Jiang, Jiming, Putta, Karthik, Jugulam, Mithila, Friebe, Bernd, & Gill, Bikram S, “Extrachromosomal circular DNA-based amplification and transmission of herbicide resistance in crop weed Amaranthus palmeri,” Proceedings of the National Academy of Sciences of the United States of America, 2018, 115(13), 3332-3337. DOI: 10.1073/pnas.1719354115.

ABSTRACT:

Gene amplification has been observed in many bacteria and eukaryotes as a response to various selective pressures, such as antibiotics, cytotoxic drugs, pesticides, herbicides, and other stressful environmental conditions. An increase in gene copy number is often found as extrachromosomal elements that usually contain autonomously replicating extrachromosomal circular DNA molecules (eccDNAs). Amaranthus palmeri, a crop weed, can develop herbicide resistance to glyphosate [N-(phosphonomethyl) glycine] by amplification of the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene, the molecular target of glyphosate. However, biological questions regarding the source of the amplified EPSPS, the nature of the amplified DNA structures, and mechanisms responsible for maintaining this gene amplification in cells and their inheritance remain unknown. Here, we report that amplified EPSPS copies in glyphosate-resistant (GR) A. palmeri are present in the form of eccDNAs with various conformations. The eccDNAs are transmitted during cell division in mitosis and meiosis to the soma and germ cells and the progeny by an as yet unknown mechanism of tethering to mitotic and meiotic chromosomes. We propose that eccDNAs are one of the components of McClintock’s postulated innate systems [McClintock B (1978) Stadler Genetics Symposium] that can rapidly produce soma variation, amplify EPSPS genes in the sporophyte that are transmitted to germ cells, and modulate rapid glyphosate resistance through genome plasticity and adaptive evolution. FULL TEXT

Kongtip et al., 2017

Kongtip, Pornpimol, Nankongnab, Noppanun, Phupancharoensuk, Ratanavadee, Palarach, Chonlada, Sujirarat, Dusit, Sangprasert, Supha, Sermsuk, Malasod, Sawattrakool, Namthip, & Woskie, Susan Renee, “Glyphosate and Paraquat in Maternal and Fetal Serums in Thai Women,” Journal of Agromedicine, 2017, 22(3), 282-289. DOI: 10.1080/1059924x.2017.1319315.

ABSTRACT:

OBJECTIVES: This longitudinal study measured the glyphosate and paraquat concentrations found in maternal and umbilical cord serum in 82 pregnant women who gave birth in three provinces of Thailand.

METHODS: Through questionnaires and biological samples collected at childbirth, factors such as personal characteristics, family members occupation, agricultural activities, and herbicide use in agricultural work were evaluated as predictors of glyphosate and paraquat levels in the pregnant women. Statistical analysis used univariate and binary multiple logistic regression, where the outcome was the probability of exposure to paraquat or glyphosate above the limit of detection associated with occupation and household factors.

RESULTS: The glyphosate concentrations in the pregnant women’s serum at childbirth (median: 17.5, range: 0.2-189.1 ng/mL) were significantly higher (P < .007) than those in the umbilical cord serum (median: 0.2, range: 0.2-94.9 ng/mL). However, the paraquat concentrations in the serum of the pregnant women at childbirth (83% </=limit of detection [LOD], with maximum of 58.3 ng/mL) were similar to those in the umbilical cord serum (80% <LOD, with maximum of 47.6 ng/mL). Women with glyphosate levels >LOD in serum at childbirth were 11.9 times more likely to report work as an agriculturist (P < .001), 3.7 times more likely to live near agricultural areas (P = .006), and 5.9 times more likely to have a family member who worked in agriculture (P < .001). The only factors affecting paraquat exposures in pregnant women at childbirth were reporting the agricultural activity of digging in farm soil and working in the agricultural fields in the third trimester of pregnancy.

CONCLUSIONS: These results show that pregnant women who work in agriculture or live in families that work in agriculture have higher exposures to the herbicides glyphosate and paraquat. The potential for long-term health impacts of these prenatal exposures to children should be evaluated, and greater regulation of the sale and use of herbicides should be considered in Thailand. FULL TEXT

Kasuba et al., 2018

Kasuba, Vilena, Milic, Mirta, Rozgaj, Ruzica, Kopjar, Nevenka, Mladinic, Marin, Zunec, Suzana, Vrdoljak, Ana Lucic, Pavicic, Ivan, Cermak, Ana Marija Marjanovic, Pizent, Alica, Lovakovic, Blanka Tariba, & Zeljezic, Davor, “Effects of low doses of glyphosate on DNA damage, cell proliferation and oxidative stress in the HepG2 cell line,” Environmental Science and Pollution Research, 2017, 24(23), 19267-19281. DOI: 10.1007/s11356-017-9438-y.

ABSTRACT:

We studied the toxic effects of glyphosate in vitro on HepG2 cells exposed for 4 and 24 h to low glyphosate concentrations likely to be encountered in occupational and residential exposures [the acceptable daily intake (ADI; 0.5 μg/mL), residential exposure level (REL; 2.91 μg/mL) and occupational exposure level (OEL; 3.5 μg/mL)]. The assessments were performed using biomarkers of oxidative stress, CCK-8 colorimetric assay for cell proliferation, alkaline comet assay and cytokinesis-block micronucleus (CBMN) cytome assay. The results obtained indicated effects on cell proliferation, both at 4 and 24 h. The levels of primary DNA damage after 4-h exposure were lower in treated vs. control samples, but were not significantly changed after 24 h. Using the CBMN assay, we found a significantly higher number of MN and nuclear buds at ADI and REL after 4 h and a lower number of MN after 24 h. The obtained results revealed significant oxidative damage. Four-hour exposure resulted in significant decrease at ADI [lipid peroxidation and glutathione peroxidase (GSH-Px)] and OEL [lipid peroxidation and level of total antioxidant capacity (TAC)], and 24-h exposure in significant decrease at OEL (TAC and GSH-Px). No significant effects were observed for the level of reactive oxygen species (ROS) and glutathione (GSH) for both treatment, and for 24 h for lipid peroxidation. Taken together, the elevated levels of cytogenetic damage found by the CBMN assay and the mechanisms of primary DNA damage should be further clarified, considering that the comet assay results indicate possible cross-linking or DNA adduct formation.

Jiang et al., 2018

Jiang, X., Zhang, N., Yin, L., Zhang, W. L., Han, F., Liu, W. B., Chen, H. Q., Cao, J., & Liu, J. Y., “A commercial Roundup(R) formulation induced male germ cell apoptosis by promoting the expression of XAF1 in adult mice.,” Toxicology Letters, 2018, 296, 163-172, DOI: 10.1016/j.toxlet.2018.06.1067.

ABSTRACT:

Roundup(R) is extensively used for weed control worldwide. Residues of this compound may lead to side effects of the male reproductive system. However, the toxic effects and mechanisms of Roundup(R) of male germ cells remain unclear. We aimed to investigate the apoptosis-inducing effects of Roundup(R) on mouse male germ cells and explore the role of a novel tumor suppressor XAF1 (X-linked inhibitor of apoptosis-associated factor 1) involved in this process. We demonstrated that Roundup(R) can impair spermatogenesis, decrease sperm motility and concentration, and increase the sperm deformity rate in mice. In addition, excessive apoptosis of germ cells accompanied by the overexpression of XAF1 occurred after Roundup(R) exposure both in vitro and in vivo. Furthermore, the low expression of XIAP (X-linked inhibitor of apoptosis) induced by Roundup(R) was inversely correlated with XAF1. Moreover, the knockdown of XAF1 attenuated germ cell apoptosis, improved XIAP expression and inhibited the activation of its downstream target proteins, caspase-3 and PARP, after Roundup(R) exposure. Taken together, our data indicated that XAF1 plays an important role in Roundup(R)-induced male germ cell apoptosis. The present study suggested that Roundup(R) exposure has potential negative implications on male reproductive health in mammals.

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