Raise awareness of environmental health issues in order to better protect our children and future generations.

EMF Studies

31 March 2014

Study: Roundup Disrupts Male Reproductive Functions By Triggering Calcium-Mediated Cell Death in Rat Testis and Sertoli Cells

Glyphosate acts as a toxicant by activating voltage-gated calcium channels, the same mechanism activated by Electro Magnetic Fields
Martin Pall, 3 February 2014 (via WEEP News, Canada)

A number of people with these diseases (see http://www.thetenthparadigm.org/index.html) have reported apparent sensitivity to roundup herbicide and its "active" ingredient, glyphosate and there has been concern because the EPA has apparently already approved of allowing much higher levels of glyphosate in non-organic foods. I recently found a paper showing that glyphosate acts as a toxicant by activating voltage-gated calcium channels, the same mechanism activated by electromagnetic field exposure. There is no reason to doubt that such increased intracellular calcium levels should be able to up-regulate the NO/ONOO- cycle and therefore most if not all NO/ONOO- cycle caused diseases. I think that there is reason for concern here. It may well be the case that glyphosate may act synergistically with EMF exposures to together produce much higher pathophysiological responses.

You are welcome to freely forward this message.

Martin Pall

Roundup disrupts male reproductive functions by triggering calcium-mediated cell death in rat testis and Sertoli cells.

Free Radical Biology and Medicine. 2013 Dec;65:335-46. doi: 10.1016/j.freeradbiomed.2013.06.043. Epub 2013 Jun 29.

de Liz Oliveira Cavalli VL, Cattani D, Heinz Rieg CE, Pierozan P, Zanatta L, Benedetti Parisotto E, Wilhelm Filho D, Mena Barreto Silva FR, Pessoa-Pureur R,Zamoner A.


Abstract

Glyphosate is the primary active constituent of the commercial pesticide Roundup. The present results show that acute Roundup exposure at low doses (36 ppm, 0.036 g/L) for 30 min induces oxidative stress and activates multiple stress-response pathways leading to Sertoli cell death in prepubertal rat testis. The pesticide increased intracellular Ca(2+) concentration by opening L-type voltage-dependent Ca(2+) channels as well as endoplasmic reticulum IP3 and ryanodine receptors, leading to Ca(2+) overload within the cells, which set off oxidative stress and necrotic cell death. Similarly, 30 min incubation of testis with glyphosate alone (36 ppm) also increased (45)Ca(2+) uptake. These events were prevented by the antioxidants Trolox and ascorbic acid. Activated protein kinase C, phosphatidylinositol 3-kinase, and the mitogen-activated protein kinases such as ERK1/2 and p38MAPK play a role in eliciting Ca(2+) influx and cell death. Roundup decreased the levels of reduced glutathione (GSH) and increased the amounts of thiobarbituric acid-reactive species (TBARS) and protein carbonyls. Also, exposure to glyphosate-Roundup stimulated the activity of glutathione peroxidase, glutathione reductase, glutathione S-transferase, γ-glutamyltransferase, catalase, superoxide dismutase, and glucose-6-phosphate dehydrogenase, supporting downregulated GSH levels. Glyphosate has been described as an endocrine disruptor affecting the male reproductive system; however, the molecular basis of its toxicity remains to be clarified. We propose that Roundup toxicity, implicated in Ca(2+) overload, cell signaling misregulation, stress response of the endoplasmic reticulum, and/or depleted antioxidant defenses, could contribute to Sertoli cell disruption in spermatogenesis that could have an impact on male fertility.

Copyright © 2013 Elsevier Inc. All rights reserved.

http://www.ncbi.nlm.nih.gov/pubmed/23820267

No comments:

Post a Comment