From our friends at the Naturally Better Clinic
How much longer will we deny the growing body of research linking Roundup to infertility before calling this chemical a contraceptive?
Following closely on the heels of the EPA’s decision to allow Roundup herbicide residues in your food at concentrations a million times higher than shown carcinogenic, a concerning new study published in the journal Free Radical Medicine & Biology implicates the herbicide, and its main ingredient glyphosate, in male infertility, at concentration ranges well within the EPA’s “safe level” for food.
Performed by Brazilian researchers, the study found acute Roundup exposure at low doses (36ppm, 0.036g/L) for 30 minutes induced cell death in Sertoli cells in prepubertal rat testis. Sertoli cells are known as “mother” or “nurse” cells within the testicles, as they are responsible for maintaining the health of sperm cells, and are required for normal male sexual development.
Roundup herbicide exposure was found to induce oxidative stress and to activate multiple-stress response pathways within affected cells, and was associated with an increase in intracellular calcium (Ca2+) concentration leading to Ca2+ overload, and cell death.
Thirty minute incubation tests with glyphosate alone (36 ppm) also increased Ca2+ uptake, and both Roundup and glyphosate were observe to downregulate reduced glutathione levels. As glutathione is an antioxidant (electron donor) found within every cell in the human body, protecting it against oxidative stress, as well as maintaining a wide range of biochemical reactions such as DNA and protein synthesis and repair, amino acid transport, prostaglandin synthesis, amino acid and enzyme activation, a dysregulation of glutathione can result in a wide range of adverse effects.
The researchers noted “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 could propose that Roundup® toxicity, implicating in Ca2+ overload, cell signaling misregulation, stress response of the endoplasmic reticulum and/or depleted antioxidant defenses could contribute to Sertoli cell disruption of spermatogenesis that could impact male fertility.”