The toxic effects and possible mechanisms of glyphosate on mouse oocytes

Abstract

Glyphosate is a high-efficiency, low-toxicity, broad-spectrum herbicide. The residues of glyphosate-based herbicides are frequent pollutants in the environment. However, the effects of glyphosate on oocyte maturation, as well as its possible mechanisms, remain unclear. The present study revealed that mouse oocytes had reduced rates of germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE) after treatment with 500 μM glyphosate. Reactive oxygen species (ROS) were found in mouse oocytes exposed to glyphosate, as shown by changes in the mRNA expression of related antioxidant enzyme genes (cat, sod2, gpx). After 14 h of exposure to glyphosate, metaphase II (MII) mouse oocytes displayed an abnormal spindle morphology and DNA double-strand breaks (DNA-DSBs). Simultaneously, mitochondria showed an aggregated distribution and decreased membrane potential in mouse oocytes exposed to glyphosate. The protein expression levels of apoptosis factors (Bax, Bcl-2) and the mRNA expression levels of apoptosis-related genes (bax, bcl-2, caspase3) were measured by Western blot and qRT-PCR, respectively. Meanwhile, the expression levels of autophagy-related genes (lc3, atg14, mtor) and proteins (LC3, Atg12) were significantly decreased in the glyphosate treatment group compared with the control group. Collectively, our results indicated that glyphosate exposure could interfere with mouse oocyte maturation by generating oxidative stress and early apoptosis.