Aminomethylphosphonic acid (AMPA) alters oxidative status during embryonic development in an amphibian species

Glyphosate's primary metabolite (aminomethylphosphonic acid, AMPA) is known to alter embryonic development at environmentally relevant concentrations in amphibians. However, we have limited understanding of the physiological mechanisms through which AMPA affects organisms. In this study, we tested whether alteration of the oxidative status is one mechanism through which AMPA affects organism performance. To this end, we analysed several oxidative status markers in hatchling tadpoles that were exposed to sublethal concentrations of AMPA during embryonic development (~16 days). We compared the influence of environmentally relevant concentrations of AMPA (from 0.07 to 3.57 μg l−1) on the relation between developmental traits (i.e, embryonic development duration, embryonic mortality and hatchling size) and oxidative status markers known to alter homeostasis when unbalanced (superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), thiols and ratios thereof). We included measures of telomere length as an indicator of physiological state. We found that AMPA concentrations induce non-monotonic effects on some oxidative status markers with hatchlings displaying elevated antioxidant responses (elevated thiols and unbalanced SOD/(GPx + CAT) ratio). The lack of effect of AMPA on the relation between developmental traits, oxidative status and telomere length suggests that selective mortality of embryos susceptible to oxidative stress may have occurred prior to hatching in individuals less resistant to AMPA which display lower hatching success. Future studies are required to disentangle whether oxidative unbalance is a cause or a consequence of AMPA exposition. This study highlights the need to investigate effects of the metabolites of contaminants at environmental concentrations to comprehensively assess impacts of anthropogenic contamination on wildlife.