A step further toward glyphosate-induced epidermal cell death: Involvement of mitochondrial and oxidative mechanisms

A deregulation of programmed cell death mechanisms in human epidermis leads to skin pathologies. We previously showed that glyphosate, an extensively used herbicide, provoked cytotoxic effects on cultured human keratinocytes, affecting their antioxidant capacities and impairing morphological and functional cell characteristics. The aim of the present study, carried out on the human epidermal cell line HaCaT, was to examine the part of apoptosis plays in the cytotoxic effects of glyphosate and the intracellular mechanisms involved in the apoptotic events. We have conducted different incubation periods to reveal the specific events in glyphosate-induced cell death. We observed an increase in the number of early apoptotic cells at a low cytotoxicity level (15%), and then, a decrease, in favor of late apoptotic and necrotic cell rates for more severe cytotoxicity conditions. At the same time, we showed that the glyphosate-induced mitochondrial membrane potential disruption could be a cause of apoptosis in keratinocyte cultures.

► Glyphosate is an herbicide that provokes intracellular and membrane impairments. ► Flow cytometry is the primary approach to exactly quantify intracellular mechanisms. ► Glyphosate-treated HaCaT represents a well-tried epidermal oxidative stress model. ► A mitochondrial membrane potential disruption is provoked by the glyphosate treatment. ► Glyphosate induces apoptosis via the mitochondrial oxidative pathway.