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Glyphosate is the most widely used herbicide in the world. Although some studies have shown cardiac electrophysiological changes associated to glyphosate, the histopathological changes that this herbicide may cause in the cardiovascular system are not yet established. The aim of this study was to evaluate the cardiovascular effects of subchronic oral and inhalation exposure to the glyphosate herbicide in rats. Eighty albino Wistar rats were distributed into eight groups (five males and five females/group): inhalation control: nebulization with sodium chloride solution (NaCl); oral control: nebulized feed with NaCl; low inhalation concentration: nebulization with 3.71 × 10 -3 grams of active ingredient per hectare (g.a.i./ha) of glyphosate; low oral concentration: nebulized feed with 3.71 × 10 -3 g.a.i./ha of glyphosate; medium inhalation concentration: nebulization with 6.19 × 10 -3 g.a.i./ha of glyphosate; medium oral concentration: nebulized feed with 6.19 × 10 -3 g.a.i./ha of glyphosate; high inhalation concentration: nebulization with 9.28 × 10 -3 g.a.i./ha of glyphosate; and high oral concentration: nebulized feed with 9.28 × 10 -3 g.a.i./ha of glyphosate. After 75 days of exposure, the animals were euthanized, and aortas and hearts were collected for histopathological analysis. Fatty streaks were observed in most animals exposed to glyphosate and were more prevalent in male rats, regardless of the route of exposure ( p < 0.05). There were no differences in the measurements of the thickness of the right and left ventricle or in the collagen density of both ventricles in any of the groups evaluated ( p > 0.05). Our study suggests that glyphosate has atherogenic potential, regardless of the concentration and route of exposure.

The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is the second most widely used herbicide in the world. The objective of this study was to evaluate the neurotoxic effects and the possible role of the dysregulation of apoptosis in the genesis of brain damage in chronic exposure to 2,4-D in rats. Eighty adult male rats were distributed into eight groups (n = 10) and exposed orally (contaminated feed) and via inhalation, with two groups exposed to distilled water (control) and six to 2,4-D in three distinct concentrations. They were exposed for 6 months. A neurobehavioral assessment was performed, and the brain was collected for histopathology and immunohistochemistry. The animals in the control groups showed greater motility in the open-field test and a greater number of entries in the elevated-plus-maze test than those exposed to 2,4-D ( p  < 0.05). Neuronal necrosis was more incident in animals exposed to 2,4-D ( p  < 0.05). There was a negative correlation between the expression of BAX and the measurement of the cerebral cortex thickness (r = -0.713; p  = 0.047). Regardless of the route of exposure, 2,4-D led to a deficit in neurobehavioral tests and decreased thickness of the cerebral cortex associated with increased expression of the pro-apoptotic protein BAX.