Background: The herbicide dichlorophenoxyacetic acid (2,4-D) is one of the most widely used crop spraying products in the world. Some pesticides induce the degranulation of mast cells and increase allergic responses. This is the first study to evaluate the damage to the oral mucosa after an experimental simulation of environmental inhalation exposure to the 2,4-D herbicide. The aim of this study was evaluate the possible oral damage caused by acute inhalation exposure to the herbicide 2,4-D. Results: There was a difference between the exposure concentrations in relation to tissue congestion intensity (p = 0.002) and mast cell counts (p = 0.002), a difference in the evaluation of the interaction between the exposure concentrations and nebulization time in the dorsum epithelium thickness (p = 0.013), and a significant correlation between the epithelial thickness and the number of nucleoli organizing regions on the dorsum of the tongue (p = 0.048). Conclusions: Even after acute exposure, the herbicide 2,4-D had the potential to damage the oral epithelium, especially at higher doses.
The uncontrolled production of the reactive oxygen species (ROS) generates oxidative stress and the development of chronic diseases, such as hypertension. Antioxidant enzymes can reduce the cellular level of ROS. Nuclear erythroid factor 2 (Nrf-2) favors the expression and activity of antioxidant enzymes. In hypertensive rats, Nrf-2 expresssion appears to be reduced in blood vessels and, consequently, it favors the oxidative stress and vascular dysfunction. Apocynin (APO) has been considered a new antioxidant drug. APO reduces blood pressure, decreases ROS production, and improves endothelial function in spontaneously hypertensive rats (SHR). We hypothesized that the role of Nrf-2 in vascular reactivity is altered in SHR and APO-treatment prevents this alteration. To test this hypothesis, we evaluated aorta reactivity to phenylephrine (PE) and acetylcholine (ACh), in the absence and presence of Brusatol, Nrf-2 inhibitor. We used aortas from normotensive Wistar rats and SHR, untreated or treated with APO. Brusatol increased the reactivity of the aortas from SHR to PE, but did not change the reactivity of Wistar rat aortas. In APO-treated SHR aortas, the effect of Brusatol was not observed. The vasodilator responses to ACh were not modified by Brusatol in aortas from normotensive or hypertensive rats, untreated or treated with APO. These results suggest that Nrf-2 is activated in the contractile response to PE. In SHR aortas, exacerbated generation of ROS induces the activation of Nrf-2. This suggestion is reinforced by the lack of Brusatol effect in APO-treated SHR aortas. As APO is an antioxidant drug, the reduction of ROS in vascular cells would not lead to Nrf-2 activation.
Background: The herbicide dichlorophenoxyacetic acid (2,4-D) is one of the most widely used crop spraying products in the world. Some pesticides induce the degranulation of mast cells and increase allergic responses. This is the first study to evaluate the damage to the oral mucosa after an experimental simulation of environmental inhalation exposure to the 2,4-D herbicide. The aim of this study was evaluate the possible oral damage caused by acute inhalation exposure to the herbicide 2,4-D.Methods: A total of 80 Swiss male mice were divided into 4 groups (n = 20) and evaluated at different time intervals (24 h, 48 h, 72 h and 8 days), with 5 animals / period. The animals were divided into the following groups: SG: nebulization with sodium chloride solution; LCG: pesticide nebulization with 3.71 x 10-3 grams of active ingredient per hectare (g.i.a. / ha); MCG: pesticide nebulization with 6.19 x 10-3 g.i.a. /ha; and HCG: pesticide nebulization with 9.28 x 10-3 g.i.a. /ha. The tongues of the mice were collected for histopathological analysis.Results: There was a difference between the exposure concentrations in relation to tissue congestion intensity (p = 0.002) and mast cell counts (p = 0.002), a difference in the evaluation of the interaction between the exposure concentrations and nebulization time in the dorsum epithelium thickness (p = 0.013), and a significant correlation between the epithelial thickness and the number of nucleoli organizing regions on the dorsum of the tongue (p = 0.048).Conclusions: Even after acute exposure, the herbicide 2,4-D had the potential to damage the oral epithelium, especially at higher doses.
Background The herbicide dichlorophenoxyacetic acid (2,4-D) is one of the most widely used crop spraying products in the world. Some pesticides induce the degranulation of mast cells and increase allergic responses. This is the first study to evaluate the damage to the oral mucosa after an experimental simulation of environmental inhalation exposure to the 2,4-D herbicide. The aim of this study was evaluate the possible oral damage caused by acute inhalation exposure to the herbicide 2,4-D. Methods A total of 80 Swiss male mice were divided into 4 groups (n = 20) and evaluated at different time intervals (24 h, 48 h, 72 h and 8 days), with 5 animals / period. The animals were divided into the following groups: SG: nebulization with sodium chloride solution; LCG: pesticide nebulization with 3.71 x 10 -3 grams of active ingredient per hectare (g.i.a. / ha); MCG: pesticide nebulization with 6.19 x 10 -3 g.i.a. /ha; and HCG: pesticide nebulization with 9.28 x 10 -3 g.i.a. /ha. The tongues of the mice were collected for histopathological analysis. Results There was a difference between the exposure concentrations in relation to tissue congestion intensity (p = 0.002) and mast cell counts (p = 0.002), a difference in the evaluation of the interaction between the exposure concentrations and nebulization time in the dorsum epithelium thickness (p = 0.013), and a significant correlation between the epithelial thickness and the number of nucleoli organizing regions on the dorsum of the tongue (p = 0.048). Conclusions Even after acute exposure, the herbicide 2,4-D had the potential to damage the oral epithelium, especially at higher doses.
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