CAT and SOD activity.

<p>Erythrocytes were pretreated with resveratrol (RSV, 100 μM and 1000 μM) for 1 h at 37°C and incubated for 30 min with DDS-NHOH (2.5 μg/ml) or T-BHP (200 μM). Results are expressed as mean ± S.E.M. *P < 0.05 compared to methanol group.</p

Effect of treatment with resveratrol on DNA damage induced by DDS-NHOH.

<p>Tail Length (μm—<b>A</b>), DNA in tail (%—<b>B</b>) Tail Moment (TM—<b>C</b>) and Olive Moment (OM—<b>D</b>) were used as a marker of DNA damage in lymphocyte using Comet assay. As positive control was used H₂O₂ (200 μM). All values are depicted as mean ± S.E.M.</p

Comparative effect of post-treatment with resveratrol (RSV) or methylene blue (MET) on methemoglobin formation induced by DDS-NHOH.

<p>Erythrocytes were incubated for 1 h with DDS-NHOH (2.5 μg/mL), then these cells were incubated with RSV (100μM) for 1 h or MET(40 nM). Data are reported as mean ± S.E.M. *P < 0.05 compared to methanol group. ^#P < 0.05 compared to DDS-NHOH group.</p

Redox mechanism.

<p>Ionization potential and stabilization energy of dapsone hydroxylamine (DDS-NHOH), resveratrol (RSV), and methylene blue (MET) on antioxidant and methemoglobinemia reversion.</p

Determination of nitric oxide (NO) in serum (a), percentage of blood methemoglobin (b) levels of malondialdehyde (MDA) in plasma (c) of patients with untreated leprosy (MDT 0) and after the third dose supervised treatment (MDT 3).

<p>Figures in the chart are expressed as mean ± SD. *p<0.05 compared to MDT0 (ANOVA).</p

Effect of the DDS-NHOH on methemoglobin formation in human erythrocytes.

<p>Erythrocytes were incubated with different concentrations of DDS-NHOH (2.5; 5.0 and 7.5 μg/mL) for 1 h at 37°C. Data are reported as means ± S.E.M from three independent experiments done in triplicate. *P < 0.05 compared to methanol group.</p

HOMO surface.

<p>Structure for HOMO of the dapsone hydroxylamine (DDS-NHOH), resveratrol (RSV), and methylene blue (MET). All nodal patterns related to individual group contributions are presented by blue or yellow for negative or positive wave function, respectively.</p

Proposal for a possible action mechanism of resveratrol (RSV) in inhibiting methemoglobin formation and DNA damage induced by DDS hydroxylamine (DDS-NHOH) <i>in vitro</i> model.

<p>Proposal for a possible action mechanism of resveratrol (RSV) in inhibiting methemoglobin formation and DNA damage induced by DDS hydroxylamine (DDS-NHOH) <i>in vitro</i> model.</p

Representation of the CYP 2C19.

<p>Area covered (depicted as <i>light blue</i> transparent <i>solid surface</i>) by the two internal cavities (catalytic site cavity and adjacent cavity) of human microsomal cytochrome P450 (CYP) 2C19 (<i>brown</i>). The heme prosthetic group is represented in <i>green</i> and the molecule of dapsone in the color <i>red</i> (<b>a</b>). Delimitation of the area occupied by the two internal cavities (catalytic site cavity and adjacent cavity) of the CYP2C19 (<b>b</b>).</p

Effect of the pretreatment with different concentration of resveratrol (RSV) on methemoglobin formation induced by DDS-NHOH.

<p>Erythrocytes were pretreated with different concentrations of RSV(10, 100, 200 and 1000 μM) for 1 h at 37°C, then these cells were incubated with different concentrations of DDS-NHOH (2.5; 5.0 and 7.5 μg/mL) for 1 h at 37°C. Data are reported as means ± S.E.M from three independent experiments done in triplicate. ^<b>#</b>P < 0.05 compared to DDS-NHOH group.</p