In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells

Rosyana V. Albuquerque, Nívea S. Malcher, Lílian L. Amado, Michael D. Coleman, Danielle C. dos Santos, Rosivaldo Sa. Borges, Sebastião Aldo S. Valente, Vera C. Valente, Marta Chagas Monteiro

Research output: Contribution to journalArticle

Abstract

Dapsone (DDS) hydroxylamine metabolites cause oxidative stress- linked adverse effects in patients, such as methemoglobin formation and DNA damage. This study evaluated the ameliorating effect of the antioxidant resveratrol (RSV) on DDS hydroxylamine (DDSNHOH) mediated toxicity in vitro using human erythrocytes and lymphocytes. The antioxidant mechanism was also studied using in-silico methods. In addition, RSV provided intracellular protection by inhibiting DNA damage in human lymphocytes induced by DDS-NHOH. However, whilst pretreatment with RSV (10-1000 μM significantly attenuated DDS-NHOH-induced methemoglobinemia, but it was not only significantly less effective than methylene blue (MET), but also post-treatment with RSV did not reverse methemoglobin formation, contrarily to that observed with MET. DDS-NHOH inhibited catalase (CAT) activity and reactive oxygen species (ROS) generation, but did not alter superoxide dismutase (SOD) activity in erythrocytes. Pretreatment with RSV did not alter these antioxidant enzymes activities in erythrocytes treated with DDS-NHOH. Theoretical calculations using density functional theory methods showed that DDS-NHOH has a pro-oxidant effect, whereas RSV and MET have antioxidant effect on ROS. The effect on methemoglobinemia reversion for MET was significantly higher than that of RSV. These data suggest that the pretreatment with resveratrol may decrease heme-iron oxidation and DNA damage through reduction of ROS generated in cells during DDS therapy.

LanguageEnglish
Article numbere0134768
Number of pages24
JournalPLoS ONE
Volume10
Issue number8
DOIs
Publication statusPublished - 18 Aug 2015

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dapsone
resveratrol
protective effect
Antioxidants
Cells
antioxidants
methylene blue
Methylene Blue
Reactive Oxygen Species
methemoglobinemia
DNA damage
cells
DNA Damage
Methemoglobinemia
reactive oxygen species
Methemoglobin
Hydroxylamine
erythrocytes
Lymphocytes
pretreatment

Bibliographical note

© 2015 Albuquerque et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Cite this

Albuquerque, R. V., Malcher, N. S., Amado, L. L., Coleman, M. D., dos Santos, D. C., Borges, R. S., ... Chagas Monteiro, M. (2015). In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells. PLoS ONE, 10(8), [e0134768]. https://doi.org/10.1371/journal.pone.0134768
Albuquerque, Rosyana V. ; Malcher, Nívea S. ; Amado, Lílian L. ; Coleman, Michael D. ; dos Santos, Danielle C. ; Borges, Rosivaldo Sa. ; Valente, Sebastião Aldo S. ; Valente, Vera C. ; Chagas Monteiro, Marta. / In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells. In: PLoS ONE. 2015 ; Vol. 10, No. 8.
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Albuquerque, RV, Malcher, NS, Amado, LL, Coleman, MD, dos Santos, DC, Borges, RS, Valente, SAS, Valente, VC & Chagas Monteiro, M 2015, 'In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells' PLoS ONE, vol. 10, no. 8, e0134768. https://doi.org/10.1371/journal.pone.0134768

In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells. / Albuquerque, Rosyana V.; Malcher, Nívea S.; Amado, Lílian L.; Coleman, Michael D.; dos Santos, Danielle C.; Borges, Rosivaldo Sa.; Valente, Sebastião Aldo S.; Valente, Vera C.; Chagas Monteiro, Marta.

In: PLoS ONE, Vol. 10, No. 8, e0134768, 18.08.2015.

Research output: Contribution to journalArticle

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T1 - In vitro protective effect and antioxidant mechanism of Resveratrol induced by Dapsone Hydroxylamine in human cells

AU - Albuquerque, Rosyana V.

AU - Malcher, Nívea S.

AU - Amado, Lílian L.

AU - Coleman, Michael D.

AU - dos Santos, Danielle C.

AU - Borges, Rosivaldo Sa.

AU - Valente, Sebastião Aldo S.

AU - Valente, Vera C.

AU - Chagas Monteiro, Marta

N1 - © 2015 Albuquerque et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PY - 2015/8/18

Y1 - 2015/8/18

N2 - Dapsone (DDS) hydroxylamine metabolites cause oxidative stress- linked adverse effects in patients, such as methemoglobin formation and DNA damage. This study evaluated the ameliorating effect of the antioxidant resveratrol (RSV) on DDS hydroxylamine (DDSNHOH) mediated toxicity in vitro using human erythrocytes and lymphocytes. The antioxidant mechanism was also studied using in-silico methods. In addition, RSV provided intracellular protection by inhibiting DNA damage in human lymphocytes induced by DDS-NHOH. However, whilst pretreatment with RSV (10-1000 μM significantly attenuated DDS-NHOH-induced methemoglobinemia, but it was not only significantly less effective than methylene blue (MET), but also post-treatment with RSV did not reverse methemoglobin formation, contrarily to that observed with MET. DDS-NHOH inhibited catalase (CAT) activity and reactive oxygen species (ROS) generation, but did not alter superoxide dismutase (SOD) activity in erythrocytes. Pretreatment with RSV did not alter these antioxidant enzymes activities in erythrocytes treated with DDS-NHOH. Theoretical calculations using density functional theory methods showed that DDS-NHOH has a pro-oxidant effect, whereas RSV and MET have antioxidant effect on ROS. The effect on methemoglobinemia reversion for MET was significantly higher than that of RSV. These data suggest that the pretreatment with resveratrol may decrease heme-iron oxidation and DNA damage through reduction of ROS generated in cells during DDS therapy.

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