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Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin

Cypermethrin (CYP), a synthetic pyrethroid is a common environmental toxicant owing to its wide usage as a broad-spectrum insecticide. Its exposure to non-target organisms, including man, elicits numerous adverse effects making it a major public health issue. Epicatechin (EC) has proven anti-oxidati...

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Autores principales: Afolabi, Olusegun Kayode, Aderibigbe, Felix Adesola, Folarin, Dasola Teslim, Arinola, Abimbola, Wusu, Adedoja Dorcas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700339/
https://www.ncbi.nlm.nih.gov/pubmed/31440603
http://dx.doi.org/10.1016/j.heliyon.2019.e02274
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author Afolabi, Olusegun Kayode
Aderibigbe, Felix Adesola
Folarin, Dasola Teslim
Arinola, Abimbola
Wusu, Adedoja Dorcas
author_facet Afolabi, Olusegun Kayode
Aderibigbe, Felix Adesola
Folarin, Dasola Teslim
Arinola, Abimbola
Wusu, Adedoja Dorcas
author_sort Afolabi, Olusegun Kayode
collection PubMed
description Cypermethrin (CYP), a synthetic pyrethroid is a common environmental toxicant owing to its wide usage as a broad-spectrum insecticide. Its exposure to non-target organisms, including man, elicits numerous adverse effects making it a major public health issue. Epicatechin (EC) has proven anti-oxidative and anti-inflammatory properties. The present study was undertaken to evaluate the protective efficacy of epicatechin with regards to altered oxidative and inflammatory parameters subsequent to CYP treatment in rats. Animals were divided into four groups. The first group served as the control, while groups 2, 3, and 4 were orally treated with EC (30 mg kg(−1) body weight), CYP (25 mg kg(−1) body weight), and CYP plus EC, respectively. Oral administration of CYP for 14 days increased the levels of oxidative stress markers such as malondialdehyde, lipid hydroperoxides, and advanced oxidized protein products in the liver and kidney. These were accompanied by a decrease in glutathione and total antioxidant capacity levels. The activity of the enzyme superoxide dismutase was increased while catalase and glutathione peroxidase activities were decreased in these organs. Moreover, CYP increased plasma levels of the pro-inflammatory cytokines, interleukin-6 and tumor necrosis factor alpha. The plasma content of the nitrative nucleic acid marker, 8-nitroguanine was also markedly elevated by CYP. Administration of EC to CYP-exposed rats mitigated the induced oxidative and inflammatory effects. These data suggest that EC can attenuate the toxic effects induced by CYP exposure.
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spelling pubmed-67003392019-08-22 Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin Afolabi, Olusegun Kayode Aderibigbe, Felix Adesola Folarin, Dasola Teslim Arinola, Abimbola Wusu, Adedoja Dorcas Heliyon Article Cypermethrin (CYP), a synthetic pyrethroid is a common environmental toxicant owing to its wide usage as a broad-spectrum insecticide. Its exposure to non-target organisms, including man, elicits numerous adverse effects making it a major public health issue. Epicatechin (EC) has proven anti-oxidative and anti-inflammatory properties. The present study was undertaken to evaluate the protective efficacy of epicatechin with regards to altered oxidative and inflammatory parameters subsequent to CYP treatment in rats. Animals were divided into four groups. The first group served as the control, while groups 2, 3, and 4 were orally treated with EC (30 mg kg(−1) body weight), CYP (25 mg kg(−1) body weight), and CYP plus EC, respectively. Oral administration of CYP for 14 days increased the levels of oxidative stress markers such as malondialdehyde, lipid hydroperoxides, and advanced oxidized protein products in the liver and kidney. These were accompanied by a decrease in glutathione and total antioxidant capacity levels. The activity of the enzyme superoxide dismutase was increased while catalase and glutathione peroxidase activities were decreased in these organs. Moreover, CYP increased plasma levels of the pro-inflammatory cytokines, interleukin-6 and tumor necrosis factor alpha. The plasma content of the nitrative nucleic acid marker, 8-nitroguanine was also markedly elevated by CYP. Administration of EC to CYP-exposed rats mitigated the induced oxidative and inflammatory effects. These data suggest that EC can attenuate the toxic effects induced by CYP exposure. Elsevier 2019-08-09 /pmc/articles/PMC6700339/ /pubmed/31440603 http://dx.doi.org/10.1016/j.heliyon.2019.e02274 Text en © 2019 Published by Elsevier Ltd. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Afolabi, Olusegun Kayode
Aderibigbe, Felix Adesola
Folarin, Dasola Teslim
Arinola, Abimbola
Wusu, Adedoja Dorcas
Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title_full Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title_fullStr Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title_full_unstemmed Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title_short Oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
title_sort oxidative stress and inflammation following sub-lethal oral exposure of cypermethrin in rats: mitigating potential of epicatechin
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700339/
https://www.ncbi.nlm.nih.gov/pubmed/31440603
http://dx.doi.org/10.1016/j.heliyon.2019.e02274
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