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Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients

OBJECTIVE: To investigate the link between Human Herpesvirus 8 (HHV8) infection and plasma oxidative stress in patients with diabetes mellitus type 2 (DM2). RESULTS: Blood samples collected from DM2 and control subjects were screened for the presence of antibodies against HHV8 and for biomarkers of...

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Autores principales: Incani, Alessandra, Marras, Luisa, Serreli, Gabriele, Ingianni, Angela, Pompei, Raffaello, Deiana, Monica, Angius, Fabrizio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020602/
https://www.ncbi.nlm.nih.gov/pubmed/32054515
http://dx.doi.org/10.1186/s13104-020-4935-3
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author Incani, Alessandra
Marras, Luisa
Serreli, Gabriele
Ingianni, Angela
Pompei, Raffaello
Deiana, Monica
Angius, Fabrizio
author_facet Incani, Alessandra
Marras, Luisa
Serreli, Gabriele
Ingianni, Angela
Pompei, Raffaello
Deiana, Monica
Angius, Fabrizio
author_sort Incani, Alessandra
collection PubMed
description OBJECTIVE: To investigate the link between Human Herpesvirus 8 (HHV8) infection and plasma oxidative stress in patients with diabetes mellitus type 2 (DM2). RESULTS: Blood samples collected from DM2 and control subjects were screened for the presence of antibodies against HHV8 and for biomarkers of oxidative stress. We determined the products of radical damage on the plasma lipid fraction, such as malondialdehyde (MDA), fatty acid hydroperoxides (HP) and 7-ketocholesterol (7-keto), the oxidation products of unsaturated fatty acids (UFA) and cholesterol, respectively. The level of plasma antioxidant α-tocopherol (α-toc) was also assessed. Relevant differences were observed in the redox status in DM2 and either HHV8-positive or -negative control subjects. The level of α-toc significantly decreased in both DM2 and HHV8-positive subjects. Levels of MDA, HP and 7-keto were much higher in HHV8-positive and DM2 subjects, indicating that plasma oxidative stress is a common feature in both DM2 and HHV8-infection. In addition, 7-keto was further increased in HHV8-positive DM2 patients. We hypothesized that the HHV8-infection may contribute to the production of ROS, and hence to the oxidative stress closely related to the pathogenesis and development of DM2.
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spelling pubmed-70206022020-02-20 Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients Incani, Alessandra Marras, Luisa Serreli, Gabriele Ingianni, Angela Pompei, Raffaello Deiana, Monica Angius, Fabrizio BMC Res Notes Research Note OBJECTIVE: To investigate the link between Human Herpesvirus 8 (HHV8) infection and plasma oxidative stress in patients with diabetes mellitus type 2 (DM2). RESULTS: Blood samples collected from DM2 and control subjects were screened for the presence of antibodies against HHV8 and for biomarkers of oxidative stress. We determined the products of radical damage on the plasma lipid fraction, such as malondialdehyde (MDA), fatty acid hydroperoxides (HP) and 7-ketocholesterol (7-keto), the oxidation products of unsaturated fatty acids (UFA) and cholesterol, respectively. The level of plasma antioxidant α-tocopherol (α-toc) was also assessed. Relevant differences were observed in the redox status in DM2 and either HHV8-positive or -negative control subjects. The level of α-toc significantly decreased in both DM2 and HHV8-positive subjects. Levels of MDA, HP and 7-keto were much higher in HHV8-positive and DM2 subjects, indicating that plasma oxidative stress is a common feature in both DM2 and HHV8-infection. In addition, 7-keto was further increased in HHV8-positive DM2 patients. We hypothesized that the HHV8-infection may contribute to the production of ROS, and hence to the oxidative stress closely related to the pathogenesis and development of DM2. BioMed Central 2020-02-13 /pmc/articles/PMC7020602/ /pubmed/32054515 http://dx.doi.org/10.1186/s13104-020-4935-3 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Note
Incani, Alessandra
Marras, Luisa
Serreli, Gabriele
Ingianni, Angela
Pompei, Raffaello
Deiana, Monica
Angius, Fabrizio
Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title_full Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title_fullStr Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title_full_unstemmed Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title_short Human Herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
title_sort human herpesvirus 8 infection may contribute to oxidative stress in diabetes type 2 patients
topic Research Note
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7020602/
https://www.ncbi.nlm.nih.gov/pubmed/32054515
http://dx.doi.org/10.1186/s13104-020-4935-3
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