Incani Alessandra, Marras Luisa, Serreli Gabriele, Ingianni Angela, Pompei Raffaello, Deiana Monica, Angius Fabrizio
Unit of Experimental Pathology, Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Section of Applied Microbiology, Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
BMC Res Notes. 2020 Feb 13;13(1):75. doi: 10.1186/s13104-020-4935-3.
To investigate the link between Human Herpesvirus 8 (HHV8) infection and plasma oxidative stress in patients with diabetes mellitus type 2 (DM2).
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.
探讨2型糖尿病(DM2)患者中人类疱疹病毒8(HHV8)感染与血浆氧化应激之间的联系。
对从DM2患者和对照受试者采集的血样进行HHV8抗体检测以及氧化应激生物标志物检测。我们测定了血浆脂质部分的自由基损伤产物,如丙二醛(MDA)、脂肪酸氢过氧化物(HP)和7-酮胆固醇(7-keto),它们分别是不饱和脂肪酸(UFA)和胆固醇的氧化产物。还评估了血浆抗氧化剂α-生育酚(α-toc)的水平。在DM2患者以及HHV8阳性或阴性对照受试者的氧化还原状态中观察到了相关差异。在DM2患者和HHV8阳性受试者中,α-toc水平均显著降低。HHV8阳性患者和DM2患者的MDA、HP和7-keto水平要高得多,表明血浆氧化应激是DM2和HHV8感染的共同特征。此外,HHV8阳性的DM2患者中7-keto水平进一步升高。我们推测,HHV8感染可能导致活性氧的产生,进而导致与DM2发病机制和发展密切相关的氧化应激。