Both HIV infection and Methamphetamine (Meth) use disorders are associated with greater depressive symptoms and oxidative stress; whether the two conditions would show additive or interactive effects on the severity of depressive symptoms, and whether this is related to the level of oxidative stress in the CNS is unknown. 123 participants were evaluated, which included 41 HIV-seronegative subjects without substance use disorders (Control), 25 with recent (<6 months) moderate to severe Meth use disorders (Meth), 34 HIV-seropositive subjects without substance use disorders (HIV) and 23 HIV+Meth subjects. Depressive symptoms were assessed with the Center for Epidemiologic Studies-Depression Scale (CES-D), and oxidative stress markers were evaluated with glutathione (GSH), 4-hydroxynonenal (HNE), and activities of gamma-glutamyltransferase (GGT) and glutathione peroxidase (GPx) in the cerebrospinal fluid (CSF). Compared with Controls, HIV subjects had higher levels of HNE (+350 %) and GGT (+27 %), and lower level of GSH (−34 %), while Meth users had higher levels of GPx activity (+23 %) and GSH (+30 %). GGT correlated with GPx, and with age, across all subjects (p < 0.0001). CES-D scores correlated with CSF HNE levels only in Control and HIV groups, but not in Meth and HIV+Meth groups. HIV and Meth use had an interactive effects on depressive symptoms, but did not show additive or interactive effects on oxidative stress. The differential relationship between depressive symptoms and oxidative stress response amongst the four groups suggest that depressive symptoms in these groups are mediated through different mechanisms which are not always related to oxidative stress.
Bibliographical noteFunding Information:
This study was made possible by National Institutes of Health grants U54NS56883 (SNRP), 5P20RR016467-11 and 8P20GMl03466-11 (INBRE II), 5G12RR003061, 8G12MD007601 (RCMI/BRIDGES), 2R24DA027318 (DIDARP) and 2K24DA016170 (to LC). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Author contributions: J.P. designed the experiments reported herein, interpreted the data, and contributed to the writing of the manuscript. X. P. performed all the assays from the CSF, analyzed the data, and contributed to the writing of the manuscript. S. M. contributed to subject recruitment and evaluation, CSF preparation and organized and presented the clinical data collected from the participants. M.J. B. supervised the study and edited the manuscript. L.C. designed and directed all clinical aspects of this study, collected the CSF samples, and critically reviewed and edited the manuscript and interpreted the data. We would like to thank Ms. Caroline Jiang and Mr. Ahnate Lim for their assistance in statistical analysis, and thank Dr. Vanessa Douet for her assistance in the quality assurance of the clinical data.
© 2015, Springer Science+Business Media New York.
- Oxidative stress