Abstract

Abstract Background: Depression is one of the significant problems in adults that accounts for up to five percent of cases worldwide. Methods: Volunteers were divided into eight groups, and their serum samples were tested for FBG, carbonyl contents, IFN-γ and TNF-α. Reactive oxygen species (ROS) modified human serum albumin (HSA) (ROSHSA) was used as an antigen and levels of serum autoantibodies were estimated by direct binding and inhibition ELISA in all subjects. Results: Significant biophysical structural modifications were observed in ROS-HSA with increased carbonyl contents compared to native-HSA (N-HSA). Significantly high levels of carbonyl content (2.68 ± 0.33 nmol/mg protein; p > 0.001) and pro-inflammatory cytokines IFN-γ (7.4 ± 0.61 pg/ml; p > 0.001) and TNF-α (1.47 ± 0.23 pg/ml; p > 0.001) were detected in serum samples from F-D-S. Similarly, a high level of autoantibodies against ROS-HSA was observed in females who were depressed and smokers (F-D-S) group (0.89 ± 0.07; p > 0.001) compared to males who were both depressed and smokers (M-D-S) (0.66 ± 0.049). Furthermore, inhibition ELISA results exhibited high recognition of serum autoantibodies from F-D-S subjects (78.6 ± 5.7 mean maximum percentage inhibition MMPI) compared to M-D-S (58.8 ± 5.2 MMPI) subjects. Conclusion: Incoherence, long term unchecked chronic psychological stress may cause oxidation of blood proteins, which subsequently result in structural alterations of biomolecules, thus generating new-epitopes, capable of inducing autoantibodies specific for ROS-modified proteins. These autoantibodies may be a potential marker for subjects suffering from depression to understand the state of immune imbalance.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.