Variations of Serum Oxidative Stress Biomarkers under First-Line Antituberculosis Treatment: A Pilot Study

Abstract

Tuberculosis (TB) is one of the highest infectious burdens worldwide, and pathogenesis is yet incompletely elucidated. Bacilli dissemination is due to poor antioxidant defense mechanisms and intensified oxidative stress. There are few recent studies that analyzed and compared free radicals or antioxidant status before and after anti-TB treatment. Hence, the present study underlines the need to identify oxidative stress as it could be a useful tool in TB monitorisation. Thirty newly diagnosed patients with pulmonary TB were included after signing an informed consent. Blood was collected before receiving first-line anti-tubercular therapy (T0) and after 60 days (T2). Spectrophotometric methods were used to quantify oxidative parameters (TBARS—thiobarbituric acid reactive species); enzymatic antioxidants such as SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), and TAC (total antioxidant capacity); and non-enzymatic antioxidants such as GSH (reduced glutathione). A moderate positive correlation was found between GSH and TAC (r = 0.63, p-value = 0.046) and GSH and SOD (r = 0.64, p-value = 0.041) at T2. Increased values of GSH, CAT, and SOD were noted at T2 in comparison with T0, while GPx, TAC, and TBARS decreased at T2. A better monitorisation in TB could be based on oxidative stress and antioxidant status. Nevertheless, restoring redox host balance could reduce TB progression.

Oxidative Stress and Inflammatory Mediators in Exhaled Breath Condensate of Patients with Pulmonary Tuberculosis. A Pilot Study with a Biomarker Perspective

“…Circulating antioxidant effectors are insufficient to counteract the oxidative stress in TB, and free radicals presumably accumulate within pulmonary tissue attacking membrane lipids, leading to lipid peroxidation [30,31]. Here, we confirm a deficiency in the antioxidant system at the alveolar level in TB.…”

“…We also found this GSH reduction in the serum. The reduction in the circulating levels of antioxidant molecules such as GSH and others has been reported in TB [7,31,32].…”

“…Oxidative stress is provoked by exacerbating ROS production through the respiratory burst and reducing the antioxidant effectors [30,31]. This condition affects normal lung function and the host immune responses contributing to disease pathogenesis due to the inability to remove the oxidative burden properly, ultimately generating pulmonary dysfunction [7,31].…”

Screening performance of C-reactive protein for active pulmonary tuberculosis in HIV-positive patients: A systematic review with a meta-analysis

“…The particularity of PTB lies in the immunological fight between M.tb. and the host, based on the interaction of bacterial strains and inflammatory biomarkers released by macrophages, monocytes, neutrophils, and lymphocytes ( 30 – 34 ). C-reactive protein (CRP) is also a non-specific biomarker in TB, with highly increased plasmatic concentrations, due to sputum bacillary load and severity of inflammation ( 30 , 35 ).…”

The Role and Mechanism of Oxidative Stress and Nuclear Receptors in the Development of NAFLD

“…Under conditions of normal antioxidant homeostasis, cells can effectively remove physiological ROS through protection systems consisting of enzymatic and nonenzymatic components. Some of the most relevant enzymes that detoxify ROS are superoxide dismutases (SODs), catalase (CAT), and glutathione peroxidase and reductase (GSH-Px) [ 18 ]. The nonenzymatic components including some small molecules such as vitamin A/C/E and glutathione act as cell structures or electron receptors against the damage from free radicals [ 19 ].…”