DISCUSSION
Tuberculosis is major public health problem worldwide [21]. It is estimated that approximately one-third of the world’s population is living with latent TB. Until recent years, it remains as one of the most important causes of death. Therefore, biomarkers are very important for effective and accurate determinations in the diagnosis, treatment monitoring and result of tuberculosis disease. The currently available diagnostic technology for TB detection is inadequate. Novel biomarkers are needed in the prognosis and treatment process of the disease [22].
Free radical production has been described in different cancers, lung injury and pulmonary emphysema [23-26]. Also degenerative lung diseases such as tuberculosis are associated with lung oxidant-antioxidant imbalance [27]. Mycobacterium tuberculosis is intracellular pathogens, which grow and replicate in the host macrophages. It is well known that macrophages undergo respiratory burst after contact with this microorganism. Increased amounts of ROS are produced as a result of respiratory burst. ROS released from macrophages cause tissue damage in respiratory tract infections [23]. Containing sulfurous amino acid molecules are more sensitive to free radicals. The sulphurous amino acids cysteine ​​and cystine are also sensitive to free radical attack. Proteins with a large number of disulfide bonds such as IgG and albumin break down their three-dimensional structure. Thus, they can not perform their normal functions. Changes in protein structure can lead to changes in antigenicity and proteolysis. Radicals can react with membrane proteins and cause impairment of the functions of enzyme, neurotransmitter and receptor proteins [28, 29].
The plasma thiol pool mainly comprises albumin thiols and protein thiols, smaller amounts of low-molecular-weight thiols such as cysteine ​​(Cys), cysteinyl glycine, homocysteine, glutathione, and γ-glutamyl Cys [12]. Measuring plasma total thiol levels and defining thiol / disulfide homeostasis is a good indicator of excessive free radical formation in many diseases. it also provides important information about the extent of free radical-mediated oxidation that causes protein damage [14, 30].
Erel and Neselioğlu reported higher plasma disulfide levels in degenerative diseases such as obesity, pneumonia, bronchiolitis and diabetes mellitus than healthy groups; In another word, thiol / disulfide homeostasis has shifted towards disulfide [12]. Topuz et al. detected that serum thiol levels in acute pulmonary thromboembolism (APE) patients were significantly low compared to a control group and disulfide level and disulfide/total thiol ratio were higher in APE group than control group [31]. Recent studies have shown that the thiol/disulphide homeostasis is disturbed in lung diseases such as infectious pneumonia [32], obstructive sleep apnea syndrome [33], COPD, asthma [34] and silicasis [35]. Plasma total thiol levels are reduced in patients with COPD or asthma [36]. Solak et al have found NT and TT levels significantly lower in smokers in comparison with the control group [37]. In a previous study, serum SOD activities were significantly decreased in tuberculosis patients compared to healthy controls, and serum MDA levels were increased [38, 39]. This result indicates that oxidative stress is increased in patients with lung tuberculosis. Durak et al. investigated pleural fluid and serum superoxide dismutase (SOD) values ​​in patients with lung cancer, tuberculosis and heart failure, and found that pleural fluid and serum SOD values ​​of all patient groups, being the highest in the tuberculosis group, were higher than the control group values. As a result, they stated that this enzyme activity could be used as a nonspecific prognostic indicator in detecting cellular and mitochondrial tissue damage [24].
Limited data is available on the relationshipbetween thiol/disulphide homeostasis and lung diseases. Determination of dynamic thiol/disulphide status in diseases where oxidative stress plays a major role in pathogenesis would be important. There has been no report about thiol levels in lung tuberculosis patients, so far. To our knowledge, this study is the first study that investigates thiols and thiol/disulphide homeostasis in patients with lung tuberculosis. In this study, we found that native and total thiol levels were significantly decreased in patients with lung tuberculosis. We think that the ROS released from the increased macrophages in lung tuberculosis patients decrease the thiol levels by oxidizing the thiols. In this study, disulfide/native thiol and disulfide/total thiol levels were found to be higher in lung tuberculosis patients when compared with the control group. However, disulfide levels were higher in the control group than in the patient group.