INTRODUCTION
Tuberculosis (TB) is a chronic, necrotic infection created by a group of mycobacteria, defined primarily as Mycobacterium tuberculosis (MTB) complex in all organs of the body, primarily the lung [1]. TB is a communicable disease that is a major cause of ill health, one of the top 10 causes of death worldwide and the leading cause of death from a single infectious agent (ranking above HIV/AIDS) according to World Health Organization (WHO) report in 2019 [2]. Lung tuberculosis is tuberculosis which attacks the lung tissue. Transmission generally occurs from an infected person to another person via droplets or with coughing up blood or contaminated sputum [3].
Most of the radicals formed in the human body are derived from oxygen [4]. The formation of highly reactive oxygen containing molecular species is a normal consequence of a variety of essential biochemical reactions. In healthy conditions at the cellular level, there is a critical balance exists between the free radical generation and the antioxidant defense [5]. Oxidative stress is excessive exposure to oxidant and / or decreased antioxidant capacity. Free radicals react with many organic and inorganic compounds, including polyunsaturated fatty acids of DNA, protein and cell phospholipids. Free radicals play a role in the pathogenesis of many diseases such as atherosclerosis, neurodegenerative diseases, cancer, allergies, diabetes, cataracts [6, 7].
Lung is the organ most affected by oxidants because it is under the influence of air pollution and blood-borne oxidants. It is also the organ that meets the most oxygen. It was observed that oxidative stress was increased in tuberculosis, and it was stated in the researches that the incidence of lung cancer was higher, especially in patients with chronic lung tuberculosis [8].
The oxidative environment normally helps to kill pathogenic microorganisms. However, in the intracellular pathogen of MTB, the opposite can grow well in macrophages in environments with high oxygen concentrations [9]. Macrophages undergo respiratory burst upon contact with this microorganism. These cells are capable of producing large amounts of reactive oxygen species (ROS) [10]. MTB infection can induce oxidative stres [11].
Recent studies have revealed significant correlations between oxidative stress (OS) and certain diseases. There are various biochemical markers used with the aim of identifying OS and inflammation. One of these markers is dynamic thiol/disulphide balance. Thiol / disulphite homeostasis (TDH) plays a critical role in many cellular activities such as antioxidant protection, detoxification, cell growth, aopoptosis, signal transduction, and enzyme activities [12, 13]. Thiols, forming a significant proportion of total antioxidants in the body. They are compositions containing sulfur and play a substantial role in aiding the body’s defense versus reactive oxygen species. Plasma thiols scavenge free radicals through a variety of mechanisms. They are commonly accepted as playing a physiologic role by acting as antioxidants [14].
There is increasing evidence showing that abnormal thiol/disulphide homeostasis situations play a role in pathogenesis of a variety of diseases such as diabetes, cancer, cardiovascular disease, chronic kidney disease, liver disorder and autoimmune subclinical hypothyroidism (Hashimoto thyroiditis) [15-20].