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].