INTRODUCTION
Mycobacterium tuberculosis (MTB), the etiological agent of tuberculosis
(TB), infects nearly a quarter of the world’s population and remains the
leading cause of death by a single pathogen [1]. The vast majority
of this infection settles in the lungs. Transmission occurs from an
infected person to another person via droplets or with coughing up blood
or contaminated sputum [2].
It derived most of the radicals formed in the human body from oxygen
[3]. 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 [4]. Oxidative stress (OS) arises because of an
imbalance between the free reactive oxygen species (ROS) and the
antioxidant mechanisms [5,6]. 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.
There is a higher risk of OS in the lung compared to other organs
[7,8]. Excess formation of ROS can start a series of chemical
reactions and cause damage to cellular components, including proteins,
lipids, and nucleic acids [5,9]. Many studies have linked OS to
various lung disorders, including asthma, chronic obstructive pulmonary
disease (COPD), acute pulmonary distress syndrome, and TB [10,11].
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 [12]. As an immune response, the infected macrophage
starts a respiratory burst and produces high levels of ROS to counteract
and kill the mycobacteria [13] MTB infection can induce oxidative
stres [14].
There are various biochemical markers used to identify OS and
inflammation. One of these markers is ischemia-modified albumin. Albumin
plays a major role in regulating oncotic pressure with antioxidant,
anti-inflammatory, and antithrombotic effects [15]. In case of
oxidative stress, certain alterations occur in the N terminal portion of
albumin, leading to reduced binding to heavy metals such as copper and
cobalt. This new chemical structure of albumin is termed as ischemia
modified albumin (IMA) [16]. The IMA was first identified in the
early 1990s and has since been widely studied in patients presenting
with myocardial ischemia IMA is one of the earliest predictors of
ischemia [17,18]. However, new studies have shown that IMA, which is
evaluated as a cardiac ischemia marker, may also increase in different
pathologies and affect other organs [19]. Studies on patients with
acute mesenteric ischemia, pulmonary embolism, cardiopulmonary
resuscitation, end-stage renal failure cerebrovascular ischemia,
systemic sclerosis, arthroscopic knee surgery, post-exercise skeletal
ischemia and diabetes mellitus have reported increased serum IMA level
[20].
The goal of this study was to evaluate IMA as a novel marker of OS in TB
patients and to investigate changes occurring in patients.