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.