Free Radicals and Tuberculosis

Tuberculosis (TB), developed by the Gram-positive bacterium Mycobacterium tuberculosis, is the prominent cause of demise globally due to high antibiotic resistance. Approximately 1.5 million people deceased of TB in 2020 worldwide. The causative pathogen of tuberculosis spreads majorly by droplets like aerosols through coughing, sneezing, or spitting, affecting alveolar macrophages inside the lungs. The tuberculosis infection prompts the development of ROS (reactive oxygen species) due to the phagocytic cells of the host. Further, TB with HIV infection induces a high level of ROS &RNS through the activation of phagocytes. Oxidative stress is developed due to an imbalance between the functionality of free ROS and associated antioxidant mechanisms. These free radicals can significantly destroy DNA, biological lipids, proteins, and other vulnerable cellular constituents. This results in an imbalance of normal redox status, physiologically increasing oxidative stress. The biological antioxidants significantly neutralize the free radicals produced via multiple physiological functions of the body, but these natural antioxidants are not adequate to scavenge the surplus reactive oxygen species. The major challenge associated with managing TB is the resistance to commonly prescribed antibiotics, developing multidrug-resistant tuberculosis. Researchers are increasing their focus on exploring novel 482combinational approaches, which can be analyzed to combat drug resistance in managing tuberculosis. The present chapter focuses on the overview of tuberculosis, pathogenesis, clinical manifestations, diagnostic assessments, free radical scavenging enzymes, the redox status of patients with tuberculosis, and new therapies based on epidemiological data and clinical studies. Also, it will correlate between free radicals and their role in the development of MDR and XDR.