Distinct gene expression patterns of mono-isoniazid resistant Mycobacterium tuberculosis uncover divergent responses to isoniazid in host-mimicked condition.

Isoniazid stands as a frontline antibiotic utilized in the treatment of tuberculosis (TB), predominantly impacting the mycolic acid component within the cell wall of Mycobacterium tuberculosis (Mtb). It also affects the formation of lipoarabinomannan (LAM), an essential glycolipid in the cell envelope of Mtb. Despite the effectiveness of antibiotics for TB treatment, drug tolerance development in mycobacteria frequently stems from their adaptation to the hostile environment within the host, leading to treatment failure.

Adaptation in Response to Isoniazid Treatment in a Multi-Stress System That Mimics the Host Environment.

Isoniazid (INH) is an antibiotic that is widely used to treat tuberculosis (TB). Adaptation to environmental stress is a survival strategy for and is associated with antibiotic resistance development. Here, mycobacterial adaptation following INH treatment was studied using a multi-stress system (MS), which mimics host-derived stress.

The Regulation of ManLAM-Related Gene Expression in with Different Drug Resistance Profiles Following Isoniazid Treatment.

Introduction: Tuberculosis (TB) caused by (MTB) remains a global health concern because of the development of drug resistance. The adaptability of MTB in response to a variety of environmental stresses is a crucial strategy that supports their survival and evades host defense mechanisms. Stress regulates gene expression, particularly virulence genes, leading to the development of drug tolerance.

Effects of ascorbic acid supplementation on oxidative stress markers in healthy women following a single bout of exercise.

Background: Ascorbic acid is a water-soluble chain breaking antioxidant. It scavenges free radicals and reactive oxygen species (ROS), which are produced during metabolic pathways. Exercise can produce an imbalance between ROS and antioxidants, leading to oxidative stress-related tissue damages.