Nitric Oxide, Carbonyl Protein, Lipid Peroxidation in Tuberculosis
Journal name: The Malaysian Journal of Medical Sciences
Original article title: Nitric Oxide, Carbonyl Protein, Lipid Peroxidation and Correlation Between Antioxidant Vitamins in Different Categories of Pulmonary and Extra Pulmonary Tuberculosis
The Malaysian Journal of Medical Sciences (MJMS) is a peer-reviewed, open-access journal published online at least six times a year. It covers all aspects of medical sciences and prioritizes high-quality research.
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Shubhangi Mahesh Dalvi, Vinayak Wamanrao Patil, Nagsen Nirgun Ramraje, Jaising Marutrao Phadtare, Sarita Uday Gujarathi
The Malaysian Journal of Medical Sciences:
(A peer-reviewed, open-access journal)
Full text available for: Nitric Oxide, Carbonyl Protein, Lipid Peroxidation and Correlation Between Antioxidant Vitamins in Different Categories of Pulmonary and Extra Pulmonary Tuberculosis
Year: 2013
Copyright (license): CC BY 4.0
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Summary of article contents:
Introduction
Tuberculosis (TB) remains a significant global health concern, characterized by high morbidity and mortality rates, particularly in individuals of lower socioeconomic status. This study investigates the biochemical changes associated with TB, focusing on oxidative stress and its correlation with the levels of antioxidant vitamins (A, C, and E) in patients. The mechanisms by which Mycobacterium tuberculosis exacerbates oxidative and nitrosative stress through reactive oxygen and nitrogen intermediates are explored, illustrating the detrimental effects these processes have on cellular functions, including potential DNA damage and protein modification.
The Impact of Oxidative Stress on Tuberculosis Patients
Oxidative stress is a critical concept highlighted in this study, manifesting through increased levels of malondialdehyde (a product of lipid peroxidation), nitric oxide, and carbonyl proteins in TB patients. The findings reveal that oxidative stress elevates with the severity of the disease, particularly from pulmonary categories I to III, correlating with increased bacillary loads. This heightened oxidative state not only damages cellular components but also adversely affects the patients' immune response. Notably, antioxidant vitamins A, C, and E were found to be significantly reduced in TB patients, illustrating a direct link between antioxidant status and oxidative damage. Interestingly, after a six-month directly observed short-course treatment, some oxidative stress markers showed a decrease, yet the balance wasn't entirely restored, indicating ongoing challenges in recovery.
Conclusion
The study concludes that increased oxidative and nitrosative stress, along with significant reductions in antioxidant vitamins, plays a vital role in the pathophysiology of tuberculosis. Establishing the intricate connection between these stress parameters and the clinical severity of tuberculosis underscores the importance of monitoring and potentially supplementing antioxidant vitamins as part of TB management strategies. Despite improvements post-treatment, the persistence of oxidative stress exemplifies the need for continued research into supportive therapies that can help restore balance and improve patient outcomes. Overall, maintaining the equilibrium between free radical generation and neutralization is crucial for the health and recovery of tuberculosis patients.
FAQ section (important questions/answers):
What factors contribute to oxidative stress in tuberculosis patients?
Oxidative stress in tuberculosis patients is caused by lipid peroxidation, nitric oxide, and carbonyl protein formation. It is linked to the disease's severity, which increases the levels of these reactive species leading to cellular damage.
What role do antioxidant vitamins play in tuberculosis?
Antioxidant vitamins E, C, and A help neutralize oxidative stress in tuberculosis by inhibiting lipid peroxidation and protecting against free radical damage, which is essential for cellular health and immune function.
How does treatment affect oxidative stress levels in tuberculosis patients?
After six months of directly observed treatment, there was a significant decrease in oxidative stress markers. However, while improvements were noted, the oxidative stress levels did not completely return to normal.
What correlations were found between oxidative stress and vitamin levels?
Positive correlations were observed among oxidative stress markers, while negative correlations existed between these markers and antioxidant vitamin levels. This indicates a direct relationship between disease severity, oxidative stress, and vitamin deficiencies.
Other Science Concepts:
Discover the significance of concepts within the article: ‘Nitric Oxide, Carbonyl Protein, Lipid Peroxidation in Tuberculosis’. Further sources in the context of Science might help you critically compare this page with similair documents:
Tuberculosis, Financial support, Vicious cycle, Disease classification, Conflict of interest, Significant reduction, Pulmonary tuberculosis, Socio-economic status, Nutritional status, Oxidative stress, Morbidity and Mortality, Lipid peroxidation, Immune response, Vitamin C, Significant decrease, Dietary factor, Biochemical changes, Nutritional diet, Nitric oxide, Malondialdehyde, Bacterial load, Immuno-modulator, Free radical generation, Vitamin A, Immuno Suppression, Cellular function, Cell membrane, Cytotoxic effect, Biochemical reaction, Arachidonic Acid, Antitubercular treatment, Societal factors, Vitamin C levels, Free Radical, Antioxidant defence, DNA damage, Mycobacterium tuberculosis, Vitamin E, Oxidative stress parameters, Biological marker, Enzyme inhibition, Genotoxic effect, Malondialdehyde Level, Oxidative degradation, Extra-pulmonary tuberculosis, White blood cell, Carbonyl protein, Gene expression study, Protein carbonyl formation, Macrophage function, Quenching mechanisms, Reactive oxygen, Antioxidant vitamin, Medical ethical committee, Ministry of Health, Nitric Oxide Level, Reactive nitrogen intermediates, Vitamin E level, Nitrosative stress, Polyunsaturated fatty acid, Lymphoid organ, Macrophage.