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High Altitude-Induced Oxidative Stress, Rheumatoid Arthritis, and Proteomic Alteration

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High Altitude Sickness – Solutions from Genomics, Proteomics and Antioxidant Interventions

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Abstract

Oxidative stress is the disruption in the equilibrium between the production of pro-oxidants such as peroxynitrite (ONOO−), reactive oxygen species (ROS), reactive nitrogen species (RNS), and superoxide anion (.O2−), etc. and antioxidants such as catalase, dismutase, etc. Two major sources of oxidative stress are endogenous and exogenous. Enhanced hyperoxia or aerobic metabolism is assumed to have high levels of reactive oxygen and nitrogen species (RONS) that have a high ability to oxidative damage to the lipids, DNA, and protein. High altitude increased the generation of ROS or reduced antioxidants that are the major causes of oxidative damage to macromolecules. Excess supply of oxygen can increase mitochondrial ROS production. In hypoxia, the mitochondrial electron transport system causes the generation of ROS. Short- and long-term exposure to hypoxia can enhance the level of oxidative stress. Rheumatoid arthritis (RA) is a chronic autoimmune condition that can cause joint damage and deterioration of the bone. Oxidative stress in RA includes various causes such as the irregular distribution of adhesive molecules, autophagy induction, and synoviocyte resistance for apoptosis. Several hours of exposure to higher humidity and reduced pressure have a major worse effect on RA. In vivo, ex vivo, and in-cell oxidative stress can be calculated using various instruments such as flow cytometry, fluorescence microplate reader, and confocal microscopy, etc. Increased altitude is related to physiological responses to hypobaric hypoxia stress by an increment in oxygen supply and usage of oxygen for tissue via metabolic modulation.

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Abbreviations

5-LO:

5-Lipoxygenase

AGE:

Advanced glycation end product

AOPP:

Advanced oxidation of protein products

CL-HPLC:

Chemiluminescence-high performance liquid chromatography

CPT1B:

Carnitine palmitoyltransferase 1

CT:

3-Chlorotyrosine

CYP2E1:

Cytochrome P450 2E1

DAF-2DA:

Diaminofluorescein diacetate

DCF:

Dichlorofluorescein

DCFDA:

Dichlorofluorescein diacetate

DHR:

Dihydrorhodamine 123

DPPP:

Diphenyl-1-pyrenylphosphine

ESR:

Electron spin resonance

FAO:

Fatty acid oxidation

GSH:

Glutathione

HIF:

Hypoxia Induce factor

IgG:

Immunoglobulin

IR:

Ionization Radiation

LDH:

Lactate Dehydrogenase

MBL:

Mannose-Binding Lectin

MDA:

Malondialdehyde

NO:

Nitric oxide

NQO:

Quinine oxidoreductase

OA:

Osteoarthritis

PC:

Protein carbonyls

PCOOH:

Phosphatidylcholine

PEOOH:

Phosphatidylethanolamine

PPARα:

Peroxisome proliferator-activated receptor α

RA:

Rheumatoid Arthritis

ROS:

Reactive Oxygen Species

SOD:

Superoxide dismutase

TBARS:

Thiobarbituric acid reactive substances

TLRs:

Toll-like receptors

TRX:

Thioredoxin

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Authors and Affiliations

  1. Department of Biotechnology, Indian Institute of Technology Roorkee, Roorkee, Uttarakhand, India

    Vikram Dalal & Vishakha Singh

  2. Department of Genomics and Molecular Medicine, CSIR-Institute of Genomics and Integrative Biology, New Delhi, Delhi, India

    Sagarika Biswas

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  1. Vikram Dalal
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Correspondence to Sagarika Biswas .

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  1. Department of Bioscience and Biotechnology, Banasthali Vidyapith, Tonk, Rajasthan, India

    Narendra Kumar Sharma

  2. National Institute of Malaria Research, Indian Council of Medical Research, New Delhi, India

    Aditya Arya

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Dalal, V., Singh, V., Biswas, S. (2022). High Altitude-Induced Oxidative Stress, Rheumatoid Arthritis, and Proteomic Alteration. In: Sharma, N.K., Arya, A. (eds) High Altitude Sickness – Solutions from Genomics, Proteomics and Antioxidant Interventions. Springer, Singapore. https://doi.org/10.1007/978-981-19-1008-1_4

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