Hyperhomocysteinemia and cardiovascular disease: The nutritional perspectives

Pandey, Rajesh; Gupta, Seema; Lal, Harbans; Mehta, Harish C.; Aggarwal, Sameer

doi:10.1007/bf02867541

Cited by 9 publications

(4 citation statements)

References 53 publications

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“…When the generation of ROS/RNS exceeds the ability of ADS to neutralize and eliminate them, such an imbalance can cause oxidative/nitrosative stress and it results in a damage to the cellular constituents (phospholipids, proteins, lipoproteins, nucleic acids and sugar) [31]. Because of this, oxidative/nitrosative stress has been implicated in cardiovascular diseases such as atherosclerosis, ischaemia/reperfusion injury, restenosis and hypertension; in cancer, in inflammatory diseases such as Acute Respiratory Distress Syndrome (ARDS), asthma, Inflammatory Bowel Disease (IBD), dermal and ocular inflammation and arthritis; in metabolic diseases, such as diabetes; in diseases of the Central Nervous System (CNS), such as Amyotrophic Lateral Sclerosis (ALS), Alzheimer's disease, Parkinson's disease and stroke, as well as in the aging processes [32,33].…”

Section: The Biochemical Basis Of the Oxidative/ Nitrossive Stress Inmentioning

confidence: 99%

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Pandey

Singh²,

Singhal³

et al. 2013

JCDR

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The understanding of the pathobiology of Chronic Obstructive Pulmonary Disease (COPD) has undergone a major change in the past three decades. The classical 'protease-antiprotease' hypothesis still holds true, nevertheless, the sequence of the biochemical events which lead to the protease/antiprotease imbalance have been unraveled. For instance, tobacco smoke, a primary risk factor for COPD, contains a plethora of reactive Oxygen/ Nitrogen Species (ROS/RNS) that serve to initiate the oxidant/ antioxidant imbalance in the respiratory tract of chronic smokers, a phenomenon that is amplified if certain other risk factors co-exist (e.g. a genetic deficiency of the major antiproteases, a suboptimal antioxidant defense system, airway hyper responsiveness etc.). The inflammatory response that ensues as a result of the initial occult exogenous oxidative/ nitrosative stress becomes a secondary endogenous source of ROS/RNS. This perpetuates the ongoing lung damage, even though the primary insult may no longer be present (abstinence). Depletion of the pulmonary antioxidants, damage to the local antiprotease protective screen, a decreased immune response, hypersecretion of mucus, superadded infections, oxygen therapy-induced oxidant production, etc. are some of the critical factors which account for the oxidative/ nitrosative stressmediated pulmonary as well as extrapulmonary features of COPD. In the light of the recent developments, remarkable efforts are being made, either to develop novel therapeutic strategies or to improve the existing ones, which are aimed at treating different aspects of the disease. Thus, it is reasonable to recommend antioxidants as a useful adjunct to the more conventional treatment options, keeping in view the 'oxidant/antioxidant' hypothesis as a unifying theme for the 'protease/antiprotease' theory of COPD. INTRODUCTIONChronic Obstructive Pulmonary Disease (COPD) is characterized by a poorly reversible airflow limitation that is usually progressive and associated with the abnormal inflammatory response of the lung to noxious particles and/ or gases which are present in cigarette smoke [1,2]. The characteristic features of the disease are chronic inflammation of the peripheral airways, chronic bronchitis and destruction of the lung parenchyma (emphysema), which include systemic extra-pulmonary manifestations [3]. The patients can suffer from one, some or all of these conditions. The peripheral airways inflammation or small-airway disease involves various morphological abnormalities such as airway narrowing with goblet cell hyperplasia, smooth muscle hypertrophy, excess mucous, oedema and inflammatory cellular infiltration. Airway remodeling with sub-epithelial and peribronchial fibrosis has been postulated as the critical factor in the small-airway narrowing and the fixed airway obstruction in the small-airways of the patients with COPD [4].Anatomically, the disease can be viewed as a part of a spectrum, with chronic bronchitis at one end and emphysema at the other. Chronic bronchitis is ...

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Section: The Biochemical Basis Of the Oxidative/ Nitrossive Stress Inmentioning

confidence: 99%

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Pandey

Singh²,

Singhal³

et al. 2013

JCDR

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“…It is well known that increasing level of homocysteine is a risk factor for cardiovascular disease and plays a significant role in the incidence of CVD [ 48 ] via different mechanisms including endothelial dysfunction, superoxide and hydrogen peroxide generation, and promoted proliferation of the aortic smooth muscle cells. However, in the present study, the level of homocysteine did not change after treatment of rats with most of N-nitrosamines except NEBA and NDMA decreased such level ( Table 1 ).…”

Section: Discussionmentioning

confidence: 99%

Novel Study on N-Nitrosamines as Risk Factors of Cardiovascular Diseases

Sheweita

El-Bendery

Mostafa

2014

BioMed Research International

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Millions of people are exposed daily to N-nitrosamines from different environmental sources. The present study aims at investigating the role of N-nitrosamines in the alteration of homocysteine, lipid profile, oxidative stress, paraoxonase activity, antioxidant enzymes, and free radicals which are important risk factors for CVD. In addition, biomarkers of cardiovascular diseases such as creatine kinase MB activity (CK-MB) and lactate dehydrogenase (LDH) as well as protein expression of both glutathione peroxidase and glutathione S-transferase π isozyme were assayed after treatment of rats with 0.2 mg/kg body weight of N-nitrosodibutylamine (NDBA), N-nitrosoethylbutylamine (NEBA), N-nitrosobutylpropylamine (NBPA), N-nitrosodiethylamine (NDEA), N-nitrosodimethylamine (NDMA), and N-nitrosodiphenylamine (NDPA) as a daily dose for two weeks. LDL levels, paraoxonase activity, reduced glutathione levels, and glutathione reductase activities were increased, whereas HDL levels decreased after treatment of rats with most of N-nitrosamines compared to control group. Moreover, levels of free radicals and catalase activity increased, whereas protein expression of both glutathione peroxidase and glutathione S-transferase decreased after treatment of rats with some N-nitrosamines. The data showed that most N-nitrosamines increased CK-MB and LDH activities. It is concluded that N-nitrosamines increased levels of free radicals, and decreased the activity of antioxidant enzymes which may consequently increase the incidence of CVDs.

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“…Homocysteine is thought to cause the oxidative stress to the vascular endothelium, impaired endothelium-dependent vasomotor regulation, reduced antithrombin III attachment to endothelium, favored affinity between lipoprotein(s) and fibrin, augmentation of tissue factor expression, and altered platelet activity. 54,[56][57][58][59][60][61] Several cases of PA with hyperhomocysteinemia-associated thrombosis have been reported in the Refs. ( 46), ( 62), (63).…”

Section: Pa Presenting With Hyperhomocysteinemia-associated Thrombosismentioning

confidence: 99%

Pernicious anemia: Pathophysiology and diagnostic difficulties

Htut

Thein

2021

J Evidence Based Medicine

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Pernicious anemia (PA) is the most common cause of vitamin B12 (cobalamin) deficiency anemia in the world. It is an autoimmune disease, comprising of salient features of autoimmune chronic atrophic gastritis (CAG) and cobalamin deficiency (CD).Although the anemia was first described as pernicious, it may well be controlled with vitamin B12 replacement. The onset and progression of PA is often insidious. Alternatively, patients may have no anemic symptoms since they become acclimatized to the subtle nature of the disease. Oftentimes, there is a possibility that the underlying disease may be missed unless a full blood count (FBC) is investigated, leading to hindrance in the treatment journey. Diagnostic challenges remain tangible for many practicing clinicians, since there is lack of reliable cobalamin assays to diagnose CD as well as clinical mimics, which simulate many other hematological conditions, such as myelodysplastic syndrome, acute leukemia, sideroblastic anemias, bone marrow failure states, thrombotic microangiopathy, and thromboembolism. Moreover, prompt recognition of the symptoms of CD is also vital, because some neurologic sequalae may become irreversible despite replenishing cobalamin. Herein, we discuss a literature review on the pathophysiology, challenging clinical presentations and diagnostic difficulties of PA.Since the cobalamin replacement therapy for PA is straightforward, it will not be discussed in this review.

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Hyperhomocysteinemia and cardiovascular disease: The nutritional perspectives

Cited by 9 publications

References 53 publications

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Novel Study on N-Nitrosamines as Risk Factors of Cardiovascular Diseases

Pernicious anemia: Pathophysiology and diagnostic difficulties

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