Serum malanodialdehyde (TBA reactive substance) levels in cigarette smokers

Nadiger, H. A.; Mathew, Cherian; Sadasivudu, B.

doi:10.1016/0021-9150(87)90056-6

Cited by 29 publications

(13 citation statements)

References 5 publications

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“…Lipid peroxidation products acid-reacting substances) were increased in the plasma and lung lavages of healthy cigarette smokers (24,166,(199)(200)(201)(202)(203)(204)(205)(206), and patients with emphysema, chronic bronchitis, and asthma (203)(204)(205). In addition, increased LPO products correlated in versely with the time elapsed from the last exposure to to bacco smoke and the degree of small airway obstruction in COPD patients (205).…”

Section: Dna Damagementioning

confidence: 98%

Oxidative Stress in Chronic Obstructive Pulmonary Disease

Repine

Bast

Lankhorst

1997

Am J Respir Crit Care Med

746

428

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Section: Dna Damagementioning

confidence: 98%

Oxidative Stress in Chronic Obstructive Pulmonary Disease

Repine

Bast

Lankhorst

1997

Am J Respir Crit Care Med

746

428

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“…7 Malondialdehyde (MDA) is the end product of lipid peroxidation and reflects the oxidative status of the biological system 8 which causes damage to LDL molecules. The oxidized LDL is taken up by macrophages via scavenger receptors and form foam cells 9 resulting in atherogenesis.…”

Section: Introductionmentioning

confidence: 99%

Role of dyslipidaemia and lipid peroxidation in pregnancy induced hypertension

Saxena¹,

Thimmaraju²,

Srivastava³

et al. 2015

J Clin Sci Res

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Background: Pregnancy induced hypertension (PIH) contributes greatly to maternal morbidity and mortality. Altered lipid profile and increased lipid peroxidation activate endothelial dysfunction and atherothrombosis leading to PIH. Therefore, estimation of lipid profile with serum malondialdehyde (MDA) in pregnancy may be helpful in predicting the development of PIH and further progression. Material and methods:In this prospective case-control study, serum lipid profile and MDA were estimated in 70 PIH subjects with gestational hypertension, pre-eclampsia, eclampsia; and 70 normotensive pregnant women aged 18 -40 years, with gestational age of over 20 weeks.Results: A statistically significant higher serum total cholesterol, very low density lipoprotein cholesterol (VLDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides (TG), TC/HDL-C, LDL-C/HDL-C and MDA, and a significantly lower HDL-C was noted in PIH subjects as compared to control subjects. When compared with the severity of PIH, all the lipoproteins (except HDL-C) along with MDA were found to be higher in women with eclampsia when compared with gestational hypertension, pre-eclampsia and normotensive pregnant women. Conclusions:An abnormal lipid metabolism along with oxidative stress may add to the promotion of vascular dysfunction leading to PIH. Lipoproteins and MDA alter significantly in eclampsia. Therefore, during pregnancy, early diagnosis and management of dyslipidaemia may prevent lipid peroxidation and progression of PIH thereby preventing obstetric complications.

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“…This indicates that self defense mechanisms in the lung did not sufficiently protect the respiratory system from smoke mediated oxidative injury because TBA reactive substances have been used as a convenient index of the oxidative damage to tissues. Serum MDA levels are higher in smokers than in non-smokers (Nadiger et al 1987;Kalra et al 1991). Red blood cells of smokers have increased levels of GPXase and catalase when compared with cells from non-smokers (Toth et al 1986).…”

Section: Discussionmentioning

confidence: 95%

Effect of subchronic administration of antioxidants against cigarette smoke exposure in rats

et al. 1993

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Effects of subchronic administration of antioxidants against pulmonary damage mediated by cigarette smoke were investigated in rats. Rats were continuously received ascorbic acid, N-acetylcysteine and ginseng extract together drinking water from day 25 after birth. After 30 days of antioxidant supplementation, rats were exposed to cigarette smoke generated from six cigarettes (11 mg tar) for 20 min per day throughout 30 days, and then several biochemical markers related to the redox status in vivo were analyzed in the respiratory system. The cigarette smoke induced mild histological changes in trachea and lungs. The activity of superoxide dismutase (SOD) in the lung was significantly increased, and catalase and glutathione peroxidase activities were increased less than SOD, but total sulfhydryl compounds (Total-SH) content was decreased by cigarette smoking. In spite of the increase in activities of antioxidant enzymes, the inhibitory capacity of lung preparations on in vitro lipid peroxidation using ox brain homogenates was decreased and the change in the capacity was not related to the changes of these intracellular enzymes activities, but with the content of Total-SH. On the other hand, the content of thiobarbituric acid reactive substances and the ratio of elastase to anti-protease in the lung homogenates were significantly increased. Supplementation of antioxidants, however, effectively attenuated all of such alterations induced by cigarette smoke. These results indicate that although cigarette smoking induces antioxidant enzymes in the lung as a self defense mechanism, it seems to be not sufficient to protect the pulmonary system, and that chronic antioxidant feeding could be effective to reduce pulmonary damage induced by free radicals.

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Serum malanodialdehyde (TBA reactive substance) levels in cigarette smokers

Cited by 29 publications

References 5 publications

Oxidative Stress in Chronic Obstructive Pulmonary Disease

Oxidative Stress in Chronic Obstructive Pulmonary Disease

Role of dyslipidaemia and lipid peroxidation in pregnancy induced hypertension

Effect of subchronic administration of antioxidants against cigarette smoke exposure in rats

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