[28] Lipid peroxidation-induced membrane structural alterations

Ginkel, G. van; Sevanian, Alex

doi:10.1016/s0076-6879(94)33031-x

Cited by 118 publications

(50 citation statements)

References 22 publications

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“…Free radical induced lipid peroxidation causes a loss of cell homeostasis by modifying the structure and functions of cell membrane. The most important characteristic of lipid peroxidation is to cause a considerable DNA-MDA adducts by interacting with cellular DNA [16,17]. The decrease in lipid peroxidation recorded as the final result in our study thus may be due to radical scavenging activity of anti oxidants.…”

Section: Does Antioxidant Therapy Influence Lipid Peroxidase?supporting

confidence: 55%

Role of Measurement of Antioxidant Enzymes in Evaluation of Antioxidant Therapy in Tobacco Abusers with Oral Leukoplakia

Jain

Singh

et al. 2011

Indian J Otolaryngol Head Neck Surg

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Antioxidants are widely used in chemoprevention of malignancy. Numerous studies in medical literature have reported the evaluation of this treatment protocol by indirect methodology-epidemiology, invitro studies, pharmacology and animal models etc. However, there is a paucity of literature on the measurement of antioxidant enzymes as a parameter for assessing the outcome of antioxidant therapy. This study explores the efficacy and outcome of antioxidant enzyme assay in relation to antioxidant therapy in tobacco abusers, hitherto unreported in medical literature. A prospective cohort study with control in 50 patients carried out at a tertiary care teaching Institution (Institute of Medical Sciences, Banaras Hindu University, Varanasi, India). Out of these patients, 10 patients acted as control, rest 40 patients-all tobacco users in some form, were divided into three groups on the basis of histopathological grading of dysplasia-no dysplasia, mild or moderate dysplasia. The levels of Lipid peroxidase (LPO), Superoxide dismutase (SOD) and Catalase (CAT) in mucosa and serum were assayed in each group, and re-evaluated at the end of 3 months after intervention with antioxidant treatment. To detect any alteration in degree of dysplasia a repeat biopsy was also done at the end of 3 months. The results were statistically analysed using paired t test. A statistically significant decrease in level of LPO and SOD, and an increase in CAT levels were recorded both in mucosa and serum. However, no change in dysplasia and no new case of dysplasia were observed. Further, antioxidant treatment was continued for a year and the final out come of the lesion was assessed by ''Carter's criteria''. A final success rate of 74.19% was recorded in terms of partial or complete regression of the lesion. This study confirms the therapeutic efficacy of antioxidants in oral leukoplakia, and cites the importance of LPO, SOD and CAT in evaluating the efficacy of antioxidant treatment. However, the study failed to elucidate any relationship between enzyme measurement and the final outcome of the lesion.

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Section: Does Antioxidant Therapy Influence Lipid Peroxidase?supporting

confidence: 55%

Role of Measurement of Antioxidant Enzymes in Evaluation of Antioxidant Therapy in Tobacco Abusers with Oral Leukoplakia

Jain

Singh

et al. 2011

Indian J Otolaryngol Head Neck Surg

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“…By-products of lipid peroxidation can change the properties of the red blood cell membrane including permeability, fluidity, and membrane enzyme activities and ultimately cell dysfunction or cell death can develop. 39 In this study, we investigated the role of oxidative stress in the pathogenesis of leukemia by measuring plasma PON1 enzyme activity. When compared with the control group, we found significantly lower PON1 activities in leukemic patients.…”

Section: Resultsmentioning

confidence: 99%

Association Between PON1 L55M Polymorphism and PON1 Enzyme Activity in Patients with Leukemia.

Eras¹,

Tombak²,

Yalın³

et al. 2017

UHOD

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Paraoxonase 1 (PON1) is an important antioxidant enzyme which has a role in preventing the effects of systemic oxidative stress. The purpose of our study was to investigate the possible association between PON1 L55M polymorphism and leukemia development and to determine the relationship between PON1 genotypes and PON1 enzyme activities. Genotypes of 102 cases and 112 healthy controls were determined by PCR-RFLP. PON1 enzyme activity was determined according to Eckerson's method. The ratio of MM genotype belonging to PON1 L55M polymorphism in control group was 6.3% and was 7.8% in patients with leukemia (p= 0.39). PON1 enzyme activity was 118.8 ± 115.1 U/mL in control group, while decreased to 75.6 ± 64.4 U/mL in patients with leukemia (p= 0.004). PON1 enzyme activities of the individuals with MM genotypes belonging to PON1 L55M polymorphism was 57.43 ± 21.61 U/ mL in control group and decreased to 39.18 ± 45.61 U/mL in leukemic patients. Our results suggest that, PON1 L55M polymorphism genotype ratios do not affect leukemia development. However, reduced PON1 enzyme activity and also the combination of PON1 L55M polymorphism with reduced PON1 enzyme activity are associated with the increased risk of leukemia. Furthermore, older age may be a risk factor for developing leukemia. PON1 enzim aktivitesi Eckerson yöntemi ile ölçüldü. PON1 L55M polimorfizmine ait MM genotip oranları kontrol grubunda %6.3 iken lösemili hastalarda % 7.8 idi (p= 0.39). PON1 enzim aktivitesi kontrol grubunda 118.8 ± 115.1 U/mL iken lösemili hastalarda düşük olarak saptandı (75.6 ± 64.4 U/mL, p= 0.004). PON1 L55M polimorfizmine ait MM genotipli bireylerin PON1 enzim aktivitesi kontrol grubunda 57.43 ± 21.61 U/mL iken lösemili hastalarda düşük olarak saptandı (39.18 ± 45.61 U/mL). Bizim bulgularımız PON1 L55M polimorfizmi genotip oranlarının lösemi gelişimini etkilemediğini göstermektedir. Bununla birlikte, düşük PON1 enzim aktivitesi tek başına ve PON1 L55M polimorfizmi ile birlikte lösemi riski artışı ile ilişkilidir. Ayrıca ileri yaş lösemiye yakalanma olasılığını yükseltir.

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“…Erythrocytes are more vulnerable to LPO [20]. Lipid peroxidation has been shown to cause profound alterations in the structure and functions of the cell membrane including decreased membrane fluidity, increased membrane permeability, inactivation of membrane-bound enzymes, and loss of essential fatty acids [21]. Several studies in occupationally exposed human subjects indicate that smoke enhance LPO and alter antioxidant systems in erythrocytes of human cutaneous model [22] and in electric arc welding operators [4,23].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress and Oxidative Damage in Male Rat Erythrocytes Associated with Prolonged Exposure to Smoke Pollution

Achudume¹,

Aina²

2012

JEP

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Exposure of animals to different duration of smoke can result in a wide range of adverse clinical conditions. Toxicological consequences arising from prolonged exposure may not be totally enumerated. The present study was to evaluate the oxidative stress-inducing potential of a short and long-time exposure of male rat erythrocytes to environmentally relevant to public health. Male Wistar rats were exposed to open municipal land-fill smoke for 30 and/or 60 days. The oxidative stress in erythrocytes was evaluated by assessing the magnitude of malondialdehyde production and reduced glutathione (GSH) contents and the activities of superoxide dismutase (SOD), catalase (C) and glutathione reductase (GR) after 30 and/or 60 days of exposure. After 30 days there was no change in SOD, catalase and GR activities and no alterations in GSH and lipid peroxidation (LPO). After 60 days, the levels and activities of SOD (23.62%), catalase (5.24%), GR (14.87%) decreased. Overall, the study demonstrates that the chronic exposure of male rats to smoke results in induction of oxidative stress and simultaneous reduction in antioxidative defense system in erythrocytes at 60 days of exposure.

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[28] Lipid peroxidation-induced membrane structural alterations

Cited by 118 publications

References 22 publications

Role of Measurement of Antioxidant Enzymes in Evaluation of Antioxidant Therapy in Tobacco Abusers with Oral Leukoplakia

Role of Measurement of Antioxidant Enzymes in Evaluation of Antioxidant Therapy in Tobacco Abusers with Oral Leukoplakia

Association Between PON1 L55M Polymorphism and PON1 Enzyme Activity in Patients with Leukemia.

Oxidative Stress and Oxidative Damage in Male Rat Erythrocytes Associated with Prolonged Exposure to Smoke Pollution

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