Plasma malondialdehyde (MDA) levels in breast and lung cancer patients

Gönenç, Aymelek; Özkan, Yeşim; Torun, Meral; Şimşek, Bolkan

doi:10.1046/j.1365-2710.2001.00334.x

Cited by 164 publications

(96 citation statements)

References 16 publications

(14 reference statements)

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“…The study reflects substantial increase in the peroxidation level of lipids in the serum of breast cancer patients when compared to the normal which is consistent with few studies [18]. Elevated level of MDA in serum or plasma apart from the breast cancer has also been reported in several cancer types such as oralcancer [1], uterine cancer [13] colorectal cancer [7] etc.…”

Section: Discussionsupporting

confidence: 88%

Elevated lipid peroxidants in breast cancer patients

Nath¹

2014

IOSRJPBS

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Section: Discussionsupporting

confidence: 88%

Elevated lipid peroxidants in breast cancer patients

Nath¹

2014

IOSRJPBS

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“…[41][42][43][44][45] Crucially, when examined, many such defects correlate with the degree of inflammatory activity in these disease processes. These observations support the notion that common mechanisms link immune dysregulation and metabolic dysfunction across a range of diseases that share common cellular and molecular effector pathways.…”

Section: Evidence Of Similar Metabolic Perturbances In Other Chronic mentioning

confidence: 99%

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

et al. 2003

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Abstract-There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Key Words: immune system Ⅲ risk factors Ⅲ atherosclerosis C onsiderable evidence indicates that patients with rheumatoid arthritis (RA) are at greater risk of developing coronary heart disease (CHD). 1 Seventeen of 21 relevant observational studies show an increased standardized morality ratio in RA and that life expectancy is shortened by 3 to 18 years. Pooled analysis of these studies suggests a 70% increase in risk of death in RA patients. Life expectancy is especially shortened in RA patients treated in specialist referral centers, where the prognosis is comparable to that of triple-vessel CHD or stage 4 Hodgkin's disease. 1 Cardiovascular disease accounts for 35% to 50% of excess mortality in RA patients, with cerebrovascular disease being the second leading cause of death. Intriguingly, most evidence suggests that classic risk factors do not explain excess vascular disease in RA. In an 8-year follow-up of 236 RA patients, a 3.96-fold (95% CI 1.86 to 8.43) higher incidence of cardiovascular events relative to a community-dwelling cohort was noted. 2 However, this risk ratio was only minimally attenuated (to 3.17 [95% CI 1.33 to 6.36]) by adjustment for conventional risk factors. These clinical epidemiological observations strongly suggest that mechanisms other than classic risk factors promote accelerated atherogenesis in RA, and responsible candidate pathways are explored in this review. Inflammation as a Candidate Pathway for CHDIt is firmly established that systemic markers of inflammation, albeit at considerably lower levels than those apparent in RA, independently predict CHD events in men and women with or without existing heart disease. 3,4 The levels of cytokines and other inflammatory mediators detected in CHD are such that high-sensitivity assays rather than conventional assays are required. This concept of inflammatory-driven atherogenesis is consistent with the plaque composition of unstable coronary lesions, with an abundance of inflammatory molecules and immune cells at the shoulder region that act to erode the collagen cap that separates the atheromatous material of the plaque from blood. 4 This appearance is similar to that of inflammatory synovitis in RA. 5 However, whereas in RA, C-reactive protein (CRP) is a powerful measure of synovial infla...

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“…As free radicals occur while smoking (16,17), plasma MDA level increases (18)(19)(20). Similarly, Gonenc et al observed that plasma MDA levels were signifi cantly high in breast and lung cancers (21). Recently, the studies related to smokers show that acrylamide occurs while the tobacco is burnt at a very high temperature and acrylamide is taken into the body together with the smoke.…”

Section: Introductionmentioning

confidence: 97%

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues

Altınöz¹,

Türköz²,

Vardı³

2015

BLL

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Abstract:The aim of this study was to investigate the protective effects of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues in rats. The rats were divided into four groups. Acrylamide administration increased MDA levels in all tissues significantly (p < 0.05). But acrylamide+NAC administration decreased MDA levels signifi cantly as compared to the acrylamide group, and lowered it to a level close to the control group values (p < 0.05). GSH levels in liver and small intestine tissues reduced signifi cantly in the acrylamide group (p < 0.05). But acrylamide+NAC administration increased GSH levels signifi cantly in all tissues. Whereas GST activity decreased signifi cantly in the acrylamide group in liver and small intestine tissues as compared to the other groups (p < 0.05), the GST activity increased signifi cantly in the acrylamide+NAC group in all tissues as compared to the acrylamide group (p < 0.05). Liver histopathology showed that the liver epithelial cells were damaged signifi cantly in the acrylamide group. Small intestine histopathology showed that the intestinal villous epithelial cells were damaged signifi cantly in the acrylamide group. Our results indicate that a high level of acrylamide causes oxidative damage in liver and small and large intestine tissues, while N-acetylcysteine administration in a pharmacological dose shows to have an antioxidant effect in preventing this damage (Tab. 2, Fig. 2, Ref. 66). Text in PDF www.elis.sk.

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Plasma malondialdehyde (MDA) levels in breast and lung cancer patients

Abstract: The results of this study provide further evidence of the relationship between lipid peroxidation and cancer and should contribute to the interpretation of epidemiological studies in this area and the planning of future research.

Cited by 164 publications

References 16 publications

Elevated lipid peroxidants in breast cancer patients

Elevated lipid peroxidants in breast cancer patients

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues

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