Serum malondialdehyde: possible use for the clinical management of chronic hepatitis C patients

Romero, María José Miquel; Bosch‐Morell, Francisco; Romero, Belén; Rodrigo, José; Serra, Miguel; Romero, Francisco J.

doi:10.1016/s0891-5849(98)00118-x

Cited by 84 publications

(66 citation statements)

References 24 publications

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“…This speculation is reinforced by the serum ALT activity levels (more directly attributable to the hepatic cell damage) that rapidly normalize during IFa2 treatment. Serum MDA levels, which are significantly lower after IF-a2 treatment, do not reach control values during or after treatment (3). The possible role of T cells in the development of chronicity in HCV-infected patients (23), acting probably as HCV reservoirs, has been recently confirmed (36), and again it fits with the above-mentioned lymphocytic glutathione depletion observed in CHC patients (35 HIV infection is associated with oxidative stress., in view, among other things, of the reduction of glutathione GSH contents in plasma and lung epithelial lining fluid (37) and T lymphocytes (38) of adult asymptomatic HIV seropositive individuals among other things.…”

Section: Semm Malondialdehyde In Patientsmentioning

confidence: 70%

“…LPO products, measured as thiobarbituric acid (TBA) reactive substances (TBARS) (20), and also MDA (3) concentrations decreased after IF-a2 treatment (3000 U, 3 times a week for 6 months), as well as the ALT activity, in serum of these patients. When applying a specific assay of MDA (fluorescence detection of the MDA-TBA after chromatographic separation) (3,4), the differences in serum MDA before and after IF-a2 treatment, in the responding and nonresponding IF-a2 treatment groups of patients revealed that higher MDA values before IF-aq treatment have a higher probability for a better outcome than those with relatively lower values, as confirmed histopathologically (3).…”

Section: Semm Malondialdehyde In Patientsmentioning

confidence: 94%

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Lipid Peroxidation Products and Antioxidants in Human Disease

Romero¹,

Bosch‐Morell²,

Romero³

et al. 1998

Environmental Health Perspectives

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Lipid peroxidation (LPO) is a free radical-related process that in biologic systems may occur under enzymatic control, e.g., for the generation of lipid-derived inflammatory mediators, or nonenzymatically. This latter form is associated mostly with cellular damage as a result of oxidative stress, which also involves cellular antioxidants in this process. This article focuses on the relevance of two LPO products, malondialdehyde (MDA) and 4-hydroxynonenal (HNE), to the pathophysiology of human disease. The former has been studied in human serum samples of hepatitis C virus-infected adults and human immunodeficiency virus-infected children. In these two cases it is shown that the specific assay of serum MDA is useful for the clinical management of these patients. The presence of MDA in subretinal fluid of patients with retinal detachment suggests the involvement of oxidative stress in this process. Moreover, we were able to report the dependence of this involvement on the degree of myopia in these patients. The assay of MDA contents in the peripheral nerves of rats fed a chronic alcohol-containing diet or diabetic mice also confirms the pathophysiologic role of oxidative stress in these experimental models. In these two cases, associated with an increase in tissue LPO products content, we detected a decrease of glutathione peroxidase (GSHPx) activity in peripheral nerve, among other modifications. We have demonstrated that in vitro HNE is able to inhibit GSHPx activity in an apparent competitive manner, and that glutathione may partially protect and/or prevent this inactivation. The accumulation of LPO products in the brain of patients with Alzheimer's disease has also been described, and it is on the basis of this observation that we have tried to elucidate the role of oxidative stress and cellular antioxidants in ,B-amyloid-induced apoptotic cell death of rat embryo neurons. Finally, we discuss the possible role of the observed vascular effects of HNE on human arteries.

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Section: Semm Malondialdehyde In Patientsmentioning

confidence: 70%

Section: Semm Malondialdehyde In Patientsmentioning

confidence: 94%

Lipid Peroxidation Products and Antioxidants in Human Disease

Romero¹,

Bosch‐Morell²,

Romero³

et al. 1998

Environmental Health Perspectives

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“…In particular, patients with chronic hepatitis C show an increase in the serum content of MDA, 8-isoprostane, and protein carbonyls that are associated with a reduction of the antioxidant defenses. [9][10][11][12][13][14] Moreover, immunohistochemistry has documented the presence of MDA and 4-hydroxynonenal protein adduct in liver biopsy specimens from CHC patients. 13,30 The measurement of the antibodies against the different lipid peroxidation-related antigens confirms these observations, revealing that elevated titers of IgG against MDA adducts are evident in 38% to 55% of the CHC patients, independent of the alcohol consumption.…”

Section: Discussionmentioning

confidence: 99%

“…15,34 Moreover, the plasma levels of lipid peroxidation products strictly correlate with the release of aminotransferase, 10,12 whereas oxidative injury ameliorates in the patients that respond to interferon therapy. 11,13 On this basis, it is tempting to postulate that the stimulation of oxidative stress by alcohol might have a role in worsening the evolution of CHC. In support of this hypothesis, we have observed that heavy drinkers having a high prevalence of lipid peroxidation-related antibodies suffer more severe liver damage than abstainers.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have documented an association between HCV infection and the presence of both liver and serum markers of oxidative stress. [9][10][11][12][13][14] Furthermore, the expression of HCV core protein in transgenic mice or in hepatoma cells lines alters the liver antioxidant status and promotes lipid peroxidation. 15,16 Ethanol is also known to stimulate the production of reactive oxygen species and hydroxyethyl free radicals and to lower hepatic antioxidant defense.…”

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confidence: 99%

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Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C

et al. 2003

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The mechanisms by which alcohol consumption worsens the evolution of chronic hepatitis C (CHC) are poorly understood. We have investigated the possible interaction between hepatitis C virus (HCV) and ethanol in promoting oxidative stress. Circulating IgG against human serum albumin (HSA) adducted with malondialdehyde (MDA-HSA), 4-hydroxynonenal (HNE-HSA), or arachidonic acid hydroperoxide (AAHP-HSA) and against oxidized cardiolipin (Ox-CL) were evaluated as markers of oxidative stress in 145 CHC patients with different alcohol consumption, 20 HCV-free heavy drinkers (HD) without liver disease, and 50 healthy controls. Anti-MDA IgG was increased in CHC patients irrespective of alcohol intake as well as in the HD group. CHC patients with moderate alcohol intake (<50 g ethanol/d), but not HD, also had significantly higher values of anti-AAHP-HSA, anti-HNE-HSA, and anti-Ox-CL IgG (P < .05) than controls. A further elevation (P < .001) of these antibodies was evident in CHC patients with heavy alcohol intake (>50 g ethanol/d). Anti-AAHP and anti-Ox-CL IgG above the 95th percentile in the controls were observed in 24% to 26% of moderate and 58% to 63% of heavy drinkers but only in 6% to 9% of the abstainers. The risk of developing oxidative stress during CHC was increased 3-fold by moderate and 13-to 24-fold by heavy alcohol consumption. Heavy drinking CHC patients had significantly more piecemeal necrosis and fibrosis than abstainers. Diffuse piecemeal necrosis was 4-fold more frequent among alcohol-consuming patients with lipid peroxidation-related antibodies than among those without these antibodies. In conclusion, even moderate alcohol consumption promotes oxidative stress in CHC patients, suggesting a role for oxidative injury in the worsening of CHC evolution by alcohol. (HEPATOLOGY 2003; 38:42-49.)

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Oxidative status of human milk and its variations during cold storage

et al. 2004

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Breastfeeding and human milk are widely accepted as optimal for human infants' nutrition. Nowadays lifestyle often makes it difficult to maintain or even initiate human lactation. This situation is mostly related to the workload of women away from home. New approaches are needed to enable maternal lactation under these circumstances. Human breastmilk storage for differed use is one possibility. The aim of this study was to assess changes in glutathione peroxidase (GPx) activity and in the concentration of the lipid peroxidation marker, malondialdehyde (MDA), when human milk was kept refrigerated or frozen. Thirty-two human milk samples were assayed for GPx activity and MDA concentration. Samples were divided in three aliquot portions, the first to be immediately analysed, the second to be refrigerated at 4 degrees C and analysed 24 h thereafter, and the third to be frozen at -20 degrees C and assayed after 10 days. GPx activity was significantly decreased in refrigerated and in frozen milk, when compared to their control samples. MDA was increased only in refrigerated milk but not in frozen samples. Thus, freezing seems better than refrigeration in order to prevent lipid peroxidation in stored human milk samples.

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Serum malondialdehyde: possible use for the clinical management of chronic hepatitis C patients

Cited by 84 publications

References 24 publications

Lipid Peroxidation Products and Antioxidants in Human Disease

Lipid Peroxidation Products and Antioxidants in Human Disease

Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C

Oxidative status of human milk and its variations during cold storage

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