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Biomedical subjects

E Levy

Publications and source records attributed to E Levy.

At least 55 records · Page 3Linked to original sources
PubMed2000

Modulation of endoplasmic reticulum-bound cholesterol regulatory enzymes by iron/ascorbate-mediated lipid peroxidation.

Mammalian sterol regulatory enzymes are integral membrane proteins of the endoplasmic reticulum. They play a critical role in liver cholesterol homeostasis and the maintenance of overall cholesterol balance in different species. Because lipid peroxidation has been implicated in hepatic dysfunction and atherosclerosis, we hypothesized that its occurrence could alter the composition and properties of the bilayer lipid environment, and thereby affect the functions of these membrane proteins. Preincubation of rat liver microsomes with iron (Fe)/ascorbate (50 microM/200 microM), known to induce peroxidation, resulted in a significant inhibition of (i) the rate-limiting enzyme in cholesterol biosynthesis, HMG-CoA reductase (46%, p < .01), (ii) the crucial enzyme controlling the conversion of cholesterol in bile acids, cholesterol 7alpha-hydroxylase (48%, p < .001), and (iii) the central enzyme for cholesterol esterification: Acyl-CoA:cholesterol acyltransferase (ACAT, 80%, p < .0001). The disturbances of these key enzymes took place concomitantly with the high production of malondialdehyde (350%, p < .007) and the loss of polyunsaturated fatty acids (36.19 +/- 1.06% vs. 44.24 +/- 0.41 in controls, p < .0008). While alpha-tocopherol simultaneously neutralized lipid peroxidation, preserved microsomal fatty acid status, and restored ACAT activity, it was not effective in preventing Fe/ascorbate-induced inactivation of both HMG-CoA reductase (44%, p < .01) and cholesterol 7alpha-hydroxylase (71%, p < .0001). These results indicate that Fe/ascorbate alters the activity of the rate-determining steps in liver cholesterol metabolism, either directly or via lipid peroxidation, capable of modifying their membrane environment. The present data also suggest that the three regulatory enzymes respond differently when exposed to Fe/ascorbate or antioxidants, which may be due to dissimilar mechanisms.

Animals↗
PubMed2000

Influence of radiographic technique and equipment on absorbed ovarian dose associated with uterine artery embolization.

PURPOSE: To evaluate the influence of pulsed fluoroscopy (PF), nonpulsed fluoroscopy (NPF), and various fluoroscopic techniques on the absorbed ovarian dose (AOD) associated with uterine artery embolization (UAE) of leiomyomata. MATERIAL AND METHODS: Ovarian location was estimated from preprocedural pelvic magnetic resonance images of 23 patients previously treated by means of UAE. The AOD was measured with thermoluminescent dosimeters (TLD) placed into an anthropomorphic phantom at the determined ovarian location. The following measurements from PF and NPF were obtained: 21.89 minutes of nonmagnified posterior-anterior fluoroscopy, 10 minutes of nonmagnified oblique fluoroscopy, 10 minutes of posterior-anterior magnified fluoroscopy, 10 minutes of combined oblique magnified fluoroscopy, and 47 simulated angiographic exposures. Numbers for nonmagnified posterior-anterior fluoroscopy time and exposure numbers were chosen from the average values from previous UAE procedures. AOD from pulsed and nonpulsed nonmagnified posterior-anterior fluoroscopy was compared to measurements from oblique magnified, posterior-anterior magnified, and oblique fluoroscopy. RESULTS: AOD from NPF was, on average, 1.7 times higher than from PF. When compared with nonmagnified posterior-anterior fluoroscopy, the AOD from oblique magnified fluoroscopy was 1.9 times greater; the AOD from nonmagnified oblique fluoroscopy was 1.1 times greater. The AOD from oblique magnified fluoroscopy was 1.5 times higher on the side closer to the x-ray tube than on the contralateral side. AOD from serial angiographic exposures contributed only less than 7% to the total AOD for the average UAE procedure. CONCLUSIONS: The AOD associated with UAE can best be reduced by limiting fluoroscopy time and the use of oblique or magnified fluoroscopy. Contribution of angiographic exposures to AOD is much less significant.

Arteries↗
PubMed2000

Radiation-induced bone sarcoma following total body irradiation: role of additional radiation on localized areas.

A 44-year-old patient who had had acute monoblastic leukemia developed an osteosarcoma of the pelvic bones 5 years after an allogeneic bone marrow transplant from his HLA-identical sister. He had additionally received superficial cutaneous radiation of the legs and pelvis, over the 3 weeks prior to total body irradiation (TBI), because of cutaneous leukemic lesions. The tumor was a fibrohistiocytomatous osteogenic sarcoma. The first lesion was in the right ilium, and a second lesion appeared 18 months later, symmetrically on the left ilium. Despite treatment, the patient died from metastases. At the time of diagnosis of radiation-induced sarcoma, the patient was free of leukemia and had several risk factors already reported to favor the development of solid tumors in stem cell recipients. These include acute leukemia, TBI and graft-versus-host disease. As he developed symmetrical lesions of the pelvic bone, and because of the histology of the radiation-induced tumor, we assumed that the additional radiation of the skin prior to TBI may have contributed to the pathogenesis of this malignant fibrous histiocytoma. Therefore, the risk/benefit ratio should be carefully considered in unusual indications. These patients should benefit from a close follow-up of the superimposed areas.

Adult↗
PubMed2000

Altered lipid profile, lipoprotein composition, and oxidant and antioxidant status in pediatric Crohn disease.

BACKGROUND: Growing evidence supports a role for peroxidation in the pathogenesis of Crohn disease (CD). The activation of inflammatory cells, the release of their mediators, and the excessive production of free radicals may affect circulating lipids. OBJECTIVE: We examined the lipid profile, lipoprotein composition, and oxidant-antioxidant status of children with CD. DESIGN: We studied 22 pediatric CD patients and 10 healthy control subjects. RESULTS: The proportion of saturated and monounsaturated fatty acids in plasma of CD patients was higher but that of polyunsaturated fatty acids was lower than in control subjects. This resulted in higher ratios in CD patients of palmitoleic acid to linoleic acid (P < 0. 05) and of eicosatrienoic acid to arachidonic acid (P < 0.04), 2 established indexes of essential fatty acid deficiency. Hypocholesterolemia was noted in CD patients as a result of lower LDL-cholesterol concentrations than in control subjects (P < 0.02). Plasma apolipoproteins B (P < 0.02) and A-I (P < 0.02) were also lower in CD patients, whereas plasma triacylglycerols were higher (P < 0.005). Lipoprotein composition was altered in CD patients, with relative triacylglycerol depletion and protein enrichment in VLDL. In contrast, intermediate-density lipoprotein of CD patients was characterized by an increased percentage of triacylglycerol and protein (P < 0.005) and a reduced proportion of phospholipids (P < 0. 01). Additional abnormalities were observed in the chemical distribution of HDL(2) and HDL(3) moieties. Lipid peroxidation was documented by higher plasma malondialdehyde concentrations in CD patients (P < 0.05), accompanied by lower retinol concentrations (P < 0.02). CONCLUSION: Disturbances in the lipid profile, in lipoprotein concentrations and composition, and in oxidant-antioxidant status occur in CD patients.

Adolescent↗
PubMed2000

Iron-ascorbate alters the efficiency of Caco-2 cells to assemble and secrete lipoproteins.

Although oxidative stress has been implicated in development of gut pathologies, its role in intestinal fat transport has not been investigated. We assessed the effect of Fe(2+)-ascorbate-mediated lipid peroxidation on lipid synthesis, apolipoprotein biogenesis, and lipoprotein assembly and secretion. Incubation of postconfluent Caco-2 cells with iron(II)-ascorbate (0.2 mM/2 mM) in the apical compartment significantly promoted malondialdehyde formation without affecting sucrase activity, transepithelial resistance, DNA and protein content, and cell viability. However, addition of the oxygen radical-generating system reduced 1) [(14)C]oleic acid incorporation into cellular triglycerides (15%, P < 0.0002) and phospholipids (16%, P < 0.0005); 2) de novo synthesis of cellular apolipoprotein A-I (apo A-I) (18%, P < 0.05), apo A-IV (38%, P < 0.05), and apo B-48 (45%, P < 0.003) after [(35)S]methionine addition; and 3) production of chylomicrons (50%), VLDL (40%), LDL (37%), and HDL (30%) (all P < 0.0001). In contrast, increased total cellular cholesterol formation (96%, P < 0.0001), assayed by [(14)C]acetate incorporation, was noted, attributable to marked elevation (70%, P < 0.04) in activity of DL-3-hydroxy-3-methyl-glutaryl-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. The ratio of Acyl-CoA to cholesterol acyltransferase, the esterifying cholesterol enzyme, remained unchanged. Fe(2+)-ascorbate-mediated lipid peroxidation modifies intracellular fat absorption and may decrease enterocyte efficiency in assembling and transporting lipids during gut inflammation.

Antineoplastic Agents↗
PubMed2000

Human crypt intestinal epithelial cells are capable of lipid production, apolipoprotein synthesis, and lipoprotein assembly.

The recent availability of spontaneously proliferating, non-transformed human crypt intestinal epithelial cells (HIEC) affords an opportunity to investigate lipid metabolism in undifferentiated enterocytes. The major purpose of this study was to explore the capability of undifferentiated crypt cells to synthesize, assemble, and secrete lipids and apolipoproteins. HIEC were cultured in medium with 5% fetal bovine serum for 5 to 21 d. The cells were clearly able to incorporate [(14)C]oleic acid (dpm/mg protein) into triglycerides (128,279 +/- 16,988), phospholipids (30, 278 +/- 2,107), and cholesteryl esters (2,180 +/- 207). Although improvement in lipid secretion was noted with prolongation of cell culture periods, low efficiency of lipid export (10.3 +/- 2.2% of intracellular content) characterized the HIEC. All phospholipid classes were elaborated, with phosphatidylcholine accounting for 79. 3 +/- 1.3% of cellular phospholipids. Chylomicrons were the dominant (46.4%) lipoproteins secreted, followed by high, low, and very low density lipoproteins (HDL, LDL, and VLDL) comprising 22.5, 20.2, and 10.8% of the total, respectively. HIEC elaborated most of the major apolipoprotein (apo) classes (A-I, A-IV, B-100, C, and E), but were less efficient in producing apoB-48. In contrast to the production of apoA-I and C as early as 5 days after confluence, apoA-I and A-IV were maximally expressed at 11 d. Culture media accumulated much more apoB-100 than apoB-48 (B-48/B-100 ratio 0.21 +/- 0.03), reflecting limited apoB mRNA editing. HIEC demonstrated both endogenous cholesterol synthesis and LDL receptor expression. Cholesterol synthesis was sensitive to 25-hydroxycholesterol and mevinolin, but unresponsive to LDL treatment, suggesting independent regulation pathways. In contrast, LDL inhibited receptor activity. The present findings provide the first solid evidence that immature HIEC are capable of key fat absorptive functions of well-differentiated enterocytes. The intracellular mechanisms required for lipid and apolipoprotein synthesis as well as for lipoprotein assembly are already present in intestinal crypt cells. These cells also retain the capacity for sterol enzyme and receptor expression. However, certain limitations, especially apoB-48 production and lipoprotein secretion as well as unresponsiveness of cholesterol synthesis to LDL, may be ascribed to the lack of differentiation.

Animals↗
PubMed2000

Metabolic syndrome X: a review.

Metabolic syndrome X is a multifaceted syndrome, which occurs frequently in the general population. It is more common in men than in women. A large segment of the adult population of industrialized countries develops the metabolic syndrome, produced by genetic, hormonal and lifestyle factors such as obesity, physical inactivity and certain nutrient excesses. This disease is characterized by the clustering of insulin resistance and hyperinsulinemia, and is often associated with dyslipidemia (atherogenic plasma lipid profile), essential hypertension, abdominal (visceral) obesity, glucose intolerance or noninsulin-dependent diabetes mellitus and an increased risk of cardiovascular events. Abnormalities of blood coagulation (higher plasminogen activator inhibitor type 1 and fibrinogen levels), hyperuricemia and microalbuminuria have also been found in metabolic syndrome X. This review summarizes the present knowledge of abnormalities in this syndrome. Each risk factor is reviewed, and potential criteria for diagnosis and therapeutic targets are discussed. Because patients with metabolic syndrome X accumulate cardiac risk factors, they should be given special attention in terms of diagnosis and treatment.

Blood Glucose↗
PubMed2000

Software development for registration of digital subtraction angiography (DSA) images in uterine fibroid embolization.

The ISIS Center at Georgetown University Medical Center has developed a comprehensive program for image-guided procedures in the spine. As part of this program, ISIS has developed a software application known as I-SPINE (ISIS's Spine Procedure Imaging Navigation Engine). I-SPINE is a Windows NT application, which is based on the Analyze/AVM libraries. The software architecture follows the Microsoft Foundation Classes (MFC) single document, multiple view paradigm. This has allowed the developers to add new visualization modules to I-SPINE that aid physicians in procedures outside the spine. One such procedure I-SPINE has been expanded for is uterine fibroid embolization. The idea is that by registering and subtracting post-embolization angiographic images from pre-treatment images the resulting image can be used to quantify the embolization effect on the fibroid circulation and predict the treatment response. The I-SPINE digital subtraction angiography (DSA) module allows the interventional radiologist to open a series of pre and post-embolization DSA images that shows the vascular structures of the uterus and the fibroid or fibroids. From these images, the radiologist selects an appropriate image from each series. The selected images are then hand registered using pixel shifting. Once the images are registered, the pixels are subtracted resulting in an image that shows the embolized arteries that were supplying the fibroids.

Angiography, Digital Subtraction↗
PubMed1999

Modulation of apo A-IV transcript levels and synthesis by n-3, n-6, and n-9 fatty acids in CACO-2 cells.

It has been postulated that apolipoprotein (apo) A-IV plays various significant roles in lipid transport and lipoprotein metabolism. Although it is controlled by fat feeding, so far little else is known about its regulation by specific fatty acids. In this study, we focused on the modulation of apo A-IV mRNA levels, mass, and biogenesis by mono- and polyunsaturated fatty acids (FA) in the human intestinal Caco-2 cell line. In confluent cells incubated with 1 mM oleic (n-9), linoleic (n-6), alpha-linolenic (n-3), or docosahexaenoic (n-3) acids for a long-term period, both apo A-IV protein levels and de novo synthesis were increased. The induction resulted from the up-regulation of apo A-IV mRNA transcripts. In contrast, an inhibitory effect was evident with short-term incubation. FA chain length and degree of unsaturation had little effect altering apo A-IV transcript and biogenesis. These data offer evidence that isolated fatty acids regulate gene expression and the production of apo A-IV in the enterocyte.

Apolipoproteins A↗
PubMed1999

Caco-2 cells and human fetal colon: a comparative analysis of their lipid transport.

Caco-2 cells and human colonic explants were compared for their ability to esterify lipid classes, synthesize apolipoproteins and assemble lipoproteins. Highly differentiated cells and colonic explants were incubated with [(14)C]oleic acid or [(35)S]methionine for 48 h. Caco-2 cells demonstrated a higher ability to incorporate [(14)C]oleic acid into cellular phospholipids (13-fold, P<0.005), triglycerides (28-fold, P<0.005) and cholesteryl ester (2-fold, P<0. 01). However, their medium/cell lipid ratio was 11 times lower, indicating a limited capacity to export newly synthesized lipids. De novo synthesis of apo B-48 and apo B-100 was markedly increased (7%0 and 240%, respectively), whereas the biogenesis of apo A-I was decreased (60%) in Caco-2 cells. The calculated apo B-48/apo B-100 ratio was substantially diminished (107%), suggesting less efficient mRNA editing in Caco-2 cells. When lipoprotein distribution was examined, it displayed a prevalence of VLDL and LDL, accompanied along with a lower proportion of chylomicron and HDL. In addition, differences in lipoprotein composition were evidenced between colonic explants and Caco-2 cells. Therefore, our findings stress the variance in the magnitude of lipid, apolipoprotein and lipoprotein synthesis and secretion between the two intestinal models. This may be due to various factors, including the origin of Caco-2 cell line, i.e., colon carcinoma.

Apolipoproteins↗
PubMed1999

TNFalpha-induced IEC-6 cell apoptosis requires activation of ICE caspases whereas complete inhibition of the caspase cascade leads to necrotic cell death.

Tumor necrosis factor (TNF)alpha is considered to play a key pathogenetic role in inflammatory bowel diseases. In this study we analyzed the mechanisms by which TNFalpha induces intestinal epithelial cell apoptosis. TNFalpha alone, and more potently in combination with IFNgamma, induced a high degree of IEC-6 cell apoptosis. This effect was more than 100-fold stronger if both of the TNF-R were stimulated, compared to stimulation of the p55-TNF-R alone, indicating an important apoptosis enhancing effect of the p75-TNF-R. TNFalpha-induced apoptosis required activation of ICE caspases and was completely abolished by its inhibitor, zVAD-fmk. Specific inhibition of caspase-3 with zDEVD-fmk did not alter the effect of TNFalpha. Western blot analyses confirmed that caspase-3 was not activated in response to TNFalpha. In the presence of complete inhibition of the caspase cascade with zVAD-fmk (>/=50 microM), TNFalpha induced cell necrosis rather than apoptosis. Our data reveal that TNFalpha can trigger enterocyte cell death via apoptosis or necrosis, depending upon the activation or blockade of specific caspases.

Amino Acid Chloromethyl Ketones↗
PubMed1999

Cell-lysate conversion of prion protein into its protease-resistant isoform suggests the participation of a cellular chaperone.

A conformational transition between the normal cellular prion protein (PrPC) and the beta-sheet-rich pathological isoform (PrPSc) is a central event in the pathogenesis of spongiform encephalopathies. The prion infectious agent seems to contain mainly, if not exclusively, PrPSc, which has the ability to propagate its abnormal conformation by transforming the host PrPC into the pathological isoform. We have developed an in vitro system to induce the PrPC --> PrPSc conversion by incubating a cell-lysate containing mouse PrPC with partially purified mouse PrPSc. After 48 h of incubation with a 10-fold molar excess of PrPSc, the cellular protein acquired PK-resistance resembling a PrPSc-like state. Time course experiments suggest that the conversion follows a stepwise mechanism involving kinetic intermediates. The conversion was induced by PrPSc extracted from mice infected with two different prion strains, each propagating its characteristic Western blot profile. The latter results and the fact that all the cellular components are present in the conversion reaction suggest that PrPC-PrPSc interaction is highly specific and required for the conversion. No transformation was observed under the same conditions using purified proteins without cell-lysate. However, when PrPC-depleted cell-lysate was added to the purified proteins the conversion was recovered. These findings provide direct evidence for the participation of a chaperone-like activity involved in catalyzing the conversion of PrPC into PrPSc.

Animals↗
PubMed1999

The direct costs of insomnia in France.

Several reports indicate that use of hypnotics is significantly higher in France relative to other European countries, but few reports exist concerning the cost of this high consumption of psychotropic medications. The purpose of the present study was to estimate the direct costs that may be attributed to insomnia in France. Data were derived from previously published surveys in this field. It includes the cost of sleep medications and of substances used to promote sleep, outpatient visits to physicians or to other health professionals and sleep recordings and treatment by sleep specialists. The final estimate of the total direct cost of insomnia in France in 1995 was FF 10,232,992,500 ($2,067,271,100). Public authorities have to understand that an increase in the direct costs of insomnia may be balanced by the reduction of the daytime consequences of insomnia and then by the reduction of the indirect costs of insomnia.

Adolescent↗
PubMed1999

[Arterial hypertension due to compression of the renal artery, revealing ovarian cancer].

BACKGROUND: The etiologic work-up of hypertension with hyperaldosteronism and elevated serum renin includes search for renal artery stenosis. Intrinsic stenosis is a common finding, but hypertension secondary to extrinsic compression of the renal artery is exceptional. CASE REPORT: A 48-year-old woman with an uneventful history was hospitalized for recent onset hypertension. Laboratory tests showed hypokaliemia, and elevated aldosterone and renin. Duplex Doppler exploration of the renal vessels evidenced extrinsic compression of the left renal artery by a tumoral mass found to be a nodal metastasis at surgery. Pathology reported cancer of the ovary. Blood pressure, and aldosterone and renin levels returned to normal after complete tumor resection. No antihypertensive treatment was required. CONCLUSION: This is undoubtedly the first case of metastatic cancer of the ovary revealed by hypertension; it can be added to the list of 49 other published cases of extrinsic compression of the renal artery by various causes leading to hypertension. In most cases, surgical removal of the obstacle or nephrectomy provided cure of the hypertension.

Female↗
PubMed1999

Susceptibility to FAS-induced apoptosis in human nontumoral enterocytes: role of costimulatory factors.

FAS-FAS ligand interaction has been implicated in increased enterocyte apoptosis seen in immune-mediated bowel injury. However, scant information exists on the role of FAS in physiological enterocyte turnover. In the present study, the regulation of enterocyte FAS and FAS ligand expression by cytokines and its functional role in human intestinal epithelial cell apoptosis and proliferation were analyzed with two different models: a nontransformed human intestinal epithelial cell line (HIEC) and normal colonic explant cultures. HIEC constitutively expressed FAS, as analyzed by flow cytometry. However, stimulation with agonistic anti-FAS antibody (1-500 ng/ml) did not induce HIEC apoptosis. In contrast, in the presence of tumor necrosis factor alpha (TNFalpha) and/or interferon gamma (IFNgamma), HIEC became highly susceptible to FAS-induced apoptosis. The sensitizing effect to FAS-induced apoptosis was mediated via TNFalpha- and IFNgamma-induced upregulation of FAS expression (maximally 348%). Receptor studies showed that the effect of TNFalpha on FAS was mediated via the p55 TNF receptor. In colonic organ cultures, IFNgamma and TNFalpha also enhanced colonocyte FAS expression, resulting in a markedly increased apoptotic response to stimulation of this receptor, as shown by in situ terminal deosyuridine triphosphate nick-end staining. Neither FAS ligand expression nor its induction by cytokines was observed in HIEC or colonic explants. Proliferation studies showed that FAS is not implicated in regulating HIEC growth. These findings suggest that, despite the fact that normal human enterocytes express FAS, costimulatory factors, such as TNFalpha or IFNgamma, abundantly secreted under inflammatory conditions, are necessary to sensitize intestinal epithelial cells to FAS-induced apoptosis by upregulating this receptor.

Antigens, CD↗
PubMed1999

Amplifications of DNA primase 1 (PRIM1) in human osteosarcoma.

We studied the involvement of PRIM1 in osteosarcoma by differential display, Northern and Southern hybridization, as well as fluorescence in situ hybridization (FISH) on interphase nuclei. In total, 22 pediatric oncology specimens were tested. PRIM1 was found to be amplified in 41% of the samples. PRIM1 is coamplified with the core 12q13 amplicon genes CDK4, SAS, and OS9, and was physically mapped very close to them. PRIM1 is therefore a new candidate for the role of a major target gene of 12q13 amplifications in human cancers. Genes Chromosomes Cancer 26:62-69, 1999.

Blotting, Northern↗
PubMed1999

Dietary iron overload and induced lipid peroxidation are associated with impaired plasma lipid transport and hepatic sterol metabolism in rats.

Although hemochromatosis is characterized by dramatic morphological and functional alterations in the liver, little is known about the effects of an excess of iron on lipid metabolism. Therefore, we determined the effect of chronic iron overload on plasma lipid profile and lipoprotein composition, as well as on hepatic cholesterol metabolism and biliary sterol output. Rats administered a diet enriched with 3% iron carbonyl for 12 weeks displayed a 30-fold increase in iron (P <.0001) and a 5-fold rise in malondialdehyde (P <.001) in the liver. When compared with pair-fed controls, iron-overload rats showed a significant increase in triglycerides (P <.005), free cholesterol (P <.006), cholesteryl ester (P <.007), and high-density lipoprotein (HDL)-cholesterol (P <. 003). Triglyceride and cholesteryl ester enrichment, protein depletion, size increase, and apolipoprotein composition alterations characterized the very low density lipoprotein (VLDL) and HDL particles of iron-overload rats. Assessment of the activity of intracellular key enzymes for cholesterol homeostasis in these rats disclosed a reduction in 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (66%, P <.005) and cholesterol 7alpha-hydroxylase (58%, P <.0004) with an increment of acyl-CoA: cholesterol acyltransferase (62%, P <.002). The lack of optimal enzymatic activity may be a result of marked membrane lipid peroxidation that brings about fluidity drop (P <.029) in microsomes of iron-overload rats (5.00 +/- 0.013) versus controls (8.20 +/- 0. 03), reflected by polarization. A decline of the pool size of cholesterol and bile acids was noted in iron-overload rats during a 6-hour bile drainage. Our results show that experimental iron overload causes marked perturbations in plasma lipid transport and hepatobiliary sterol metabolism. Given the positive correlation of malondialdehyde with most of the altered parameters, iron-catalyzed lipid peroxidation may well be one of the involved mechanisms.

Alanine Transaminase↗