Cholesterol Journal Articles

Record 7021 to 7040

Hyperlipidemia induced by a cholesterol-rich diet leads to enhanced peroxynitrite formation in rat hearts
Onody, A., C. Csonka, et al. (2003), Cardiovasc Res 58(3): 663-70.
Abstract: OBJECTIVE: We investigated the influence of experimental hyperlipidemia on the formation of cardiac NO, superoxide, and peroxynitrite (ONOO(-)) in rat hearts. METHODS: Wistar rats were fed 2% cholesterol-enriched diet or normal diet for 8 weeks. Separate groups of normal and hyperlipidemic rats were injected twice intraperitoneally with 2 x 20 micromol/kg FeTPPS (5,10,15,20-tetrakis-4-sulfonatophenyl-porphyrinato-ironIII), a ONOO(-) decomposition catalyst, 24 h and 1 h before isolation of the hearts. RESULTS: A cholesterol diet significantly decreased myocardial NO content, however, myocardial Ca(2+)-dependent and Ca(2+)-independent NO synthase activity and NO synthase protein level did not change. Myocardial superoxide formation and xanthine oxidase activity were significantly increased; however, cardiac superoxide dismutase activity did not change in the cholesterol-fed group. Dityrosine in the perfusate, a marker of cardiac ONOO(-) formation, and plasma nitrotyrosine, a marker for systemic ONOO(-) formation, were both elevated in hyperlipidemic rats. In cholesterol-fed rats, left ventricular end-diastolic pressure (LVEDP) was significantly elevated as compared to controls. Administration of FeTPPS normalized LVEDP in the cholesterol-fed group. CONCLUSION: We conclude that cholesterol-enriched diet-induced hyperlipidemia leads to an increase in cardiac ONOO(-) formation and a decrease in the bioavailability of NO which contributes to the deterioration of cardiac performance and may lead to further cardiac pathologies.

Hyperlipidemia induced by high cholesterol diet inhibits heat shock response in rat hearts
Csont, T., G. Balogh, et al. (2002), Biochem Biophys Res Commun 290(5): 1535-8.
Abstract: We examined whether heat shock response is affected by experimental hyperlipidemia in rat hearts. Therefore, isolated hearts of male Wistar rats fed a 2% cholesterol-enriched diet or standard diet for 12 weeks were subjected to either 20 min heat stress at 42 degrees C or global normothermic ischemia followed by 120 min normothermic, normoxic perfusion. Both heat stress and ischemia resulted in a significant increase in cardiac mRNA and protein levels of the inducible member of the 70-kDa heat shock protein family (HSP70) when compared to time-matched controls as assessed by reverse transcriptase polymerase chain reaction and Western blotting in hearts of normal rats. However, in hyperlipidemic groups, increase in cardiac hsp70 mRNA and HSP70 protein in response to heat stress and ischemia was markedly attenuated. We further observed that the basal level of hsp70 mRNA was significantly higher in the hyperlipidemic group when compared to normal controls; however, the HSP70 protein level was not different. This is the first demonstration that hyperlipidemia inhibits cardiac heat shock response. We further conclude that basal HSP70 expression might be downregulated at a posttranscriptional level in hyperlipidemia.

Hyperresistance to cholesterol hydroperoxide-induced peroxidative injury and apoptotic death in a tumor cell line that overexpresses glutathione peroxidase isotype-4
Hurst, R., W. Korytowski, et al. (2001), Free Radic Biol Med 31(9): 1051-65.
Abstract: The selenoenzyme phospholipid hydroperoxide glutathione peroxidase (PHGPX; GPX4) plays a key role in eukaryotic defense against potentially lethal peroxidative injury and also regulation of physiological peroxide tone. In this work we focused on the cytoprotective antiperoxidant effects of GPX4, using a breast tumor epithelial cell line that over-expresses the enzyme. Wild-type COH-BR1 cells, which exhibit little (if any) GPX4 activity, were transfected with a construct encoding the mitochondrion-targeted long (L) form of the enzyme. Several transfectant clones were selected which expressed relatively large amounts of GPX4, as determined by both Northern and Western analysis. Enzyme activity ranged from 15-fold to 190-fold greater than that of wild-type or null-transfected cells. The functional ramifications of GPX4 overexpression were tested by challenging cells with photochemically generated cholesterol hydroperoxides (ChOOHs) in liposomal form. Compared with vector controls, overexpressing clones were found to be substantially more resistant to ChOOH-induced killing, as determined by annexin-V (early apoptotic) and thiazolyl blue (mitochondrial dehydrogenase) reactivity. Concomitantly, the clones exhibited a striking hyper-resistance to free radical-mediated lipid peroxidation, as assessed by labeling cell membranes with (14)Ccholesterol and measuring a family of radiolabeled oxidation products (ChOX). L-form GPX4's antiperoxidant and cytoprotective effects could reflect its ability to detoxify ChOOHs as they enter cells and/or cell-derived lipid hydroperoxides arising from ChOOH one-electron turnover.

Hyperresponsiveness to dietary cholesterol in inbred rabbits is not associated with enhanced reduction in binding of beta-VLDL to liver membranes
Meijer, G. W., A. C. Beynen, et al. (1992), J Nutr 122(4): 931-9.
Abstract: In two inbred strains of rabbits with high or low response of serum cholesterol to dietary cholesterol, binding of rabbit beta-VLDL to hepatic membrane preparations was determined. The objective was to test the hypothesis that after cholesterol feeding, hyperresponders show a more dramatic reduction in hepatic apolipoprotein (apo) B/E receptors, which may explain the development of the high degree of cholesterolemia in these animals. The number of hepatic high affinity receptors for beta-VLDL in hyperresponders fed a diet without added cholesterol was, on average, 20% lower than that in hyporesponders. After the addition of increasing amounts of cholesterol to the diet, liver cholesterol concentrations were elevated to a greater extent in hyper- than in hyporesponsive rabbits. Liver free cholesterol concentrations were negatively associated with maximal binding of beta-VLDL to liver membranes. With increasing liver free cholesterol concentrations, maximal binding was less effectively depressed in hyper- than hyporesponders. We conclude that in the inbred strains of rabbits, hyperresponsiveness to dietary cholesterol is not caused by enhanced depression of hepatic apo B/E receptors.

Hypersensitivity to thromboxane A2 in cholesterol-rich human platelets
Tomizuka, T., K. Yamamoto, et al. (1990), Thromb Haemost 64(4): 594-9.
Abstract: The effect of changes in platelet membrane cholesterol content on thromboxane A2 (TXA2)-induced platelet activation was studied. Concentrations of 9,11-epithio-11,12-methano-TXA2 (STA2), a stable analogue of TXA2 which can cause half-maximal aggregation and release of 14Cserotonin in cholesterol-rich platelets were significantly lower than those in cholesterol-normal platelets. STA2-induced increase in cytosolic calcium concentration and 32Pphosphatidic acid formation in cholesterol-rich platelets were significantly greater than those in cholesterol-normal platelets. The maximal concentration of binding site (Bmax) for SQ29548 was significantly increased in cholesterol-rich platelets compared with cholesterol-normal platelets, while the equilibrium dissociation rate constant (Kd) for SQ29548 did not differ between cholesterol-rich and cholesterol-normal platelets. The present study suggested that sensitivity to TXA2 was increased by the incorporation of cholesterol into platelet membrane and that the cause of hypersensitivity to TXA2 in cholesterol-rich platelets may be partly explained by an increase in binding capacity for TXA2.

Hypertension in rats does not potentiate hypercholesterolemia and aortic cholesterol deposition induced by a hypercholesterolemic diet
Mori, H., K. Ishiguro, et al. (1993), Lipids 28(2): 109-13.
Abstract: The effect of a hypercholesterolemic diet (HCD) on hyperlipemia and atherogenesis was investigated using normotensive Wistar/Kyoto rats (WKY), spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), with systolic blood pressures increasing in that order. Feeding an HCD diet containing cholesterol, cholate and suet induced hypercholesterolemia in all the strains examined as compared with a normal diet. The plasma cholesterol levels were significantly higher in WKY than in SHR and SHRSP fed the HCD diet. The HCD diet also induced hepatic fat deposition, particularly deposition of cholesteryl esters, a slight increase in aortic cholesterol deposition, and elevation of both monoenoic/saturated fatty acid ratios and linoleate/arachidonate ratios in tissue lipids. The changes induced in the three strains by the HCD diet were not positively correlated with blood pressures. The HCD diet affected hepatic acyl-CoA:cholesterol acyltransferase and plasma lecithin:cholesterol acyltransferase activities differently in WKY and SHR which, in addition to the induction of delta 9 desaturase, may partly account for the difference in the diet-induced changes in the fatty acid compositions of plasma cholesteryl esters. The results indicate that hypertension per se does not stimulate the development of hypercholesterolemia and arterial cholesterol deposition induced by an HCD diet, suggesting that other factors are involved.

Hyperthermic sensitivity and cholesterol levels of mammalian cell lines in culture
Soejima, S., K. Hidaka, et al. (1991), Cancer Lett 60(2): 159-67.
Abstract: In this study, we asked whether cholesterol contents were specifically correlated with cellular sensitivity to hyperthermia. To examine this possibility, we employed two isogenic mammalian cell lines, Chinese hamster V79 cell line and its amphotericin B-resistant (AMBr) cell line. AMBr cells had a decreased content of membrane sterols in comparison with V79 cells. Clonogenic assays showed that AMBr cells were more sensitive to hyperthermic treatment at 45 degrees C than V79 cells. Cholesterol contents were increased in AMBr cells by exposure to liposomes containing 1:1 lecithin-cholesterol, and the sterol level was comparable to that of V79 cells. In comparison with untreated AMBr cells, AMBr cells were more resistant to hyperthermia at 45 degrees C when incubated with liposomes containing cholesterol. Treatment of V79 cells with oxygenated sterol, a potent inhibitor of endogeneous sterol synthesis, sensitized the hyperthermic cytotoxicity. Our present data present the hypothesis that cellular cholesterol contents are closely correlated with cellular heat toxicity.

Hypertriglyceridaemia and its influence on low density lipoprotein regulation of cellular cholesterol synthesis: a comparison between hypertriglyceridaemic diabetic and non-diabetic patients
Owens, D., J. Stinson, et al. (1991), Diabet Med 8(8): 745-51.
Abstract: The present investigation was undertaken to examine the relationship between serum triglyceride and composition of lipoprotein. Six groups of patients were examined, three with Type 2 (non-insulin-dependent) diabetes and three without diabetes. The groups were further categorized on the basis of their serum cholesterol and triglyceride levels into normocholesterolaemic (serum cholesterol less than 6.5 mmol l-1) and hypercholesterolaemic (serum cholesterol greater than 6.5 mmol l-1) with and without hypertriglyceridaemia (serum triglyceride greater than or less than 3.5 mmol l-1). Low density lipoprotein (LDL) composition was determined and regulation of cholesterol synthesis by LDL was assessed by measuring its effect on 14C-acetate incorporation into mononuclear leucocyte cholesterol. LDL from the hypercholesterolaemic diabetic patients had a significantly higher esterified cholesterol content when the patients were normotriglyceridaemic (1.14 +/- 0.04 vs 0.76 +/- 0.04 g g-1; p less than 0.01). The ability of LDL to suppress cholesterol synthesis (percent inhibition) was significantly less using LDL from the normocholesterolaemic diabetic patients or hypercholesterolaemic non-diabetic or diabetic patients compared with LDL from the normocholesterolaemic non-diabetic control subjects (47.4 +/- 3.9%, 39.1 +/- 5.1% and 35.2 +/- 4.1% vs 59.5 +/- 1.2%, p less than 0.01). However, hypertriglyceridaemia had no effect on LDL suppression of cholesterol synthesis. We conclude that hypertriglyceridaemia alters LDL composition but the alteration is not associated with the ability of LDL to regulate cholesterol synthesis.

Hypertriglyceridemia and low HDL cholesterol in Japanese patients with NIDDM
Okubo, M. and T. Murase (1996), Diabetes 45 Suppl 3: S123-5.
Abstract: Diabetes is frequently associated with the combination of hypertriglyceridemia and low HDL cholesterol level, a known risk factor for cardiovascular disease. We evaluated the frequency of elevated serum triglyceride and the reduced HDL cholesterol levels in Japanese male NIDDM patients. Hypertriglyceridemia (>1.69 mmol/l) and low HDL cholesterol level (<0.91 mmol/l) were frequently found in Japanese male (NIDDM patients (30.4 and 14.2%, respectively). The combined abnormality, i.e., hypertriglyceridemia with concomitant low HDL cholesterol level, was more common in patients with poor glycemic control. We observed that inpatient diet therapy markedly reduced serum triglyceride but serum HDL cholesterol did not change significantly. This is in marked contrast to primary hypertriglyceridemia, in which HDL cholesterol level generally increases in parallel with a reduction in serum triglyceride level. We discuss the defective removal of triglyceride-rich lipoproteins and ineffective HDL production caused by lipoprotein lipase (LPL) deficiency. We also discuss possible correction of this combined abnormality by certain maneuvers that increase LPL activity.

Hypertriglyceridemia and low serum HDL cholesterol are common in children after liver transplantation
Siirtola, A., T. Solakivi, et al. (2001), Transplant Proc 33(4): 2449.

Hypertriglyceridemia in lecithin-cholesterol acyltransferase-deficient mice is associated with hepatic overproduction of triglycerides, increased lipogenesis, and improved glucose tolerance
Ng, D. S., C. Xie, et al. (2004), J Biol Chem 279(9): 7636-42.
Abstract: Lecithin-cholesterol acyltransferase deficiency is frequently associated with hypertriglyceridemia (HTG) in animal models and humans. We investigated the mechanism of HTG in the ldlr-/- x lcat-/- (double knockout (dko)) mice using the ldlr-/- x lcat+/+ (knock-out (ko)) littermates as control. Mean fasting triglyceride (TG) levels in the dko mice were elevated 1.75-fold compared with their controls (p < 0.002). Both the very low density lipoprotein and the low density lipoprotein/intermediate density lipoprotein fractions separated by fast protein liquid chromatography were TG-enriched in the dko mice. In vitro lipolysis assay revealed that the dko mouse very low density lipoprotein (d < 1.019 g/ml) fraction separated by ultracentrifugation was a more efficient substrate for lipolysis by exogenous bovine lipoprotein lipase. Post-heparin lipoprotein lipase activity was reduced by 61% in the dko mice. Hepatic TG production rate, determined after intravenous Triton WR1339 injection, was increased 8-fold in the dko mice. Hepatic mRNA levels of sterol regulatory element binding protein-1 (srebp-1) and its target genes acetyl-CoA carboxylase-1 (acc-1), fatty acid synthase (fas), and stearoyl-CoA desaturase-1 (scd-1) were significantly elevated in the dko mice compared with the ko control. The hepatic mRNA levels of LXRalpha (lxralpha) and its target genes including angiopoietin-like protein 3 (angptl-3) in the dko mice were unchanged. Fasting glucose and insulin levels were reduced by 31 and 42%, respectively in the dko mice, in conjunction with a 49% reduction in hepatic pepck-1 mRNA (p = 0.014). Both the HTG and the improved fasting glucose phenotype seen in the dko mice are at least in part attributable to an up-regulation of the hepatic srebp-1c gene.

Hypo- and hyper alphalipoproteinemia and genetic abnormalities in reverse cholesterol transport system
Matsuyama, A. and S. Yamashita (1999), Nippon Rinsho 57(12): 2729-34.
Abstract: The risk of atherosclerosis has been known to be inversely correlated with the plasma concentration of high-density lipoprotein (HDL)-cholesterol, and we now know HDL plays a protective role against atherosclerosis. The most important mechanism, by which HDL could exert their anti-atherogenic role, is certainly the removal of excess cholesterol from peripheral cells and its transport to the liver, a process commonly called "reverse cholesterol transport system". In this system, many proteins are involved, i.e., ABC1, LCAT, CETP, HTGL and SR-BI. Abnormalities of these proteins reduce the efficacy of the system, and cause abnormalities of HDL and atherosclerosis. In this paper, we review the recent findings on the molecular mechanism of reverse cholesterol transport system, and then discuss hypo- and hyperalphalipoproteinemia, which are caused by genetic abnormalities of the key players.

Hypo- and hyperalphalipoproteinemia and genetic abnormalties in reverse cholesterol transport system
Matsuyama, A. and S. Yamashita (2001), Nippon Rinsho 59 Suppl 2: 539-44.

Hypo- and hyperresponse of serum cholesterol level and low density lipoprotein production and degradation to dietary cholesterol in man
Glatz, J. F., P. R. Turner, et al. (1993), Ann N Y Acad Sci 676: 163-79.
Abstract: Serum cholesterol in man rises when cholesterol intake increases, but the extent of the elevation varies between subjects. Part of the variation between subjects is spurious and not reproducible; it is caused by random diet-independent fluctuations of serum lipid levels. Part is due to consistent metabolic differences between subjects. We have earlier found that responsiveness was associated with higher initial total and HDL cholesterol, lower habitual cholesterol consumption, and lower body mass index, and unrelated to gender, age, or apo E phenotype. We have now investigated the metabolic basis of variability by measuring turnover rates of low density lipoprotein (LDL) apolipoprotein B (apo B) on a low-cholesterol diet (140 mg/day) and a high-cholesterol diet (900 mg/day) in 8 volunteers with well-defined differences in the responsiveness of their serum cholesterol to diet. Autologous 125I-LDL was injected on day 23 of each diet period. Its fractional catabolic rate (FCR) was estimated from the ratio of 125I in urine over that in plasma, seven days after injection. FCR (mean +/- SD) increased from 0.24 +/- 0.02 pools/day on the low- to 0.31 +/- 0.20 on the high-cholesterol diet. LDL-apo B concentration rose from 49 +/- 13 to 63 +/- 12 mg/dl, and LDL-apo B production rate, calculated as FCR x concentration/body weight, from 4.8 +/- 1.2 to 8.0 +/- 1.4 mg/kg/day. The individual rise in production rate was significantly correlated with the rise in the serum concentration of LDL-apo B (r = 0.90) or LDL-cholesterol (r = 0.75), and also with the rise in total serum cholesterol measured in these same subjects in similar experiments 3-4 years earlier (r = 0.74). Degradation of LDL by freshly isolated blood mononuclear cells and by mononuclear cells incubated for 72 h in lipoprotein-deficient medium (derepressed cells) was measured on both diets in these and in additional volunteers. The rate of degradation (mean +/- SD) of standard human LDL by fresh cells was 336 +/- 166 ng LDL protein/mg cell protein per 8 h on the low-cholesterol diet, and decreased by 147 +/- 180 ng/mg per 8 h or 44% on the high-cholesterol diet (n = 23, p < 0.01). The catabolic activity of derepressed cells obtained when subjects were on the low-cholesterol diet was negatively related to the LDL cholesterol response (r = -0.57, n = 18, p < 0.05), and to the total cholesterol response in earlier experiments (r = -0.45, n = 18, p < 0.10).(ABSTRACT TRUNCATED AT 400 WORDS)

Hypoantigenic (HA) milk formula and blood cholesterol level in infants at 3 months of age
Savino, F., R. Oggero, et al. (1997), Acta Paediatr 86(9): 1003-5.
Abstract: A preliminary observation is reported concerning total and high-density lipoprotein blood cholesterol levels in 36 infants at 3 months of age fed with a hypoantigenic milk formula. The values are compared with those of 66 breastfed and 76 conventional formula-fed infants. Total and high-density lipoprotein-cholesterol levels in hypoantigenic formula-fed infants (152 and 65.7 mg dl(-1), respectively) were comparable to those of breastfed infants (148 and 61.8 mg dl(-1)) and significantly (p < 0.05) higher than those of conventional formula-fed infants (130 and 42.5 mg dl(-1)).

Hypochlorite modification of high density lipoprotein: effects on cholesterol efflux from J774 macrophages
Bergt, C., H. Reicher, et al. (1999), FEBS Lett 452(3): 295-300.
Abstract: The present study was aimed at investigating effects of hypochlorite (HOCl) modification of high density lipoproteins subclass 3 (HDL3) on their ability for cellular cholesterol removal from permanent J774 macrophages. Our findings indicate that HOCl (added as reagent or generated enzymatically by the myeloperoxidase/H2O2/Cl- system) damages apolipoprotein A-I, the major protein component of HDL3. Fatty acid analysis of native and HOCl-modified HDL3 revealed that unsaturated fatty acids in both major lipid subclasses (phospholipids and cholesteryl esters) are targets for HOCl attack. HOCl modification resulted in impaired HDL3-mediated cholesterol efflux from J774 cells, regardless of whether reagent or enzymatically generated HOCl was used to modify the lipoprotein. Decreased cholesterol efflux was also observed after HOCl modification of reconstituted HDL particles. Impairment of cholesterol efflux from macrophages was noticed at low and physiologically occurring HOCl concentrations.

Hypochlorite-modified (lipo)proteins are present in rabbit lesions in response to dietary cholesterol
Malle, E., G. Wag, et al. (2001), Biochem Biophys Res Commun 289(4): 894-900.
Abstract: Myeloperoxidase (MPO), a heme enzyme secreted by activated phagocytes, generates an array of oxidants proposed to play critical roles in host defense, tissues damage, and foam cell formation. Although neutrophils are the major source for MPO, the enzyme could be identified abundantly in circulating monocytes and monocytes/macrophages in rabbit lesions. MPO is the only enzyme known to generate hypochlorous acid (HOCl) and HOCl-modified lipoproteins have pronounced atherogenic and/or proinflammatory features in vivo and in vitro. Using specific monoclonal antibodies, HOCl-modified (lipo)proteins were detected in atherosclerotic plaques of heterozygous Watanabe heritable hyperlipidemic rabbits and to a lesser extent in a specific strain of New Zealand White rabbits with a high atherosclerotic response to hypercholesterolemia. Colocalization of immunoreactive MPO and HOCl-modified-epitopes in serial sections of rabbit lesions provides convincing evidence for MPO-H2O2-chloride system-mediated oxidation of (lipo)proteins under in vivo conditions. We propose that monocyte-derived MPO could connect chronic inflammatory conditions with arterial lipid/lipoprotein deposition during diet-induced atherogenesis in rabbits.

Hypochlorite-modified high density lipoprotein, a high affinity ligand to scavenger receptor class B, type I, impairs high density lipoprotein-dependent selective lipid uptake and reverse cholesterol transport
Marsche, G., A. Hammer, et al. (2002), J Biol Chem 277(35): 32172-9.
Abstract: Hypochlorous acid/hypochlorite (HOCl/OCl(-)), a potent oxidant generated in vivo by the myeloperoxidase-H(2)O(2)-chloride system of activated phagocytes, alters the physiological properties of high density lipoprotein (HDL) by generating a proatherogenic lipoprotein particle. On endothelial cells lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) and scavenger receptor class B, type I (SR-BI), act in concert by mediating the holoparticle of and selective cholesteryl ester uptake from HOCl-HDL. We therefore investigated the ligand specificity of HOCl-HDL to SR-BI-overexpressing Chinese hamster ovary cells. Binding of HOCl-HDL was saturable, and the degree of HOCl modification was the determining factor for increased binding affinity to SR-BI. Competition experiments further confirmed that HOCl-HDL binds with increased affinity to the same or overlapping domain(s) of SR-BI as does native HDL. Furthermore, SR-BI-mediated selective HDL-cholesteryl ester association as well as time- and concentration-dependent cholesterol efflux from SR-BI overexpressing Chinese hamster ovary cells were, depending on the degree of HOCl modification of HDL, markedly impaired. The most significant findings of this study were that the presence of very low concentrations of HOCl-HDL severely impaired SR-BI-mediated bidirectional cholesterol flux mediated by native HDL. The colocalization of immunoreactive HOCl-modified epitopes with apolipoprotein A-I along with deposits of lipids in serial sections of human atheroma shown here indicates that the myeloperoxidase-H(2)O(2)-halide system contributes to oxidative damage of HDL in vivo.

Hypochlorous acid-mediated modification of cholesterol and phospholipid: analysis of reaction products by gas chromatography-mass spectrometry
van den Berg, J. J., C. C. Winterbourn, et al. (1993), J Lipid Res 34(11): 2005-12.
Abstract: Oxidative modification of membrane lipids by hypochlorous acid could be an important element in the mechanism of membrane disruption by activated neutrophils. We have previously shown that hypochlorous acid reacts with unsaturated fatty acids of membrane phospholipids to give fatty acid chlorohydrins (Winterbourn et al. 1992. Arch. Biochem. Biophys. 296: 547-555). In the present study, we examined the reaction of cholesterol in bilayers with an inert phospholipid carrier. Product separation and identification was performed using gas chromatography-mass spectrometry after trimethylsilyl-derivatization. Unlike the reaction of hypochlorous acid with unsaturated fatty acids, no chlorohydrin derivatives were found with cholesterol. Instead, the main oxidation products were identified as the epimeric cholesterol 5,6-epoxides and 4-hydroxycholesterol, while several other hydroxy- and keto-derivatives were also found in smaller amounts. Analysis of the products obtained after reaction of vesicles composed of a mixture of several unsaturated phospholipid species plus cholesterol revealed that the individual fatty acids and cholesterol all exhibit comparable susceptibilities toward hypochlorous acid. Using myeloperoxidase to generate hypochlorous acid, basically the same products and product distribution were obtained. These studies show that unsaturated phospholipids and cholesterol can be profoundly modified by reaction with hypochlorous acid. This warrants further investigation to define the role of lipid modifications in neutrophil-mediated membrane disruption.

Hypocholesterolaemic effect of banana (Musa sapientum L. var. Cavendishii) pulp in the rat fed on a cholesterol-containing diet
Horigome, T., E. Sakaguchi, et al. (1992), Br J Nutr 68(1): 231-44.
Abstract: The pulp of banana fruit (Musa sapientum L. var. Cavendishii) was examined for its cholesterol-lowering effect with male rats fed on a diet containing lard (50 g/kg) and cholesterol (5 g/kg). Freeze-dried banana pulp showed a marked cholesterol-lowering effect when incorporated into a diet at the level of 300 or 500 g/kg, while the banana pulp dried in a hot-air current (65 degrees) did not. Starch and tannin prepared from banana pulp were not responsible for the cholesterol-lowering effect. The results also suggest that banana lipids did not affect the concentration of serum cholesterol. Feeding of dopamine, n-epinephrine and serotonin tended to raise the concentration of serum cholesterol. Thus, all the substances tested which were thought to be susceptible to influence by hot-air drying were unlikely to be responsible for the hypocholesterolaemic effect. However, both soluble and insoluble fibres fractionated from banana pulp had a cholesterol-lowering effect, with the exception of cellulose. It was assumed that a browning reaction undergone during hot-air drying might be related to the disappearance of the hypocholesterolaemic effect of banana pulp dried in a hot-air current. The results obtained support the conclusion that soluble and insoluble components of dietary fibre participate in the hypocholesterolaemic effect of banana pulp.

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Cholesterol Journal Articles