Cholesterol synthesis and esterification in experimental xanthoma tissues.

Kodama, Hajime; Nagao, Yo; Arakawa, Kiyoshi; Tada, Jôji; Nohara, Nozomi

doi:10.1016/s0022-2275(20)40660-1

Cited by 10 publications

References 25 publications

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Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions

Nakajima

Ikeda

Hirata

et al. 2007

Euro J Lipid Sci & Tech

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Oxidized LDL has been obtained by incubation with copper ions (Cu‐LDL) or various kinds of cells. LDL incubated with xanthoma tissues (x‐LDL) is considered a model of in vivo oxidized LDL that has extravasated into xanthoma lesions. To investigate the mechanism of x‐LDL formation, we studied the effects of various enzyme inhibitors or antioxidants on the oxidation process of LDL. Thiobarbituric acid‐reactive substance (TBARS) levels, electrophoretic mobility and spectrophotometric pattern of the oxidized LDL were examined. Antioxidants suppressed TBARS formation in both x‐LDL and Cu‐LDL. Enzyme inhibitors inhibited TBARS levels in x‐LDL, but not in Cu‐LDL. All the enzyme inhibitors and antioxidants, except for the cyclooxygenase inhibitor, inhibited the anodic electrophoretic mobility of x‐LDL. The anodic electrophoretic mobility of Cu‐LDL was suppressed only with antioxidants. Spectrophotometry indicated that an increase in the absorbance at 240 nm was observed in Cu‐LDL, but not in x‐LDL. x‐LDL oxidation is primarily catalyzed by phospholipase A2, and subsequently generated polyunsaturated free fatty acids propagate the peroxidation. Fatty acid hydroperoxides conjugated with dienes are not synthesized in x‐LDL. On the other hand, non‐enzymatic oxidants, such as superoxide anion and hydroxyl radicals generate Cu‐LDL with diene‐conjugated fatty acid hydroperoxides.

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Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions

Nakajima

Ikeda

Hirata

et al. 2007

Euro J Lipid Sci & Tech

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Hypolipidaemic Agents in the Treatment of Xanthomata

Miller¹

1989

Pharmacology of the Skin II

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Persistence of foam cells in rabbit xanthoma after normalization of serum cholesterol level

et al. 1988

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Xanthoma was produced in diet-induced hypercholesterolemic rabbits by intradermal dextran sulfate injections. The serum cholesterol level returned to the normal range at about 10 weeks after ending the cholesterol diet. Gross observations after cessation of the cholesterol diet revealed a decrease in xanthomatous infiltrations. However, the dense foam cell infiltrations and cholesterol accumulations showed no signs of regression at even 9 months after ending the cholesterol diet. Signs of foam cell migration into the blood stream were not observed. The persistence of the xanthoma may be due to a lack of acceptors, such as high-density lipoproteins, that remove the cholesterol from the foam cells. During our 9-month observation period, some foam cells were degenerated and a few were fused with each other to transform into Touton-type giant cells. Nonfoamy histiocytes were infiltrated around these degenerating foam cells. The histiocytes may have transformed into foam cells by incorporating the lipids of the degenerated foam cells.

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Cholesterol synthesis and esterification in experimental xanthoma tissues.

Cited by 10 publications

References 25 publications

Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions

Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions

Hypolipidaemic Agents in the Treatment of Xanthomata

Persistence of foam cells in rabbit xanthoma after normalization of serum cholesterol level

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Cholesterol synthesis and esterification in experimental xanthoma tissues.

Cited by 10 publications

References 25 publications

Low‐density lipoprotein is oxidized by phospholipase A2 and lipoxygenase in xanthoma lesions

Low‐density lipoprotein is oxidized by phospholipase A2 and lipoxygenase in xanthoma lesions

Hypolipidaemic Agents in the Treatment of Xanthomata

Persistence of foam cells in rabbit xanthoma after normalization of serum cholesterol level

Contact Info

Product

Resources

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Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions

Low‐density lipoprotein is oxidized by phospholipase A₂ and lipoxygenase in xanthoma lesions