The conversion of cholest-5-en-3beta-ol into cholest-7-en-3beta-ol by the echinoderms Asterias rubens and Solaster papposus. (1/11)

1. The echinoderms Asterias rubens and Solaster papposus (Class Asteroidea) metabolize injected [4(-14)C]cholest-5-en-3beta-ol to produce labelled 5alpha-cholestan-3beta-ol and 5alpha-cholest-7-en-3beta-ol. 2. Conversion of 5alpha-[4(-14)C]cholestan-3beta-ol into 5alpha-cholest-7-en-3beta-ol was demonstrated in A. Rubens. 3. Incubations of A. rubens with [4(-14)C]cholest-4-en-3-one resulted in the production of labelled 5alpha-cholestan-3-one, 5alpha-cholestan-3beta-ol and 5alpha-cholest-7-en-3beta-ol. 4. [4(-14)C]Sitosterol was metabolized by A. rubens to give 5alpha-stigmastan-3beta-ol and 5alpha-stigmast-7-en-3beta-ol. 5. The significance of these results in relation to the presence of alpha7 sterols in starfish is discussed.  (+info)

A major ozonation product of cholesterol, 3beta-hydroxy-5-oxo-5,6-secocholestan-6-al, induces apoptosis in H9c2 cardiomyoblasts. (2/11)

Cholesterol, a major neutral lipid component of biological membranes and the lung epithelial lining fluids, is susceptible to oxidation by reactive oxygen and nitrogen species including ozone. The oxidation by ozone in biological environments results in the formation of 3beta-hydroxy-5-oxo-5,6-secocholestan-6-al (cholesterol secoaldehyde or CSeco, major product) along with some other minor products. Recently, CSeco has been implicated in the pathogenesis of atherosclerosis and Alzheimer's disease. In this communication, we report that CSeco induces cytotoxicity in H9c2 cardiomyoblasts with an IC(50) of 8.9+/-1.29 microM (n=6). The observed effect of CSeco at low micromolar concentrations retained several key features of apoptosis, such as changes in nuclear morphology, phosphatidylserine externalization, DNA fragmentation, and caspase 3/7 activity. Treatment of cardiomyocytes with 5 microM CSeco for 24h, for instance, resulted in 30.8+/-3.28% apoptotic and 1.8+/-1.11% of necrotic cells as against DMSO controls that only showed 1.3+/-0.33% of apoptosis and 1.6+/-0.67% of necrosis. In general, the loss of cellular viability paralleled the increased occurrence of apoptotic cells in various CSeco treatments. This study, for the first time, demonstrates the induction of apoptotic cell death in cardiomyocytes by a cholesterol ozonation product, implying a role for ozone in myocardial injury.  (+info)

Formation of cholesterol ozonolysis products in vitro and in vivo through a myeloperoxidase-dependent pathway. (3/11)

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Akt-dependent anabolic activity of natural and synthetic brassinosteroids in rat skeletal muscle cells. (4/11)

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Anabolic effect of plant brassinosteroid. (5/11)

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Polyhydroxylated steroids from the bamboo coral Isis hippuris. (6/11)

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A phytooxysterol, 28-homobrassinolide modulates rat testicular steroidogenesis in normal and diabetic rats. (7/11)

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Cytotoxic effects of secosterols and their derivatives on several cultured cells. (8/11)

The cytotoxic effects of various oxysterols on several culture cells were examined. Ozonolysis products of cholesterol, secosterols (3beta-hydroxy-5-oxo-5,6-secocholestan-6-al) and its aldolization product (3beta-hydroxy-5beta-hydroxy-B-norcholestane-6beta-carboxaldehyde) and their keto alcohol and acid derivatives, were found to have potent cytotoxic activities, as compared with major endogenous oxysterols such as 5beta,6beta-epoxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, and 25-hydroxycholesterol. Secosterols might play important roles in tissue damage and inflammation-associated diseases.  (+info)

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