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Medical Forum / General / General / June 2005Oxidation / small dense LDL
Bioorg Med Chem Lett. 2005 Jun 2;15(11):2781-2785. Related Articles, Links Decrease in the particle size of low-density lipoprotein (LDL) by oxidation. Hidaka A, Inoue K, Kutsukake S, Adachi M, Kakuta Y, Kojo S. Department of Food Science and Nutrition, Nara Women's University, Kita-Uoya, Nara 630-8506, Japan. A radical reaction of low-density lipoprotein (LDL) causes fragmentation and cross-link of apolipoprotein B-100 (apoB). LDL (50mug/ml) was subjected to the well-studied oxidation with Cu(2+) (1.67muM). The concentration of alpha-tocopherol decreased to 10% of the initial level during the first 30min. After this lag time, the conjugated diene content, as measured by absorption at 234nm, started increasing and the residual apoB at 512kDa determined by immunoblot after SDS-PAGE (sodium dodecylsulfate-polyacrylamide gel electrophoresis) was also decreased. The particle size of LDL determined by nondenaturing gradient gel electrophoresis decreased steadily during the initial 120min, when residual native apoB was only 30% of the initial level. Plasma was also oxidized with Cu(2+) (400muM). Under this condition, a clear lag time was not observed and alpha-tocopherol content, apoB, and the LDL particle size were decreased simultaneously. Based on these experiments, we propose that an oxidation reaction is involved in the formation of small dense LDL. PMID: 15911255 [PubMed - as supplied by publisher] -------------------------------------------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking I made this point on this NG more than a year ago, because one guy was saying that only small LDL was a problem, but I made the point that the free radical reactions were causing there to be more of this form. It's amazing how these "researchers" keep discovering the same things and claiming that it's something new. They don't seem to read the literature that they like to claim they are experts in. >I made this point on this NG more than a year ago, because one guy was > saying that only small LDL was a problem, but I made the point that the > free radical reactions were causing there to be more of this form. > It's amazing how these "researchers" keep discovering the same things > and claiming that it's something new. They don't seem to read the > literature that they like to claim they are experts in. you don't seem to understand the difference between: thinking it so and _prooving_ it is so. I didn't do the experiment, but it has been done. Instead of auditioning for a role on the Sopranos, perhaps you should actually do some research. I will involve typing in www.pubmed.com and then a few more words, and then hitting the enter key, but I've got a lot of confidence it you. Just keep saying to yourself, "I think I can, I think I can..." Took me about a minute to find this one: Ann Med. 2002;34(1):48-54. Susceptibility of LDL to oxidation in vitro and antioxidant capacity in familial combined hyperlipidemia: comparison of patients with different lipid phenotypes. Liu ML, Ylitalo K, Vakkilainen J, Nuotio I, Valkonen M, Lahdenpera S, Viikari J, Taskinen MR. Department of Medicine, Helsinki University Central Hospital, Finland. BACKGROUND: There is increasing evidence that oxidation of low-density lipoprotein (LDL) plays an important role in atherogenesis. AIM: To explore the LDL oxidizability and its determinants in familial combined hyperlipidemia (FCHL) patients with different phenotypes. METHOD: The study included 59 FCHL family members with different lipid phenotypes, 39 non-affected relatives, and 30 spouses as healthy controls. RESULTS: The lag time for LDL oxidation was significantly shorter in FCHL patients with different lipid phenotypes as compared to healthy controls. There were no significant differences in the propagation rate and conjugated diene formation and alpha-tocopherol content in LDL between the FCHL groups and healthy controls. Plasma concentrations of alpha-tocopherol in all FCHL patients and uric acid in FCHL patients with IIB and IV phenotypes were significantly higher than in healthy controls. Plasma total peroxyl radical trapping capacity measured (TRAPmea) and TRAPcalc tended to be higher in affected FCHL groups, but the difference was significant only for IIB phenotype. The peak LDL particle size in the combined group of FCHL patients was significantly smaller than in healthy controls. The lag time for LDL oxidation correlated significantly with LDL size both in the group of FCHL family members (r = 0.477, P<0.001) and in the healthy controls (r = 0.482, P<0.01). CONCLUSIONS: LDL from FCHL patients irrespectively of lipid phenotypes is more susceptible to oxidation in vitro than LDL from healthy controls. This increased susceptibility of LDL to oxidation in vitro seems to be attributed to the abundance of small dense LDL particles and not to the defect of antioxidant capacity in FCHL. It doesn't matter whether you are "genetically predisposed" to small LDL, so long as you stay away from unsaturated fatty acids, except in trace amounts, such as that found in coconut oil. > Took me about a minute to find this one: > [quoted text clipped - 38 lines] > LDL, so long as you stay away from unsaturated fatty acids, except in > trace amounts, such as that found in coconut oil. I'm sorry, I'm having trouble understanding your meaning. Let me try to rephrase: Independent of genetics, as long as you keep below some level of UFA, WHAT? Something good will result? There's nothing in the thread about UFA. You're introducing it here. If you had cited anything in support of whatever you were trying to say we might have figured it out. There is certainly nothing about them in the abstract you pasted in. I'm guessing that you think too much dietary UFA is bad, but what you think happens when one bite(?) of something with more than coconut oil is unknown. I expect all will agree that some level of UFA is too much, but you seem to be trying to make a statement here about a specific level. One of the benefits of consuming UFAs may be that they react with the limited serum oxidizer supply, consuming it so as to reduce the extent to which it oxidizes LDL. I could research what you stated if you had said *anything*. > Took me about a minute to find this one: A pity you didn't take a bit longer to read it and understand it. > Ann Med. 2002;34(1):48-54. > [quoted text clipped - 11 lines] > explore the LDL oxidizability and its determinants in familial combined > hyperlipidemia (FCHL) patients with different phenotypes. <snip> >CONCLUSIONS: LDL from FCHL patients irrespectively of lipid > phenotypes is more susceptible to oxidation in vitro than LDL from [quoted text clipped - 5 lines] > LDL, so long as you stay away from unsaturated fatty acids, except in > trace amounts, such as that found in coconut oil. Clearly you don't have a clue what FCHL is, or you'd realise that regardless of what they eat or don't eat they will have high LDL and greatly increased chance of death from atherosclerosis. MattLB >I didn't do the experiment, but it has been done. Instead of > auditioning for a role on the Sopranos, perhaps you should actually do > some research. I will involve typing in www.pubmed.com and then a few > more words, and then hitting the enter key, but I've got a lot of > confidence it you. Just keep saying to yourself, "I think I can, I > think I can..." I don't doubt that the experiment has been done, I doubt that you know what a single experiment means when it comes to uncover a certain biochemical mechanism. Typing random keywords into a pubmed searchbox is not any kind of achievement, even though you seem to believe it is- understanding the principles that these studies are based on and knowing what a study says and what it really does not say is an entirely different thing.. and you are very strongly lacking in that part (I just remember that SOD/age study you posted). > I made this point on this NG more than a year ago, What point? What are you referring to? Try quoting what you're commenting on. > because one guy was > saying that only small LDL was a problem, but I made the point that the > free radical reactions were causing there to be more of this form. So you're actually agreeing with him. I couldn't find the post you're referring to, but given the various names you've had and your tendency to break threads and start new ones just to reply, it's perhaps not surprising. This thread seems pertinent though: http://groups-beta.google.com/group/sci.med.nutrition/browse_frm/thread/3e781dfb 998cc67c/5e9b11766fa1a745?q=nick+small+LDL&rnum=3&hl=en#5e9b11766fa1a745 > It's amazing how these "researchers" keep discovering the same things > and claiming that it's something new. They don't seem to read the > literature that they like to claim they are experts in. At least they research things directly, rather than picking and choosing other people's work to fit their own viewpoint. You're always going on about scientific method, yet don't seem to realise that most scientific "truth" is the result of incremental increases in supporting evidence rather than one big idea. MattLB Yes, the theory of relativity is a "little thing." All the evidence points to free radical damage, in one form or another, being the root cause of "chronic disease." If I didn't see the evidence for myself, I would not have believed it. Perhaps you should remove your head from you hind quarters and take a look for yourself. I'll guess you're replying to something I said, probably this bit: " At least they research things directly, rather than picking and choosing other people's work to fit their own viewpoint. You're always going on about scientific method, yet don't seem to realise that most scientific "truth" is the result of incremental increases in supporting evidence rather than one big idea. " > Yes, the theory of relativity is a "little thing." One: it was/is a theory. If it hadn't been supported by subsequent experimental evidence/observation that's all it would be. Two: Einstein is a household name precisely because it wasn't "most" research. I thought that was rather obvious. > All the evidence points to free radical damage, in one form or another, > being the root cause of "chronic disease." If I didn't see the > evidence for myself, Where exactly did you see free radical damage causing chronic disease? > I would not have believed it. Perhaps you should > remove your head from you hind quarters and take a look for yourself. I don't actually walk on all fours. MattLB Yes, the theory of relativity is a "little thing." All the evidence points to free radical damage, in one form or another, being the root cause of "chronic disease." If I didn't see the evidence for myself, I would not have believed it. Perhaps you should remove your head from you hind quarters and take a look for yourself. |
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